Tuesday, December 31, 2013

Women with a history of pregnancy loss are at higher risk for cardiovascular disease later

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Women with a history of pregnancy loss are at higher risk for cardiovascular disease later -

The Annals of Family Medicine published today an article detailing the research showing that women with a history of pregnancy loss are at higher risk for cardiovascular disease later in adulthood than other women, the work of doctors in the Center for primary care and prevention (PAC) at Memorial Hospital of Rhode Island.

Article "the risk of cardiovascular disease in postmenopausal women with pregnancy loss before: Initiative on women's health" derives from analysis of data from the Maternity Experiences of a sample of 77.701 women, according to Donna Parker, ScD, director of Community health and research with the PAC. Among them, 30.3 percent reported a history of miscarriage, 2.2 percent of stillbirth history, and 2.2 percent by the story of the two.

"We found that the odds adjusted for coronary heart disease in women who had a stillbirth or more was 1.27 (95 percent confidence interval (CI), which is a measure of the reliability, from 1.07 to 1.51) compared with women who had no stillbirths "says Dr. Parker. "For women with a history of miscarriage, the odds ratio was 1.19 (95 percent, 1.08 to 1.32). For women with a history of two or more miscarriages, the odds ratio was 1.18 (95 percent, 1.04 to 1.34) compared with no error. "

the researchers found no significant association of ischemic stroke and pregnancy loss, she added. The association between pregnancy loss and coronary heart disease appears to be independent of blood pressure, body mass index, waist-hip ratio and counting of white blood cells.

"These results contribute to the growing body of evidence that the metabolic, hormonal and hemostatic pathway changes associated with pregnancy loss may contribute to the development of coronary heart disease in adulthood," says Dr. Parker.

women with miscarriage history or a stillborn child should be closely monitored and receive early intervention to their primary care physician to risk factors such as diabetes, hypertension, cholesterol, obesity, smoking and diet are closely monitored and controlled.

Monday, December 30, 2013

Researchers assigned 13 National Psoriasis Foundation scholarship to study psoriasis

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Researchers assigned 13 National Psoriasis Foundation scholarship to study psoriasis -

Nearly half a million dollars given to early career physicians studying psoriatic diseases

Twelve residents and medical students each received a year, 50,000 National psoriasis Foundation scholarship to study $ psoriasis. Awards are intended to increase the number of scientists who study and treat psoriatic diseases by promoting promising doctors to devote their careers to the study of psoriasis as medical researchers.

The program pairs an early career physician with psoriatic disease researcher established to oversee their work. Learn more about the scholarship program of the Psoriasis Foundation: www.psoriasis.org/fellowships.

The National Psoriasis Foundation Medical Dermatology Fellows for 2014 are:

  • Dena Elkeeb, MD, from the University of Utah, will develop a group of pediatric study in the Utah psoriasis Initiative to assess the impact of systemic corticosteroids on physical characteristics psoriasis, its severity and the patient's overall health.
  • Aleksandra Florek, MD, from the University of Colorado Denver, will study the epidemiology of psoriatic disease and health risks, or comorbidities, and investigate issues related to treatment of psoriasis, such as cost and efficiency

the National psoriasis Foundation medical Dermatology scholarships Amgen , supported by a grant Amgen, are :.

  • Zelma Fuxench Chiesa, MD, from the University of Pennsylvania Perelman School Of Medicine, will determine the risk of major cardiovascular events in people with psoriasis and if treatment with the drug Humira (adalimumab) improves vascular inflammation. It will also study the effect of certain psoriasis treatments on the risk of skin cancer.
  • Jessica Donigan, MD, MPH, of Massachusetts General Hospital / Harvard Medical School, will evaluate why psoriasis plaques appear to be more stigmatizing than the lesions of other dermatological diseases. efficiency
  • Rivka Friedland, MD, Northwestern University, will examine the safety and systemic medications and phototherapy on psoriasis in children.
  • Dario Kivelivetch, MD, of Baylor Research Institute, will assess cardiovascular risk in people with psoriasis using coronary artery calcium scores, which are special X-ray tests that can check for early heart disease to determine its severity.
  • Davida Kornreich, MD, from Mt. Sinai Icahn School of Medicine, will analyze whether the topicals applied in different orders exchange efficiency. Kornreich also study the safety and efficacy of a moderate holistic treatment to severe plaque psoriasis.
  • Marina Li, BS, student a third year medical student at Case Western Reserve University, will examine whether reducing inflammation of the skin also reduces blood clots and other cardiovascular disease signs.
  • Forum Patel, MD, from the University of California, Davis, will identify if the glycans called complex sugars are biomarkers or biological signs psoriasis.
  • Scott Santilli, MD, University Hospital Case Medical Center, will examine the effect of systemic, or whole-body, the therapy psoriasis and its potential for regulating the cardiovascular risk in people with psoriasis.
  • Aimee Two, MD, from the University of California, San Diego, study the role of dendritic cells or pro-inflammatory cells in the immune system, in psoriasis and if hyaluronidase, an enzyme that can cause dendritic cells to move away from the skin, can be effective to stop inflammation.
  • Shaowei Wu, MD, Ph.D., Brown University, use data from two ongoing Nurses Health Studies national to study the relationship between pregnancy, menstruation, menopause and hormone use after menopause the risk of psoriatic disease.

Furthermore, the recipient Dr. Mark G. Lebwohl Medical Dermatology Fellowship , named to recognize Dr. Mark Lebwohl, president emeritus of the National Psoriasis Foundation Medical Board and a major world psoriasis experts, is

  • Emily Wicker, MD, of Rady Children's Hospital, University of California, San Diego, who will develop screening guidelines for comorbidities or risk associated health in children with psoriasis.

Sunday, December 29, 2013

CFDA approves ENMD-2076 Phase II CASI trial in breast cancer patients with triple negative

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CFDA approves ENMD-2076 Phase II CASI trial in breast cancer patients with triple negative -

CASI Pharmaceuticals, Inc. ( Nasdaq: CASI), a pharmaceutical company developing clinical stage therapies for the treatment of cancer and other diseases, today announced that the Food and Drug administration of China (CFDA) approved the company's request to conduct a clinical phase II trial in breast cancer triple negative (CSTN) patients China for its own drug candidate, ENMD-2076.

Ken K. Ren, Ph.D., CEO of CASI, commented, "CFDA approval of our application is an important and exciting step for CASI in the execution of our China and the global strategy of integrated development. TNBC our Phase II trial ENMD-2076 in the uS is on track, and we can now extend the trial in China by recruiting more patients. test data China can be combined with the data being collected in the United States, and may lead to achieve a clinical inflection point faster. in addition, China's trial will allow us to evaluate the safety and efficacy of ENMD-2076 in the Chinese population of the patient, providing the ability to meet unmet medical needs in the country. in addition, this test data can be used to support our drug registration import in China . the future "

Dr. Ren continued," our development team in Beijing works closely with our principal researcher and key opinion leaders from major oncology centers in China in preparation for the trial. We intend to conduct additional tests, it is an important part of our overall China strategy and integrated development for the development of cost-effective drugs, and to achieve our mission to make drugs safer and more efficient for patients. We look forward to the continued advancement of ENMD-2076. "

Saturday, December 28, 2013

Scientists are developing the next generation of chips bioreactor to produce functional human platelets

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Scientists are developing the next generation of chips bioreactor to produce functional human platelets -

Scientists from Brigham and Hospital (BWH) of the women developed a scalable, the next generation of platelets bioreactor to produce fully functional human platelets in vitro. The work is a major biomedical breakthrough that will contribute to the blood transfusion needs to address worldwide.

The study is published July 21, 2014 Blood .

"The ability to generate another source of functional human platelets with virtually no transmission of the disease represents a paradigm shift in how we collect platelets that can enable us to meet the needs of increasingly for blood transfusions, "said Jonathan Thon, PhD, Division of Hematology, Department of medicine at BWH, lead author of the study.

According to the researchers, more than 2.17 million units platelets from donors are transfused each year in the United States to treat patients undergoing chemotherapy, organ transplantation and surgery, and for those who need blood transfusions following a major trauma. However, growing demand, a limited life span of five days. and the risk of infection, rejection and infection were shortages of common blood platelets

"derived platelets bioreactor theoretically have several advantages over conventional platelet donors derivatives in terms of security and the use of resources, "said William Savage, MD, PhD, medical Director, blood donor Centre Kraft family at Dana-Farber Cancer Institute / Brigham and Women's Hospital, which has not contributed to the study. "An important factor that has limited our ability to compare platelet bioreactor platelet donors is inefficient increasingly wafers, a problem that slows the progress of clinical research. This study addresses this gap, while contributing to our understanding of the biology of platelets at the same time. "

blood cells such as platelets are made in the bone marrow. bioreactor-a the device that mimics a biological environment to carry a reaction on an industrial scale biologically inspired engineering applications to fully integrate the key components of the bone marrow, the modeling of both characteristics and composition of the blood. the microfluidic bioreactor wafer summarizes the characteristics such as stiffness bone marrow, the composition of the extracellular matrix, the size of microchannels, and the stability of blood flow in high-resolution microscopy of living cells to human platelets.

Application of shear forces of blood flow in the bioreactor triggered a dramatic increase in the initiation of platelet 10 percent to 0 percent, which leads to functional human platelets.

"being able to develop a device that models of successful bone marrow is an essential bridge between our understanding of physiological triggers platelet formation to support drug development and production of platelets large scale, "said study senior author Joseph Italiano, Jr., Ph.D., Division of Hematology, Department of medicine at BWH, and vascular biology Program at Boston children's Hospital.

regarding the next steps, the researchers would like to start Phase 0 / I in human clinical trials in 2017.

"the regulatory bar is set correctly for high blood products, and it is important to that we show platelet quality, function and safety over the next three years as we are likely to be recipients of these platelets ourselves at some point, "said Thon.

Friday, December 27, 2013

CRIPTO1 role in the resistance of TKI elucidated

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CRIPTO1 role in the resistance of TKI elucidated -

By Lynda Williams, first medwireNews Problem

Overexpression of CRIPTO1 may explain inhibitor intrinsic tyrosine kinase resistance (TKI) in about 10% of patients with non-small cell lung cancer (NSCLC) and receiver endothelial growth factor ( EGFR ) mutations, research indicates.

CRIPTO1 expression has been linked to the induction of epithelial cells to mesenchymal transition, the proliferation and cell migration and invasion by a CBC channel. And these biological responses are associated with resistance to targeted cancer drugs, said Giuseppe Giaccone, of Georgetown University in Washington DC, USA, and colleagues.

The researchers examined the expression of CRIPTO1 in 21 NSCLC tissue samples and found 15 expressed the protein, which also had 14 SRC phosphorylation.

Moreover, when EGFR -mutated NSCLC cell lines were engineered to express CRIPTO1, they were found to have a significantly higher value for IC TKI erlotinib and dacomitinib the lines control cells.

however, which induces the expression of CRIPTO1 in wild type EGFR cell lines had no impact on their sensitivity to TKIs. And sensitivity to cisplatin and paclitaxel did not differ significantly between cells expressing CRIPTO1 and controls, the researchers report in the Journal of Clinical Investigation .

In addition, when the researchers examined the CBC signaling pathway in NSCLC cells EGFR cell lines expressing -mutant CRIPTO1 SRC had increased mRNA and protein compared to controls, and SRC that phosphorylated AKT and MEK, while no effect was observed for wild type EGFR cell lines.

Similarly, the expression of CRIPT01 has been associated with the induction of EMT in NSCLC cell lines, especially in the mutant EGFR lines.

Finally, the researchers found that resistance to erlotinib is mediated by the CBC and the expression of CRIPTO1 may mediate its control SCR via downregulation of miR-205.

"In conclusion, we demonstrate that overexpression CRIPTO1 potentially represents a new intrinsic EGFR TKI resistance mechanism in NSCLC-host sensitizing EGFR mutations," Giaccone et al write.

"Our study suggests cotargeting EGFR and CBC as a rational approach for the potential treatment of erlotinib-resistant, positive CRIPTO1, mutated NSCLC patients EGFR."

of medwireNews license with permission of Springer Healthcare Ltd. © Springer Healthcare Ltd. All rights reserved. None of these parties endorse or recommend any commercial products, services or equipment.

Thursday, December 26, 2013

Kinex receives FDA approval to begin Phase I study of KX2-391 Ointment for actinic keratosis

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Kinex receives FDA approval to begin Phase I study of KX2-391 Ointment for actinic keratosis -

Kinex Pharmaceuticals announced the receipt of an allowance by the US FDA for the Company's 391 KX2- ointment for the start of a clinical phase I study in actinic keratosis. This is the third IND in the Company to be approved by the US FDA in the last 12 months.

KX2-391 is a synthetic, orally active, highly selective inhibitor of Src tyrosine kinase signaling and tubulin polymerization. KX2-391 promotes the induction of p53, the G2 / M arrest of proliferation of the cell population and subsequent apoptosis through the stimulation of caspase-3 and cleavage of PARP. potent inhibition of the growth of human keratinocytes, and several melanoma cell lines in vitro suggests the potential clinical activity for actinic keratosis and skin tumors. In addition, KX2-391 has also been observed to inhibit T cell migration and the formation of endothelial tubules in vitro , which suggests additional potential therapeutic benefits for skin diseases such as psoriasis, wherein the condition is supported by a lymphocyte infiltration, inflammation and / or angiogenesis.

"The encouraging preclinical data for KX2-391 ointment has allowed us to progress in this clinical study. Actinic keratosis is a premalignant condition and perfectly into our portfolio in oncology," said the dr. Rudolf Kwan, Chief medical Officer of KINEX pharmaceuticals.

Kinex has authorized the use of KX2-391 for dermatological indications in the territory of Greater China to a company specializing in pharmaceutical formulations, . PharmaEssentia Corp. (Taipei, Taiwan) the scientific head of the project at PharmaEssentia, Dr. Jer Hsu said: "I congratulate our team for the successful development of the formulation of KX2-391 in collaboration with our excellent ointment collaborative partner, KINEX Pharmaceuticals. We are also leading the effort to advance this formulation for clinical indication of psoriasis in Taiwan. " KoChung Dr. Lin, CEO of PharmaEssentia said: "We are delighted to see the successful collaboration of the provision for the KX2-391 for actinic keratosis IND by the FDA. We also look forward to ask for a Taiwan IND for KX2-391 ointment and the launch of our clinical development program for psoriasis in Taiwan. our collaboration with Kinex has been rewarding and we will use our collective drive to bring KX2-391 ointment clinical Asia quickly. "

KX2-391 is being developed as an oral agent for oncology indications and has been tested in four clinical studies to date. In defining its pharmacological activity in tumor cells , both in vitro and in vivo , KX2-391 showed potent activity against a broad range of solid tumors as well as leukemia cell lines, including lines cell resistant to anticancer drugs currently used. Kinex also collaborated with Hanmi Pharmaceuticals (Seoul, Korea) to develop the oral formulation of KX2-391 for oncology indications in Korea and China Territory. in partnership with Hanmi Pharmaceuticals, the safety, tolerability and pharmacokinetics of KX2-391 were studied in 0 patients in both solid and liquid tumors. a study of KX2-391 in combination with paclitaxel is currently being conducted in South Korea and sponsored by the collaboration with hanmi Pharmaceuticals.

Dr. Chan Wing Kai, Head of Clinical Operations for Asia-Pacific for Kinex, said: "The ability to develop new topical formulation of KX2-391 for hyper-proliferative skin diseases shows how Kinex is actually built a pipeline of drug candidates. I look forward to working with our partner PharmaEssentia to initiate clinical trials of KX2-391 ointment for psoriasis, and KX2-391 orally for leukemia and other cancer indications . "

Tuesday, December 24, 2013

adaptive response randomization approach can boost patient participation in medical studies

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adaptive response randomization approach can boost patient participation in medical studies -

This is a classic Catch-22: Medical researchers need to understand if a promising new treatment really is better than a current, assigning random half of a group of patients for each treatment.

But when they approach patients to take part in the study, 50-50 random odds don 't seem quite right - and the study struggles to get enough volunteers. This slows efforts to improve the treatment of this condition.

Now new research shows the promise of an approach that takes part of the "random" process, while preserving the ability to compare treatments.

instead of all patients to get treatment chosen at random, the approach adjusts the chances that the study goes. So if the first results show that one of the two treatments seem to work better, the chances of this increase in processing each new patient. He called adaptive or RAR response randomization.

In a new brief report in the journal Stroke , University of Michigan Medical School researchers report the results of how 418 patients Emergency services responded to the two approaches to education medical.

researchers asked the patients to imagine they had just suffered a stroke, they showed a video describing a study that needed to stroke patients, and asked them if they would volunteer for this study if they had really just had a stroke.

that patients did not know is that half of them had been shown a random video describes a classic randomized, and half had seen the same video but with an added section explaining that if the treatment seems to work better in patients earlier, their chances of getting it improve.

Only 54 percent of those shown the first video said they volunteered for the study. But 67 percent of those RAR showed the video said they would register.

If the results play in studies of emergency real time, that difference of 13 points could make a big difference in the pace of medical research, says William Meurer, MD, MS, the doctor of emergency UM who led the study.

"While this is a hypothetical scenario, it shows that we could increase recruitment for the study of acute stroke using an adaptive response randomization design," he said. "This could be particularly important in emergencies, when patients or their relatives have a few minutes to consider the options."

The new study has already led to new research that will focus on understanding the explanation of the patients their chances of getting a treatment over another

.

at the same time, a clinical trial network based UM for emergency brain has already started using the RAR approach in some studies. The network, called NETT for neurological tests emergency treatment, is a laboratory for adaptive designs (many using RAR) through a project called Adaptive Designs Accelerate promising trials on treatments (ADAPT-IT).

The main challenge to RAR studies is to ensure that researchers collect sufficient data on each treatment to make their statistical reliability -. that is, to be able to say with certainty that the treatment differences are real and not due to chance

Meurer notes that RAR approach in a study comparing the two treatments can benefit the patients most, but poses a greater challenge for researchers. Using a RAR approach in a study comparing three (or more) options, so that the least effective of the three gets used unless the study is continuing, present an opportunity to improve patient outcomes in the test and learn more effectively.

other adaptive approaches to randomization, as a study of breast cancer where patients are randomized differently depending on the specific characteristics of their cancer, are also beginning to use.

Meurer and UM emergency physician and chair William Barsan NETT, MD, helped colleagues at UM design clinical studies where randomization adapts according to various criteria, including the seriousness of the illness of a patient. They also raised clinical trials researchers what they think of the RAR approach.

Barsan says: "We believe that the use of RAR approach is very attractive in our network, which we treat patients with life-threatening neurological emergencies such as stroke and head trauma . Knowing that more patients receive the most effective treatment seems like the right thing to do. "

Conducting a study RAR no longer requires infrastructure and preparation for researchers, Meurer said - for example, instead of just make up an equal number of treatment packages when the study begins, the research team must prepare a number of packages containing the option that works best increase

It is also important to keep the doctor. " blinded "to which option they give each patient, so they do not bias the study.

Monday, December 23, 2013

Alaska being hit hard with penalties of infection in hospital

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Alaska being hit hard with penalties of infection in hospital -

Moreover, the utility of medical marijuana in the treatment of pain is reset in question after lawmakers from New York legalized.

Kaiser Health News: Medicare penalties for hospital infections Alaska Hit Hard
the four largest Alaskan hospitals are facing Medicare payment penalties for the quality of their care. Providence, regional Alaska, Alaska Native Medical Center and Fairbanks Memorial are all in the bottom 25 percent nationwide for the number of infections and serious complications patients receive in their hospitals, according to data analyzed by Kaiser Health News . The sanctions are part of a focus on the quality of care that is included in the Affordable Care Act (Feidt, 6/27)

The New York Times :. Prescriptions for politicians Marijuana Doctors Defy and data
moved to New York last week to join 22 states in legalizing medical marijuana for patients with a wide range of debilitating diseases, including epilepsy and cancer, Crohn's disease and Parkinson's disease. Yet there is no rigorous scientific evidence that marijuana effectively treats the symptoms of most diseases where states have authorized its use. Instead, experts say, lawmakers and authors of public referenda have acted largely on the basis of animal studies and heartbreaking stories. The results have sometimes confused the doctors and researchers (Saint Louis, 6/26).


http://www.kaiserhealthnews.org This article has been reprinted kaiserhealthnews.org with permission from the Henry J. Kaiser Family Foundation. Kaiser Health News, an editorially independent news service, is a program of the Kaiser Family Foundation, a professional health policy research non-partisan organization affiliated with Kaiser Permanente.

Sunday, December 22, 2013

Chesapeake Urology this $ 114.248 in Urology Care Foundation for Research on Cancer of the prostate

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Chesapeake Urology this $ 114.248 in Urology Care Foundation for Research on Cancer of the prostate -

With the continued support of research on prostate cancer Sanford Siegel, MD, president and CEO of Chesapeake Urology Associates, presented the Urology care Foundation with a check for $ 114,248 to support its research efforts on prostate cancer. The funds raised by the Zero Prostate Cancer Challenge (ZPCC) 10K / 5K race in September 2013, were presented at the annual meeting of the AUA in Orlando, Florida, May 16, 2014. The Urology Care Foundation is the official foundation of the American Urological Association (AUA) -an organization of approximately 20,000 urologists.

Chesapeake Urology Associates, a leading promoter for the advancement of research on critical prostate cancer, is proud to sponsor the prostate Fund Chesapeake Urology at the Urology Care Foundation and, to date, raised almost $ 00,000 through its fundraising efforts to benefit research on prostate cancer, education, and free screenings for men across the Greater Baltimore. Chesapeake Urology expects to meet its goal of $ 1 million endowment fund prostate in 2015.

"Prostate cancer takes the lives of more than 30,000 men each year," says Dr. Siegel. "In because of this staggering statistic, Chesapeake Urology remains determined to end prostate cancer by helping to find a cure through support of advanced research and free screening programs. "

at the support of this commitment, Chesapeake Urology created the Great prostate cancer Challenge® (GPCC) in 07, a fundraising only focused on the research initiative on prostate cancer awareness and free screenings for men in need. It is the only program of awareness and raising funds based doctor in the country and has been adopted by 40 urology practices in 36 cities since its inception. in 2013, the Great prostate cancer Challenge has become the prostate cancer ZERO Challenge to create greater awareness of cancer of the prostate and the nonprofit ZERO-the end of prostate cancer.

ZERO Prostate Cancer Challenge 5K annual run / 1 Mile Fun Walk

The collection of funds ZERO cancer of prostate Challenge efforts are focused around an annual 5K / 1 Mile Fun Walk every September during the National prostate cancer awareness Month. This event, as well as other events throughout the year, including the Great Prostate Cancer Challenge Baltimore Golf Classic, which teamed up with LPGA Tour players to help in the fight against prostate cancer generates financial support to help end prostate cancer through research. Since its inception, Chesapeake Urology physicians and staff, patients and families, and friends of ZPCC have raised more than $ 2 million to Baltimore to help find a cure and awareness of prostate cancer. Funds from the ZERO Prostate Challenge cancer are given to non-profit organizations, ZERO-The Project to End Prostate Cancer and Urology Care Foundation in an effort to advance research on prostate cancer with hope of one day finding a cure for the devastating disease.

the free prostate cancer test for men in need

Part of the money raised from the ZPCC also remain local, finance a number of free screenings for prostate cancer every year in the Baltimore Metro. The locations of screening events are carefully selected and maintained in areas with an underserved population. Since African-American men have a 60 percent greater risk of this disease, partners Chesapeake Urology with many African-American churches in the Baltimore and Chesapeake doctors and volunteers Urology staff their time and expertise to these health events. To date, Chesapeake Urology examined more than 4,000 men in this program.

Saturday, December 21, 2013

Study examines the prevalence of HPV screening methods in developing countries

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Study examines the prevalence of HPV screening methods in developing countries -

health screens for carcinogenic HPV infections like can be difficult in developing countries where living in rural areas can result in limited access to health services. A new study from the University of Alabama at Birmingham examined the prevalence of high-risk HPV in Nepal, and finds that a method of screening for it can be effective.

Almost all cases of cervical cancer are believed to be caused by HPV infection. Of the more than 270,000 deaths due to cervical cancer each year, about 85 percent are in developing countries, according to the World Health Organization. The incidence of cervical cancer in Nepal is 24.2 per 100 000, making Nepal a country with one of the highest rates of cervical cancer in South Asia.

Sadeep Shrestha, Professor Ph.D., associated with the Department of Epidemiology, is the lead author of the new study published in PLoS ONE that investigated the prevalence of HPV screening methods in a remote district called Accham Far western Nepal.

in a camp for a healthy day conducted in Nepal Fertility Care Center, including the main contributor Pema Lhaki, Shrestha team gathered samples collected clinicians, as well as cervical specimens self-collected . This was done to determine if samples of HPV self-collected specimens were comparable to clinicians collected as a form of screening for women with formal education little or no. Study first author Derek Johnson, a doctoral student in the Department of Epidemiology, stayed in Nepal for 18 months to help lead the study.

"We have learned that even in a remote area among illiterate women, collected self samples for HPV and cervical cancer screening is possible," said Shrestha. "The most of the participants had never visited a medical center, and thus an effective sampling plan will be necessary for cancer screening for HPV / cervical. "

Shrestha said their study determined the high risk of prevalence, meaning the -causing cancer, HPV was 9.6 percent in women who took part in a day camp, and at least 25 percent had abnormal cytology.

"We realized that many other women could not attend the camp health because of the distance to the camp, the potential health problems or even because of cultural taboo," said Shrestha. . "Because of these factors, we believe that the HPV prevalence in our study is an underestimation This region has a high prevalence of HIV, and therefore we believe that this area could also have a high prevalence of HPV, but several camps and creative designs to include women will be needed to prove it. "

Shrestha said a limited budget means a limited sample size. However, it was the first HPV and cytology study conducted in a rural population in Nepal, so the results should be considered useful.

"The model to the screening of projects in existing health camps, associated with self-sampling approach to HPV, would benefit the Nepalese government with its comprehensive screening plans," said Shrestha.

infrastructure for HPV testing in Nepal is not fully developed, said Shrestha. These samples were tested in the US, but Shrestha would like to see the development of better facilities for local trials Nepal to help improve the sustainability of routine HPV testing in the future.

Friday, December 20, 2013

MRCC elderly patients should not be excluded from the targeted therapy option

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MRCC elderly patients should not be excluded from the targeted therapy option -

By Sarah Pritchard, medwireNews Reporter

Advanced age is not a due to prevent patients from receiving vascular endothelial growth factor (VEGF) -targeted therapy for metastatic renal cell carcinoma (mRCC), the results show the study of a population of mixed age patients.

Not only the median duration of treatment, overall response rates and comparable overall survival among those aged 75 years and above compared to their younger counterparts, but after adjusting the data for poor prognostic factors, older had no association with poor survival.

The study cohort included 1381 MRCC patients, of which 144 were aged 75 years or more. The most common initial treatment given to these seniors was sunitinib followed by sorafenib, bevacizumab and AZD2171 (cediranib). There was no significant difference in the distribution of risk groups - defined using the Heng Journal of Clinical Oncology 09 prognostic factors -. By age

Indeed, the main differences between basic people aged 75 and older and younger patients were less nephrectomies and brain metastases in the elderly population, notes Daniel Heng, the University of Calgary in Alberta, Canada, and the team.

The median duration of treatment was similar regardless of age, 5.5 and 7.5 months for the older and younger groups, respectively. Similarly, the overall response and median survival was also similar, with a respective 18% against 25%, and 16.8 months versus19.7

Data Heng and colleagues adjusted for factors poor prognosis known :. Levels below the lower limit of hemoglobin normal, Karnofsky performance status of less than 80%, a corrected serum calcium level higher than the upper limit of normal, increased serum neutrophils and platelets, and less than one year from the time of diagnosis and treatment of RCC.

the results of the multivariate analysis showed no association between the age of 75 years and the duration of treatment or overall survival ,, reported the research team.

These results are in contrast to the idea that elderly patients with RCC also present with comorbid conditions such as hypertension, diabetes, cardiovascular and cerebrovascular disease and other respiratory diseases, the researchers write in genitourinary Cancer clinic .

"because of these comorbidities related to age, it is believed that treatment may not be well tolerated," they added, suggesting that the use of targeted therapy in elderly patients RCC warrants further study.

medwireNews licensed by permission of Springer Healthcare Ltd. © Springer Healthcare Ltd. All rights reserved. None of these parties endorse or recommend any commercial products, services or equipment.

Thursday, December 19, 2013

lung cancer patients could benefit from a new technology 'QTA'

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lung cancer patients could benefit from a new technology 'QTA' -

Lung cancer patients could benefit from a more precise treatment, and their progress can be better monitored, using a new method of high noninvasive imaging medical analysis technology, according to a study published today by the newspaper PLOS oNE .

genetic changes increasingly are recognized as driving the development of cancer. But obtaining evidence of such changes usually requires a biopsy, which can be problematic for sensitive areas of the body such as the lungs.

Based on a review of 48 cancer patients with non-small cell lung cancer (NSCLC), the study found that, by scanning their tumor cells using "based CT analysis quantitative texture "(QTA), researchers were able to determine - with almost 0 percent accuracy. - if the patient's tumor had a mutated K-ras gene causing cancer

study was conducted by researchers from the Institute of translational genomics research (TGen), Virginia G. Piper Cancer Center at Scottsdale Healthcare and Cancer Treatment Centers of America (CTCA).

NSCLC accounts for over 85 percent of all lung cancers, which kill about 159,000 Americans this year, making it the leading cause of cancer deaths. It has a survival rate five years to less than 10 percent

QTA has been shown to be accurate. - and non-invasive - alternative to surgical biopsy and other invasive ways of collecting and analyzing biological samples, the study said. This method of genomic distinctions can help physicians determine the best type of treatment to be administered to each patient.

"The ability to quickly and non-invasively characterize NSCLC tumors would be a great asset to clinical oncologists," said Dr. Glen Weiss, lead author of the study, Director of Clinical Research and oncologist medical at cancer Treatment Centers of Western Regional medical center of America in Phoenix, and clinical Associate Professor in the Division of cancer TGen and cell biology.

"QTA applied to molecularly case NSCLC is defined to have a broader precision medicine by providing a non-invasive application identify the best therapies for each patient, "said Dr. Weiss.

Dr. Ronald Korn, medical director of Virginia G. Piper Cancer Center Scottsdale Healthcare and lead author of the study, QTA described as an important step forward in the use of medical imaging: "Characterization non-invasive molecular characteristics of the tumor may improve the management of not. -invasive QTA treatment can differentiate the presence of the K-ras mutation pan-wild-type NSCLC. "

Dr. Korn is also head Executive and medical Director of imaging Endpoints, an important central imaging laboratory that provides centralized image management and advanced image interpretation for clinical trials. Thanks to Scottsdale Healthcare Research Institute, in collaboration with Imaging Endpoints central laboratory, this team has developed one of the only global radiology research laboratories specializing in the early detection and evaluation of the response (also known as the RADAR program).

"Although further studies are necessary to advance our RADAR program forward in routine medical practice, our basic laboratory remains focused on the characterization of tumors noninvasively through imaging and use of these technologies to help determine as soon as possible if the cancer treatments are working, sometimes within days to weeks after starting treatment, "said Dr. Korn.

Dr. Weiss said that future studies using QTA could also help identify other genomic subtypes of NSCLC.

Wednesday, December 18, 2013

IRF4 transcription factor plays a key role in brown fat thermogenic process

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IRF4 transcription factor plays a key role in brown fat thermogenic process -

The body contains two types of fat cells, easily distinguished by color: white and brown. While white fat is used to store excess calories until they are needed by the body, brown fat cells actually burn fat by converting it into heat. Since it was discovered that adult humans are home to substantial amounts of brown fat, the investigators worked to better understand its burning properties thermogenic fat with the ultimate goal of developing new therapies to fight against obesity and diabetes.

Now, research conducted by researchers at Beth Israel Medical Center Deaconess (BIDMC) adds another piece to the puzzle, which shows that the IRF4 transcription factor (factor regulating interferon 4) plays a key role in brown fat thermogenic process, regulation of energy expenditure and cold tolerance. The findings appear in the July 3 issue of the journal cell .

"The discovery several years ago that brown fat is active in metabolism suggested that if we could handle the number or activity of these fat cells, we could force our body to burn extra calories, "says lead author Evan Rosen study, MD, PhD, an investigator in the Division of endocrinology, diabetes and metabolism at BIDMC and Associate Professor of medicine at Harvard medical School." Now that we have identified an important factor driving this process, we can consider new approaches to exploit this for therapeutic benefit. "

Excited by cold temperatures and certain hormones and drugs, including epinephrine, brown fat generates heat through the actions of a group of genes collectively, the gene expression program thermogenic, best known coding for uncoupling protein 1 (UCP1). UCP1 dissipates, or waste, energy in the mitochondria of brown fat cells, which causes the generation of heat as a byproduct.

"It has been a keen interest in how the UCP1 gene is regulated, with most attention focused on a molecule called PGC1-alpha," says Rosen. " PGC1-alpha was discovered 15 years ago in the laboratory of co-author Bruce Spiegelman, and is a transcriptional co-factor, which means it indirectly leads to gene transcription as UCP1 because he does has not the ability to bind to DNA itself. This suggests that there must be a bona fide transcription factor, or protein binding to DNA, which has been mediating the effects of PGC-1alpha, but despite years of work and several candidates promising no clear partner to PGC-1alpha was found to increase thermogenesis. It happens that IRF4 is that partner. "

interferon regulatory factor (IRF) play an important role in regulating the immune system. The Rosen Group had already identified IRF4 as a key element in the development of adipocytes and handling of lipids, having discovered that the expression of IRF4 is induced by fasting in fat and that animals lacking IRF4 in adipose tissue are obese, insulin resistant and intolerant cold.

in this new work, led by first author Xingxing Kong, PhD, a postdoctoral fellow in the Rosen lab, scientists have speculated that, in addition to serving as a key regulator of lipolysis, IRF4 could also play thermogenic direct role in brown fat.

experiments on mouse models confirmed their hypothesis, demonstrating that IRF4 is induced by cold and cAMP in adipocytes and is sufficient to promote increasing thermogenic gene expression, energy expenditure and cold tolerance. Conversely, loss of IRF4 in brown fat resulted in reduced expression thermogenic gene and energy expenditure, obesity and intolerance to cold. Finally, the researchers showed that IRF4 physically interacts with PGC-1 alpha to promote the expression of UCP1 and thermogenesis.

"We know a lot about how these genes are activated by cold or when stimulated by catelcholamine drugs such as adrenaline," says Rosen. "But we KnowWhat turned this gene program at the molecular level. This new discovery of the role of key transcription IRF4, perhaps we can identify new drug targets that directly affect this path, what could be more specific than just give epinephrine -as drugs, which lead to heart rate and blood pressure. "

Tuesday, December 17, 2013

Pseudogenes can play a key role in the discovery of new biomarkers

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Pseudogenes can play a key role in the discovery of new biomarkers -

Unfortunately, the ungrateful pseudogene.

Dysfunctional, unloved and seemingly of little use, these genes -cousin poor parents have lost their protein coding capacity. They contain non-essential equipment for the survival of the body and are the "last stop" for the disposal of waste genomics.

No more. The day of pseudogene may have arrived with scientists from the University of Texas MD Anderson Cancer Center in Houston.

Han Liang, PhD, assistant professor in the department of bioinformatics and computational biology at Cancer Center is the advancement of knowledge of these genetic quirks largely overlooked, but increasingly attractive. He and his team conducted a study that generated the pseudogene expression profiles in 2,808 patient samples from seven types of cancer. This meant analysis 378 billion RNA sequences to measure levels of expression near 10,000 pseudogenes.

The results indicated that the science of analyzing the pseudogene expression may very well play a key role in explaining how cancer occurs in assisting medical experts to discover new biomarkers. The results of the study appear in today's issue of Nature Communications.

The understanding of biomarkers is important for the development of therapies targeting specific tumor sites and to obtain new information on how patients will in various cancers and treatments. Biomarkers are molecules that can indicate the presence of a condition or disease, and are increasingly used to measure how the body reacts to therapies. The emerging field of personalized medicine is built on customizing the treatment for patients based on biomarkers.

The Liang study is new in the understanding of pseudogenes based on the analysis of large numbers of patient samples. Previous studies have been limited by the size of the sample groups of patients. Liang The team analyzed the data provided by the research program Cancer Genome Atlas. The program is supported by the National Cancer Institute and the National Human Genome Research Institute at the National Institutes of Health and is looking at genomic changes in more than 20 different types of cancer.

"The study included seven subtypes of cancer, including breast, kidney, ovarian, colon, lung and uterus," said Liang. "through cancer types, subtypes of tumors revealed by expression of pseudogene showed significant and strong similarities with subtypes defined by other molecular data."

Liang believes the study highlights the potential of analyzing the expression of pseudogene as a new "gold standard" to investigate the mechanisms of cancer and the discovery of prognostic biomarkers. These biomarkers will allow medical experts to predict more accurately rates of cancer survival.

"pseudogene expression alone can accurately classify major subtypes of endometrial cancer," said Liang. "It is striking, in renal cancer subtypes pseudogene expression not only significantly correlated with patient survival, but also help to stratify patients in combination with clinical variables."

Monday, December 16, 2013

Scientists find a new strategy for the treatment of brain cancer

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Scientists find a new strategy for the treatment of brain cancer -

Scientists at the Montreal Neurological Institute and Hospital of McGill University and Central McGill university health showed that a member of the family of proteins known as SUMO (small ubiquitin modifier) ​​is a key to why the tumor cells multiply uncontrollably, especially in the case of glioblastoma. The proteins of the SUMO family modify other proteins and SUMOylation proteins are essential for many cellular processes. Identify the role of SUMO in the growth of cancer cells lead to a new strategy for the treatment of glioblastoma.

Glioblastoma is the most common and deadly brain cancer. Current standard treatments include surgical resection, adjuvant chemotherapy and radiotherapy. Despite treatment, patients' survive about a year and a half. Cancer continues to grow, in part because of the presence of cancer stem cells. It is essential to understand the cancer growth pathways in stem cells for the development of targeted therapies stem cells.

The molecular mechanisms that control the growth of cancer through cell cycle progression, involving many proteins and many aspects of this complex process are still unknown. A group of proteins called cyclin-dependent kinases (CDKs) driving the cell cycle; Yet we do not know why cancer cells retain a large amount of CDK proteins.

"In the investigation of human glioblastoma cell cycle, we discovered that CDK6 is amended by SUMO1.CDK6 sumoylation inhibits degradation and thus stabilizes CDK6 protein in cancer," says Dr. Anita Bellail, researcher at the Montreal neurological Institute and Hospital of McGill University and the McGill University health Centre and lead author of the article published in Nature Communications . Co-authors of the study include Jeffrey J. Olson of the University's Department of neurosurgery and Emory Chunhai "Charlie" Hao, Department of pathology, Montreal neurological Institute and Hospital of McGill University and the McGill University health Centre.

"We found that sumoylation CDK6 is required for the renewal and growth of cancer stem cells in glioblastoma. inhibition of SUMO1 removes stem cells and suppresses the progression of cancer. "

Their conclusion adds concrete evidence of recent studies on ways of sumoylation in the development of cancer in humans and progression. with the new understanding of how SUMO affect the cell cycle in cancer stem cells, this group of scientists are currently screened for targeted SUMO1 new medicines for human glioblastoma treatment.

Sunday, December 15, 2013

A new study reveals unique health issues facing urban Aboriginal people in Canada

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A new study reveals unique health issues facing urban Aboriginal people in Canada -

For the first time, researchers have access to detailed information on how urban Aboriginal population in Canada uses the health care. A new study, called Our Health Counts, uses this health database to clearly demonstrate the unique challenges facing urban Aboriginal people in Canada - according to researchers at St. Michael's Hospital

the findings, published today BMJ Open , illustrate the striking disparities between urban First Nations and the general population.

researchers interviewed 554 First Nations adults in Hamilton, Ontario. - Chosen for its large indigenous population and a strong infrastructure of social and health services and Aboriginal communities. The researchers collected data on factors that influence a person's health, such as poverty, disease and income for the First Nations population of Hamilton.

"Compared to the general adult population of Hamilton, we found high utilization

emergency room, multiple barriers to health care access and high rates of chronic disease in Aboriginal adults in urban areas "said Dr. Michelle Firestone, associate researcher at the Centre of St. Michael's Hospital research Inner City Health.

over 10 percent of adult First Nations visited the emergency room six or more times in the previous two years. - only 1.6 percent of the general adult population Hamilton could say the same thing

"Hamilton extended health and social services, but 40 percent of respondents felt that their access to health care as fair or poor, "said Dr. Firestone, who holds a doctorate in public health." This shows the geography is not the only health care barrier for First nations. "

Nearly half of the respondents indicated that the long waiting lists to see a specialist was an obstacle. Other common barriers include not being able to arrange transportation; not being able to pay the direct costs or transportation; services not covered by non-insured health benefits and lack of trust in health care providers.

Over 60 percent of Aboriginal people living in Ontario live in urban areas. A growing number of First Nations are moving to urban areas to find better housing, employment opportunities and education and to available services and facilities.

The most common chronic diseases of First Nations adults Hamilton included arthritis (30.7 percent), high blood pressure (25.8 percent), asthma (19 percent) and diabetes (15.6 percent)

Among First Nations adults living in Hamilton :.

  • 73 percent of respondents reported an infection of the upper respiratory tract in the last 12 months
  • 25 percent reported having been injured in the last 12 months
  • 78 percent earn less than $ 20,000 per year
  • 70 percent live in less income areas of the city

indigenous peoples are often excluded, unidentified or under-represented in most databases of information on health in Canada. Our heads of health accusation fills this void by using health information based on respondents sampling - a research method used to recruit hidden or stigmatized populations based on participants to identify the next wave of recruits to the study. Counts our health is the first directed sampling by respondents of the member cities of First Nations in Canada.

"Our health has an important contribution to public health," said Dr. Firestone. "These data have important implications for the provision of health services, programming and policy development. It should directly inform the strategic direction and improve the health of urban Aboriginal people in Ontario."

Saturday, December 14, 2013

New chemical compound protects against blindness and diabetes in animals

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New chemical compound protects against blindness and diabetes in animals -

In a new study by UC San Francisco (UCSF) scientists, a chemical compound designed to precisely target part of a crucial cellular quality control network provided significant protection in rats and mice against the degenerative forms of blindness and diabetes.

in addition to opening a path of development of promising drugs for the wide range of diseases caused by cell loss, new research offers a new vision of how the unfolded protein response (UPR) a network "life or death" cell signaling: When cells are under stress, the UPR ensures that they produce proteins properly configured, but these cells not to this task quickly motivated by the UPR to self-destruction.

A UPR component known as the IRE1 track was generally thought to manage the protection aspects of this response, promoting cell survival by providing cells with biological resources they need to cope with stress, while an additional track, called PERK, has been associated with cell death.

But in the new research, published in July 10, 2014 edition of cell , when the researchers used KIRA6, a small kinase inhibitor molecule they designed to inhibit the actions of IRE1 alpha -the molecular sensor that triggers the way they IRE1 blocked cell death and the conserved function in two experimental models of human diseases.

in two models of retinitis pigmentosa rats, a disease in which the light sensing cells in the eye gradually die off, causing blindness, KIRA6 retained both the number of these cells and visual function. And in mice a known strain as the Akita, which carry a genetic mutation that causes diabetes in early life that the insulin producing beta cells stressed to the degeneracy of the pancreas, KIRA6 protected beta cells of cell death, leading to a two-fold increase insulin production and improved glycemic control.

"This is a huge step forward in our field," said co-senior author Scott A. Oakes, MD, Associate Professor of Pathology at UCSF. "On the surface these seem to be two diseases very different, but the cell death induced by IRE1-is at the root of both. "

the results are the culmination of a" gigantic project, "first establish that the pathway could lead a IRE1 degenerative disease, and to develop and test compounds to address the damage, said Feroz Papa UCSF, MD, PhD, associate professor of medicine and co-lead author and a member of the California Institute for quantitative Biosciences. "It took four years, more than a hundred separate experiments in various contexts, not including replications-and involved 24 researchers in seven laboratories laboratories in four cities."

KIRA6 is the latest a series of compounds (the acronym stands for "Kinase Inhibitors RNase-attenuators) that were originally designed and synthesized in the study co-authors laboratories Dustin J. Maly, PhD, associate professor of chemistry at the University of Washington, Seattle, and Bradley J. Backes, PhD, associate professor of medicine at UCSF.

"Although KIRA6 has shown efficacy in animals," said Papa, "it is important to emphasize that most optimization through medicinal chemistry effort is needed to develop this class of compounds the stage where they could be tested for efficacy in humans through clinical trials. "

Friday, December 13, 2013

Study highlights the molecular cause of cachexia, referring to a potential treatment

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Study highlights the molecular cause of cachexia, referring to a potential treatment -

New research raises the prospect of more effective treatments for cachexia, a wasting deep fat and muscles occurring in about half of cancer patients, increasing their risk of death, according to scientists at the Dana-Farber cancer Institute.

many strategies have been tried to reverse the condition, which can cause such fragility that patients can not withstand potentially life-saving treatments, but none have had great success.

scientists reporting in the July 13 advance online edition of Nature , led by Bruce Spiegelman, PhD, found that mice with lung tumors symptoms of cachexia or improved were prevented when administered an antibody that blocks the effects of PTHrP protein secreted by tumor cells. PTHrP means related protein parathyroid hormone, and is known to be released from many types of cancer cells.

The scientists said their findings are the first to explain in detail how PTHrP tumors switches on a thermogenic (heat producing) process in adipose tissue, resulting in a loss of unhealthy weight.

This protein derived from a tumor, they found, stimulated "beige" or brown fat cells mixed with white fat stored in the body, causing white fat to 'brown' - which is , generating heat and even cause weight loss when the animals were at rest

researchers conducted two experiments using mice that developed lung tumors and cachexia .. in one case, is administered a polyclonal antibody that specifically neutralizes PTHrP and found that prevents the waste almost completely, while untreated animals became slightly cachexic.

In a second experiment, treatment with the antibody prevented loss of muscle mass and improve muscle function, while the control animals developed severe muscle atrophy.

"You would have expected on the basis of our first experiments in cell culture, the blocking of PTHrP in mice reduce browning fat," said Spiegelman. "But we were surprised that it also affected the muscle loss and better health."

Research has suggested that PTHrP alone does not directly cause muscle atrophy, but blocking the activity of the protein prevents.

Thus, the role of PTHrP "is certainly not the whole answer" to the riddle of cachexia, Spiegelman noted, but perhaps a necessary part, while other factors are also involved .

a contributor to the study, Vickie E. Baracos, PhD, of the University of Alberta in Edmonton, Canada, provided that the blood of 47 lung cancer patients or colon were cachexic. Serkan Kir, PhD, Spiegelman lab - and first author on the paper -found increased levels of PTHrP in 17 patients. These patients had body mass significantly lower lean and produce more heat energy at rest than are other patients in the group.

It may be that the mechanism of PTHrP is responsible for cachexia in a subset, but not all, cancer patients, Spiegelman suggested. Before trying the anti-PTHrP antibody in human patients, he said, "clinicians probably would not know first if the protein is elevated in certain cancers, and determine which patients are good candidates for a clinical trial. "

Barrett Rollins, MD, PhD, Scientific Director of Dana-Farber, noted that the report of Spiegelman and colleagues "provides a new roadmap for development, a rational mechanistic treatment for this condition incredibly debilitating happens in so many of our patients. so far we have had no truly effective way to reverse this horrible complication. "

patients with upper gastrointestinal and pancreatic cancers are more likely to develop cachexia, and the condition affects about 80 percent of the cancer patients in the terminal phase. The current strategy is to provide appetite stimulants and nutritional supplements and drugs to counter some of the molecular pathways underlying deemed wasting process, but with limited success.

Thursday, December 12, 2013

Metvix PDT is now available at Odette Cancer Centre as an additional treatment option for patients NMSc

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Metvix PDT is now available at Odette Cancer Centre as an additional treatment option for patients NMSc -

The Odette Cancer Centre at Sunnybrook Health Sciences Centre in collaboration with Galderma Canada are announcing that Metvix PDT (photodynamic therapy), is now available at Odette cancer Centre in Toronto as an additional treatment option for patients with NMSC (nonmelanoma skin cancer). For eligible patients the positive impact of Metvix PDT can not be overestimated in precancerous AK (actinic keratoses) and superficial BCC (basal cell carcinoma) treatment.

treatment

Metvix PDT delivers precisely targeted for AK and BCC. Metvix PDT is changing the treatment of AK and BCC patients by offering preferred advantages:

  • The clinical results comparable to current standard modes of treatment
  • procedure minimally non -invasive with superior cosmetic results
  • healing can take place in as little as 7-10 days treatment is directed precisely

the Odette Cancer Centre, one of best cancer centers in the world, always offering the highest level of patient care while conducting research and world-class education in a clinical setting. Always committed to improving treatment and patient care, Odette Cancer Centre leads once again the way in providing Metvix PDT for NMSC. Instrumental to bring Metvix PDT Centre Dr. Gregory Czarnota, principal investigator and Director, Program on the Odette Cancer, Dr. Steven Babic, medical physicist, and Dr. Toni Barnes, radiation oncologist are at the forefront of this initiative marks a new area of ​​treatment Conservatory.

the Odette Cancer Centre is a 2 e the largest center of fight against cancer in Canada and the 6 e the largest center of fight against cancer in North America, ranked among a select group of world-class institutions that engage in intense research, community outreach and provide the full range of patient care.

partnership Galderma and Odette Cancer Centre reinforces the strong commitment of both parties to continue to provide the most innovative and technologically advanced treatments to improve the experience and outcomes of patients when treated for AK and Conservatory.

Wednesday, December 11, 2013

Game theory identifies the ideal time to disrupt the cooperation of metastatic cancer cells

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Game theory identifies the ideal time to disrupt the cooperation of metastatic cancer cells -

no cancer in, but the Johns Hopkins researchers borrow ideas from the evolutionary theory of games to learn how cells cooperate in a tumor to gather energy. Their experiments, they said, could identify the perfect time to disrupt the cooperation of metastatic cancer cells and make a tumor more vulnerable to anticancer drugs.

"The reality is that we can not cure metastatic cancer that has spread to his theory of organ and primary game adds to our efforts to tackle the problem," says Kenneth J. Pienta, MD Donald S. Coffey professor of urology at Johns Hopkins Brady Urological Institute and director of the prostate cancer program at the Johns Hopkins Kimmel cancer Center. A description of the work appears in 1 June 20 report in the journal focus Interface .

Game theory is a mathematical study of strategic decision making, and has been widely used to predict the conflict and cooperation between individuals and even nations, but increasingly is applied to the forecast of cell-cell interactions in biology with an ecological perspective. Tumors contain a variety of cells shift between cooperatives as competitive as the United, said Ardeshir Kianercy, Ph.D., a postdoctoral researcher in the lab of Pienta. "To study the tumor cells in isolation is not enough," he noted. "It makes sense to study their behavior and relationships with other cells and how they co-evolve together."

In their research, the Johns Hopkins scientists use mathematical and computational tools to configure game settings based on biological interactions between the two types of tumor cells, an oxygen-rich and the other poor oxygen. The cells within a tumor are engaged in various types of energy metabolism depending on how close they are to a supply of oxygen-rich blood. Tumor cells in the oxygen poor areas use the sugar glucose to produce energy and, in the process, release a compound called lactate. the oxygen-rich cells use the lactate in a different type of energy metabolism processes and consequently the release of glucose which can be used by poor cell oxygen to burn their own energy.

In general, the process is an effective partnership that can help a tumor to thrive, but the partnership is still evolving tumor cells mutate. mutation rate affect the strength of energy partnerships between cells and the levels of glucose and lactate production and the rich absorption of oxygen and low oxygen, according to scientists.

Application of the calculations of game theory that represented the tumor mutation rates of cells and glucose levels and potential lactate, scientists have found that in certain mutation rate ranges, "there a critical transitions when a tumor suddenly moved between different types of metabolic energy strategies, "said Kianercy. This switch in the playbook of tactics energy production can occur when tumors grew and spread.

Scientists believe that tumors may be particularly vulnerable in this window switching strategy, making it a potentially ideal time for clinicians to disrupt the environment and the wreck of the tumor partnership between its cells.

Some tumor cells, for example, can cause normal cells around them to release lactate for fuel. A therapy that disrupts the transport lactate to tumor cells during a critical transition "could push a tumor to a state where the cells do not cooperate with each other," said Kianercy. "And if they become uncooperative, they are more likely to stay in this state and the tumor may become more vulnerable to anti-cancer therapies."

Pienta said he did not yet know whether this type of metabolic cooperation occurs in all tumors. But the model of game theory used in the study gives scientists a new way to understand how cancers can develop. "We want ultimately to test how we can stop this process with therapies for cancer patients," he said.

Tuesday, December 10, 2013

The current guidelines are more detailed on DMP for people with breast cancer

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The current guidelines are more detailed on DMP for people with breast cancer -

The German Institute for Quality and efficiency of health care (IQWiG) published the results of a literature search for evidence of clinical practice guidelines based on the treatment of people with breast cancer. The aim of the report is to identify the recommendations of high methodological quality current guidelines that may be relevant for the planned revision of the disease management program (DMP). According to the results of the report, there is no compelling need for revision of any part of the DMP. However, IQWiG identified some aspects that could be supplemented and specified.

PGD are reviewed regularly

After being commissioned by the Joint Federal Committee (G-BA), IQWiG systematically searched for new guidelines, assessed their methodological quality, and extracted relevant recommendations of these guidelines. The next step of the recommendations have been compared with the specifications for the German DMP.

The need for revision can occur if new studies provide new evidence about a disease and its treatment. It is therefore legally specified that a DMP should be revised at regular intervals. It is the responsibility of the Institute to identify one hand the differences between guideline recommendations and the DMP. It is then the G-BA'sresponsibility to examine whether these differences should actually lead to a revision of the DMP.

guidelines identified 26 relevant

IQWiG was able to include a total of 26 guidelines in its investigation. Six of these guidelines comprehensively address the management of patients with breast cancer. September guidelines deal exclusively with early breast cancer, four other guidelines with advanced breast cancer (stage IV). The remaining nine guidelines relate to specific aspects such as radiation therapy, breast reconstruction or a systematic adjuvant treatment.

desirable supplementation

As determined IQWiG, there are several aspects of health for the recommendations of the DMP should be revised. Among other aspects, this applies to the diagnosis and measures primary therapy: The guidelines address the performance of a magnetic resonance imaging (MRI) in specific therapeutic indications, explicitly advising against routine MRI. Regarding radiation therapy for breast cancer, the guidelines provide recommendations on hypofractionated radiotherapy -. One aspect not being considered by the DMP

The process of producing the report

IQWiG published the preliminary results in the form of the preliminary report in November 2013 and interested parties were invited to submit comments. At the end of the proceedings commenting, the preliminary report was revised and sent as a final report to the commissioning agency in May 2014. The written comments submitted are published in a separate document simultaneously with the final report. The report was produced in collaboration with external experts.

Monday, December 9, 2013

The researchers receive nearly $ 3.6 million to create new national clinical trials network

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The researchers receive nearly $ 3.6 million to create new national clinical trials network -

A team of researchers, doctors at Huntsman Cancer Institute (HCI) at the University of Utah (U of U) has received nearly $ 3.6 million over the next five years in a cooperative agreement with the National Institutes of Health (NIH) to establish a charge of academic network participant website (NLAPS). The price puts HCI in an elite group of only 30 to 40 NLAPS locations nationwide; these sites are part of the NIH effort to create a new National Clinical Trials Network (NCTN).

"We are confident that HCl can be an important asset to help update the national NIH clinical trial program," said David Gaffney, MD, PhD, principal investigator. Gaffney is vice president, medical director and professor of radiation oncology at the University of U School of Medicine and an HCI investigator. "HCI will provide scientific leadership in the development and implementation of clinical trials, and access to clinical trials for patients throughout our service area in the Intermountain West five states.

"HCI strives to provide a wide range of important clinical trials for our patients. We give our world-class patient care and are working to improve cancer treatment in the future, "Gaffney said.

The NCTN will transform, consolidate and integrate the efforts of the previous National Cancer Institute (NCI) clinical trials Group of cooperation. the objectives of the new network include the development of multi-institutional clinical trials to evaluate new therapies against cancer through a wide range of people and types of cancer.

HCl, a cancer center NCI-designated, will be a key partner in the NCTN research cooperative group, according to Gaffney. "We have a successful clinical trial infrastructure already in place, and we have active research unique, including a center for NCI quantitative Imaging excellence and the Utah population database, "said Gaffney.

"Furthermore, we have several experts in all areas of cancer medicine, and our doctors and scientists to adopt a team approach to improve cancer care," said Gaffney.
HCI Center for quantitative imaging provides cancer researchers, clinicians and patients with the most advanced cancer imaging technologies, allowing the search for the best quality, disease diagnosis and monitoring therapy. the database Utah population is a powerful resource genealogical data based on the population that in many cases extends 15 generations, in connection with the scale cancer State and medical records.

"HCI is proud to direct those resources to the success of a cooperative NTCN efforts to eradicate cancer," said Gaffney.

Sunday, December 8, 2013

New York DOH grants RPCI approval to begin the genomic test patients with cancer

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New York DOH grants RPCI approval to begin the genomic test patients with cancer -

Roswell Park Cancer Institute (RPCI) Approval The New York State Department of Health (DOH) has granted to begin the genomic test cancer patients using its test OmniSeq TargetTM advanced molecular diagnostic laboratory.

testing, approved through clinical laboratory evaluation program of the DOH (CLEP), is part of a global approach developed by RPCI Centre for personalized medicine for profiling and interpretation of the genetic information contained in the tumor tissues of cancer patients. OmniSeq TargetTM is one of three tests approved for use in New York State that use next-generation sequencing, and it is the only test to exclusively target mutations in action -. These changes for which targeted therapeutic approaches exist

OmniSeq TargetTM analyzes 23 genes associated with various cancer - such as ALK, EGFR, PTEN and KRAS RNA. The use of multiple genomic broadband technologies OmniSeq TargetTM detect specific genetic mutations, translocations and copy number changes, looking for alterations and specific aberrations that indicate specific forms or targeted molecular cancer characteristics. The test uses a double sequencing platform for mutation assays, using both sequencing platforms Ion Torrent and Illumina -. One approach that has unparalleled sensitivity and positive predictive value compared to typical single platform model

"This is a test cancer of the next generation that is both comprehensive and targeted, and n 'there is no other test like the market, "says Carl Morrison, MD, DVM, executive director of the Center for personalized medicine." this focus on mutations in action is what makes our approach and what makes this test as an important tool in the therapeutic treatment. When a doctor receives the results of our back tests, they will be able to apply this new information and adjust the treatment plan decision making patient to get the appropriate targeted therapy. "

Roswell Park Cancer Institute has also developed a software system that provides clinically relevant information OmniSeq TargetTM trials in reports that are part of the electronic health records of patients, doctors to make decisions faster and more informed treatment. the cancer center plans to incorporate OmniSeq TargetTM tests in the management of many patients from the third quarter of 2014.

"This test represents a major advance in the patient care, "said RPCI President and CEO Donald L direction. Trump, MD. "For years, the promise of genomic medicine has been largely theoretical and prospective part. OmniSeq TargetTM gives us the ability to identify for many cancer patients that the therapy will be most effective for an individual, sparing patients from having to take a drug that was never going to work for them . We can expect dramatic improvements in both outcomes and patient quality of life. "

Saturday, December 7, 2013

Study finds increased microglial neuronal discharges and improve brain cell survival after injury

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Study finds increased microglial neuronal discharges and improve brain cell survival after injury -

A type of immune cell widely believed to exacerbate adult chronic brain diseases such as Alzheimer's disease and multiple sclerosis (MS), can effectively protect the brain against traumatic brain injury (TBI) and may slow the progression of neurodegenerative diseases, according to a clinical study published in Cleveland today in the online journal Nature Communications .

The research team, led by Bruce Trapp, PhD, chair of the Department of Neurosciences at the Lerner Research Institute of Cleveland Clinic, found that microglia may help synchronize the brain fire, which protects the brain from TBI and can help relieve chronic neurological diseases. They provided the most detailed study and visual evidence of the mechanisms involved in this protection.

"Our results suggest that the innate immune system helps protect the brain after injury or during chronic diseases, and this role should be further studied," said Dr. Trapp. "We could potentially exploit the protective role of microglia to improve the prognosis of patients with TBI and delay disease progression, MS, Alzheimer's and stroke. The methods we have developed will help us further understand the mechanisms of neuroprotection. "

Microglias are primary responders to the brain after an injury or sickness. Although researchers have long believed that activated microglia causes harmful inflammation that destroys healthy brain cells, some speculate a more protective role. The team of Dr. Trapp used an advanced technique called 3D electron microscopy to visualize the activation of microglia and subsequent events in animal models.

They found that when chemically activated, microglia migrate to inhibitory synapses, the connections between brain cells that slow firing pulses. They displace the synapse (called "stripping synaptic"), thereby increasing neuronal firing, leading to a cascade of events that improve the survival of brain cells.

Trapp is internationally known for his work on the mechanisms of neurodegeneration and repair in multiple sclerosis. His research has included investigating the cause of neurological disability in patients with multiple sclerosis, the cellular mechanisms of brain repair in neurodegenerative diseases and molecular biology of myelination in the central and peripheral nervous systems.

Friday, December 6, 2013

Co-targeting strategies suggested for resistance to EGFR TKI in NSCLC

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Co-targeting strategies suggested for resistance to EGFR TKI in NSCLC
-

By Lucy Piper first medwireNews Problem

resistance mechanisms additional researchers have identified that could be targeted to improve the efficiency of the kinase inhibitors of the receptor tyrosine irreversible epidermal growth factor receptor (EGFR TKI) in patients with non-small cell lung cancer (NSCLC) harboring the two EGFR and T70M mutations.

Preclinical and clinical studies have shown limited effectiveness irreversible EGFR TKI, like afatinib, in patients EGFR TKI sensitive mutations and secondary point mutation T70M in exon 20 of EGFR which replaces methionine for threonine in amino acid position 70.

this suggests that these agents by themselves are not sufficient to overcome the resistance the study researchers explain.

to identify strategies to improve on this limited effectiveness, Eric Haura (H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA) and colleagues used tyrosine phosphorylation profiling to compare PC9 cells with TKI-sensitive EGFR mutation paired with PC9GR cells that were resistant -TKI EGFR T70M and worn.

researchers found 110 antiphosphotyrosine unique (pTyr), peptides which are more abundant in the cells of PC9GR, many of which corresponded to receptor tyrosine kinases, including AXL and IRS2, which in the correct environmental circumstances could be potential co-drivers resistance.

There was also a clear subnet characterized by hyperactive signaling facility, including TEM, and ROR1 GAB1 2 protein /. This however turned MET signaling is not secondary to amplification MET gene ,.

Abundance of PTyr peptides in PC9GR cells was amplified by the treatment with erlotinib. And when PC9GR cells were incubated with ligands upregulated receptor tyrosine kinases, for those IRS2 MET and protected the cells against afatinib exposure.

This offer proof of their ability to interact with growth factor ligands to lead the resistance to EGFR -TKI, Haura and writing team in Clinical Cancer Research .

The researchers then looked for parallel signaling pathways in the PC9 and PC9GR cells that are not inhibited by EGFR TKI and can cooperate with EGFR to maintain cell growth or survival.

They identified a kinase of the Src family network (SFK) which was independent of EGFR phosphorylation, which was not affected by erlotinib and afatinib, but completely suppressed when exposed the SFK- inhibitor dasatinib and afatinib.

This combined anti-tumor potential effect of SFKs co-targeting EGFR T70M and has been validated in the results showing dasatinib and afatinib or dasatinib, more selective T70M EGFR TKI WZ4002 reduced cell proliferation and increased apoptosis in multiple NSCLC cell lines harboring T70M. By comparison, there was no combination is EGFR mutated cells or wild-type EGFR cells.

These anti-tumor effects also improved resulted in an improvement in vivo effects on tumor growth PC9GR cells injected into mice.

"Collectively, our results suggest that dasatinib can generally be used as a combination therapy with irreversible or selective T70M EGFR TKI for NSCLC patients who acquired EGFR TKI resistance associated with T70M" the researchers reported.

They add, however, that his clinical activity in NSCLC is likely to be limited to combinations with targeted agents and T70M in specific patient genotype.

medwireNews licensed by permission of Springer Healthcare Ltd. © Springer Healthcare Ltd. All rights reserved. None of these parties endorse or recommend any commercial products, services or equipment.

Thursday, December 5, 2013

vaccination against HPV can be effective in reducing the results of abnormal Pap tests, even after the first sexual

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vaccination against HPV can be effective in reducing the results of abnormal Pap tests, even after the first sexual -

Minority women who received vaccination against human papillomavirus (HPV), even after becoming sexually active had lower rates of abnormal Pap test than those who have never been vaccinated. These findings appear in the journal Sexually Transmitted Diseases .

School Researchers from Boston University of Public Health and the School of Medicine conducted a cross-sectional study of 235 women age 21 to 30 cytological cervical undergoing routine tests. HPV status and demographic and behavioral characteristics were self-reported and verified with electronic medical records.

"Although the data clearly show better immune response and vaccine efficacy against genital warts and cervical dysplasia when vaccination occurs before 14 years, this study suggests that vaccination against HPV can be effective in reducing the results of abnormal Pap tests, even after the first sexual intercourse, "says co-author Rebecca Perkins, MD, M.Sc., assistant professor of obstetrics and gynecology at the medical faculty of the Boston University and a gynecologist at Boston Medical Center.

at the time of the study, 41 percent had received at least one vaccination against HPV; 97 percent of women were vaccinated after the sexual beginning. Ten percent of the women had abnormal cervical cytology results. The prevalence of abnormal cytology was 65 percent lower among women who received at least one vaccination against HPV compared to unvaccinated women.

The researchers continued monitoring of vaccination against HPV is necessary to identify clinical benefits, especially given the low absorption rate of the vaccine and the completion and immunization a large number of young women after sexual debut. "The studies should continue to compare the efficacy of the vaccine before and after sexual debut and vaccine doses received and to explore the role of herd immunity," said Perkins.

Wednesday, December 4, 2013

OSNP program addresses potential gaps in external parameters

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OSNP program addresses potential gaps in external parameters -

An innovative framework to identify and address potential gaps in outpatient settings in health care using clinical tools electronic surveillance was used to identify patient safety through a variety of conditions, according to a study published today in the journal eGems .

ambulatory Safety Net Program Kaiser Permanente Southern California (OSNP) harnesses the power of electronic health records as well as a proactive culture to detect clinical improvement opportunities of the potential quality and action to improve patient care.

document presents the general framework of OSNP, which was used to treat a wide range of security issues in various clinical conditions. The objectives of OSNP care deficiencies such as the use of competing drugs that could lead to drug interactions or the need for follow-up testing. This is in contrast with the majority of patient safety programs that focus on the emergency or hospital care.

"Over 98 percent of patient interactions occur in outpatient and ambulatory Security Program Net harnesses the power of electronic health records to target care gaps by scanning for things like drug interactions or follow-up testing needed, "said study author Michael H. Kanter, MD, regional medical director of quality and clinical analysis, Southern California Permanente medical Group. "For example, a patient who is on one or more drugs that require annual monitoring that has not come to get his blood drawn for necessary test will be indicated by our clinical tool of electronic surveillance, and we will remind the patient to come and having made his laboratory work. "

according to the researchers, this innovative approach can be applied by other health care organizations, provided they have key information in digital format, even if they do not have a health record electronic or integrated delivery systems.

"the Southern California safety net Outpatient program is different from other patient safety programs that are dedicated to hospital care or hospital, as it analyzes the background of all that was missed, "said Dr. Kanter. "Like other health care delivery systems to develop and implement similar tools, information sharing these methods through organizations can improve ambulatory security more broadly."

Kaiser Permanente can conduct research on transformational health such as this study partly because it has the largest electronic health system centered on private patient in the world. electronic health record system of the organization Kaiser Permanente HealthConnect-, securely connects to about 9.3 million patients to 16,000 physicians in nearly 0 medical offices and 38 hospitals. It also connects Kaiser Permanente researchers in one of the most extensive collections of longitudinal medical data available, facilitating studies and important medical discoveries that shape the future delivery of health care for patients and the medical community.

This story is part of the ongoing efforts of Kaiser Permanente to address various health care gaps in ambulatory care settings and improving the quality and safety of health care. Kaiser Permanente has published numerous studies on the benefits of Kaiser Permanente HealthConnect-, it launched in 04. In February, a Kaiser Permanente study published in the Journal of Vascular Surgery found that EHR screening program for aneurysms of the abdominal aorta reduces the number of tanks, patients at risk of over half. Another study published in the Journal of the American Medical Informatics Association in October 2013 found that the use of electronic health records to automate the reporting of quality measures reduces the time required for reporting a measurement-only set about 50 percent.

Tuesday, December 3, 2013

Study identifies genetic as dominant risk factor in breast cancer, prostate and colorectal

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Study identifies genetic as dominant risk factor in breast cancer, prostate and colorectal -

A study of individuals who were adopted identified the genetic as a dominant risk factor in 'family' breast, prostate and colorectal cancer.

researchers from the Centre for Research on Primary Health Care at the University of Lund and Region Sk-do in Sweden presented new research results based on population registers studies.

"the results of our study do not mean that the way of life of an individual is not important to the individual risk of developing cancer, but suggests that the risk for the three types most common cancer depends largely on genetics, "said Bengt Z-ller, a reader at the University of Lund, who led the study.

researchers studied adoptees born in Sweden in connection with both biological parents and adoptive parents. The Swedish Multi-Generation Register and the Cancer Registry were used to monitor 70 965 men and women adopted. They were all born between 1932 and 1969 and developed breast cancer, prostate cancer or colorectal cancer between 1958 and 2010. Using registry studies, the researchers also examined their adoptive parents and biological on same period.

cancer risk among adopted children with at least one biological parent who had the same cancer was 80 percent higher than breast cancer, prostate cancer and colorectal cancer as a control group without a biological parent with the same cancer. There were however a higher risk for people with adoptive parents with breast cancer, prostate cancer and colorectal cancer as a control group. People with a biological parent with cancer has also developed the disease at a younger age than those without a biological parent with the same cancer. The age at which an individual developed cancer, however, was not affected by whether an adoptive parent had the same cancer.

The results are an important indicator of the importance of hereditary factors for breast, prostate and colorectal cancer, according to Bengt-Z ller.

"The occurrence of breast cancer, prostate cancer and colorectal cancer in the biological parents is an important risk factor that should be included in history and medical examinations of patients. There is important that physicians ask questions about family history so they can decide if further tests are needed, "said Bengt-Z ller.

Monday, December 2, 2013

single gene defines the difference between aggressive and nonaggressive forms of thymoma

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single gene defines the difference between aggressive and nonaggressive forms of thymoma -

For a rare form of cancer called thymoma, the researchers discovered a single gene that defines the difference between a fast -growing tumors require aggressive treatment and a slow-growing tumor that does not require intensive therapy.

Thymoma is a cancer derived from epithelial cells of the thymus, an organ essential for the lymphatic system where T cells mature or so-called "killer cells". Very little is known about the role of the gene mutation GTF2l in human tumors, but scientists at Georgetown Lombardi Comprehensive Cancer Center and the National Cancer Institute say almost all indolent forms of thymoma they tested (not aggressive growth slow) have the mutation. They report their finding in the ?? issue Nature Genetics .

"thymoma indolent rarely become aggressive, so the discovery that a single gene can identify tumors that do not require aggressive treatment is an important development for our patients," says principal investigator of the study, Giuseppe Giaccone, MD, PhD, associate director of clinical research at Georgetown Lombardi.

in addition to clinical implications, the study is important because "it is very rare to find a single mutated gene that can define a class of tumors, "he said. ". Usually a large number of genes are involved in fact, we also found that the more aggressive thymoma express the well-known cancer genes found in other tumors. - Who could give us clues about a new treatment for these cancers "

thymus is in the chest behind the sternum Thymoma and a second type of thymus cancer called thymic carcinoma are rare According to.. National cancer Institute, these cancers counted together represent only 0.2 to 1.5 percent of all cancers- a case occurs in about every 700,000 individuals.

most diagnosed patients have surgery but, according to the alleged aggressiveness of the cancer, some patients have radiotherapy and / or chemotherapy in addition to or instead of surgery. "the use of these treatments in thymoma is controversial, because we know that some patients not require aggressive treatment, but so far there has not been a way to know who these patients are, "Giaccone said.

Saturday, November 30, 2013

research finding may accelerate the development of treatments for PTSD

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research finding may accelerate the development of treatments for PTSD -

TAC2 major gene for fear memory consolidation

Scientists at the Yerkes National primate Research Center, Emory University have identified a drug that seems to make memories of terrible events lasting less mice.

conclusion may accelerate the development of treatments to prevent PTSD (post-traumatic stress disorder). The drug, called osanetant targets a distinct group of brain cells in a brain region that controls the formation and consolidation of memories of fear.

The results were published in the journal Neuron .

"potentially, drugs that affect this group of cells could be used to block memory consolidation of fear shortly after exposure to trauma, which would help prevent PTSD," says Kerry Ressler, MD, PhD, professor of psychiatry and behavioral sciences at Emory University school of Medicine and Yerkes National Primate Research Center "PTSD is unique among psychiatric disorders in what we know when it begins. - when trauma of finding ways to prevent its development in the first place. - in emergency or battlefield Service - is an important and exciting avenue of research in this field "

the first author. Article is postdoctoral fellow Ra-l Ander Gal, PhD.

Ressler and Ander were sifting through a list of many genes that are activated in mouse brains after they learn to be afraid of her, because the sound is associated with a slight shock electric. The researchers were probing changes in the central amygdala, a region of the brain known to regulate learning of fear.

Of the thousands of genes they examined, their "top gene" was tachykinin 2 or TAC2. TAC2 The gene was turned on more strongly during fear learning in mice that were previously exposed a model of post-traumatic stress ..

"the gene is robust TAC2 activated after learning of fear and belongs to a path that can be specifically blocked with a drug," says Ressler. "He Interestingly TAC2 that is highly expressed in a particular part of the amygdala, but with little or no expression in other brain areas related to the formation of fear memories. In addition, we found that cells that express TAC2 are distinct from those of other investigators had previously identified as being involved in the expression of fear. "

TAC2 is part of a family of messengers in the nervous system known as tachykinins. Drugs that block a product encoded by report of TAC1 TAC2 are antiemetics, often prescribed when someone receives chemotherapy for cancer.

Osanetant, which blocks the action of TAC2, was tested in previous clinical trials for schizophrenia and was safe but not effective in the fight against this disease. He has not been tested in humans for the prevention of post-traumatic stress.

"Osanetant is a safe drug and well tolerated in humans and could be potentially used to prevent PTSD when given little after trauma, although more research is needed, "Ander said.

Under the influence of osanetant, mice could still learn to be afraid of a sound associated with a shock, but the mice did not freeze in response to sound as one day later, even if the drug was administered one hour after training.

"Our goal is to specifically impair emotional memories of a traumatic event instead of all the memories associated with it. Thus, the trauma and the circumstances are recalled, but the consolidation of fear memories is impaired, which could decrease the likelihood of developing fear-related disorders, "said Ander.

Friday, November 29, 2013

Extract from Chinese herb god of thunder vine suppresses pancreatic cancer cells

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Extract from Chinese herb god of thunder vine suppresses pancreatic cancer cells -

A diagnosis of pancreatic cancer, the fourth most common cause of cancer death in the US-can be devastating. Thanks in part to the aggressive cell replication and tumor growth, pancreas cancer progresses rapidly and has a survival rate five-year low (less than 5 percent).

GRP78, a protein that protects cells from dying, is more abundant in cancer cells and tissues than in normal organs and is thought to play a role in helping pancreatic cancer cells survive and prosper. University of Minnesota researchers have found triptolide, an extract of the Chinese herb thunder god vine ( Tirpterygium wilforii ), suppresses GRP78, possibly leading to death of pancreatic cancer cells.

For mammals to use proteins in the body, a process called protein folding must occur in the endoplasmic reticulum (ER) cells. If the proteins are folded rather quickly, the unfolded proteins and begin to build the cell becomes stressed. Stress activates extended RE a cellular process called the "unfolded protein response (UPR)." Initially, the UPR helps prime the ability of the protein-folding of the cell, enabling it to function properly again. But if the problem does not resolve, the UPR triggers cell death.

GRP78 helps cells survive long enough for the UPR to launch and correct protein folding problems. However, GRP78 is available higher amounts in cells of pancreatic cancer, which helps cancer cells to escape cell death, to live and multiply them.
Triptolide has previously been shown to have a negative effect on pancreatic cell viability cancer and growth of the block and the spread of these cells. in this study, led by Ashok Saluja, Ph.D., the researchers observed the effects of triptolide on cells of pancreatic cancer and tissue. They found that the UPR was successful in triptolide treated cells to allow cell death in cells defective.

"Our study shows that although increased expression of GRP78 confers a survival advantage to tumor cells, prolonged exposure to stress Triptolide induces chronic RE, which ultimately leads to cell death" the authors said. "In this context, inhibition of GRP78 by activation of the stress pathway RE by triptolide provides a new mechanism to inhibit the growth and survival of pancreatic cancer cells."

The article "Triptolide active response of the unfolded protein leading to chronic ER stress in cells of pancreatic cancer" is published in the American Journal of Physiology-Gastrointestinal and Liver Physiology. It is highlighted as one of the "best of the best" this month as part of APSselect program of the American Physiological Society.