راه اندازی سامانه جمع آوری نگهداری اطلاعات جهش های سرطان

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دانشمندان در دانشگاه واشنگتن سامانه ای را راه اندازی کرده اند که شبیه ویکی پدیا در جهش شناسی سرطان است. در این سامانه همه دست اندرکاران عرصه تشخیص ملکولی سرطان برای خود حساب کاربری درست می کنند . اطلاعات جهش و علامت را ثبت می کنند.

این سامانه که CIViC نام دارد به مشکلات تفسیر داده ها می پردازد چون بسیاری از اطلاعات خام اولیه برای متخصصین سرطان قابل تفسیر نیست. جزییات این خبر و جوانب علمی آن در نسخه اخیر ژورنال علمی نیچر چاپ شده است.

تعیین جهش ها در تومور بسیار آسان است اما تفسیر آنها و اینکه این یافته ها چه تاثیری در آینده بیمار دارد بسیار مشکل است.

به گفته دست اندرکاران این طرح قرار است به این مشکل پرداخته شود. و به گفته مدیران این پرژه نکته مهم و انحصاری در مورد این سامانه آن است که منبع آن باز و آزاد است و همه محققین می توانند از داده ها استفاده کنند.

 

همه افراد و محققین می توانند یک قطعه جدید از اطلاعات را ارسال کنند و یا ویرایش انجام دهند. برای آن که یک مطلب مورد تایید قرار گیرد باید مورد تایید حاقل دونفر برسد که یکی از آنها  ویرایشگر متخصص و ارشد باشد. ویراستاران ارشد  مجاز به تصویب داده های خود را ندارند. 

 

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افسردگی و اضطراب مشکل اصلی بازماندگان سرطان

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در یک مطالعه که اخیراً در ۱٬۳۶۲ بیمار بازمانده و بهبودیافته از سرطان انجام گرفته است نشان می‌دهد که از هر ۵  نفر آنان ۴ نفر مبتلا به افسردگی و اضطراب می‌باشد .
به همین دلیل است که رسیدگی به وضعیت بیماران سرطانی از ضروریا فوری برخوردار می‌باشد. و پزشکان درمان کننده نباید تنها به  درمان بالینی بیماران تمرکز داشته باشند بلکه نکات  روحی و روانی را نیز می‌بایست مدنظر قرار دهند.د 
عوامل مختلفی از قبیل مسائل مالی مشکلات خانوادگی نگرانی از آینده و به خصوص شدت و عوارض بیماری از عواملی هستند که در این اضطراب و افسردگی تأثیر مستقیم دارند.  برای مثال بیماران  سرطان دستگاه تناسلی زنان  در مقایسه با بیماران مبتلا  به  لنفوم از وضعیت روحی و روانیبهتری برخوردار هستند .  دلیل این  موضوع آن است که احتمالاً بیماری لنفوم رفتار تهاجمی تر در مقایسه با سرطان‌های زنان دارد .فاکتور مهم دیگر در این ارتباط سن می‌باشد تأثیر روانی تشخیص سرطان در سنین پایین‌تر شدیدتر از سنین بالاتر است.

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امکان پیش بینی عود سرطان گلو با یک آزمایش جدید

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۱۵تا ۲۰ در صد سرطان های گلو بعد از درمان عود می کنند. تاکنون روش موثری برای پیش بینی عود این بیماری وجود نداشته است. در یک مطالعه که در مجله Clinical Cancer Research چاپ شده است محققین از رابطه بالا رفتن دو نشانگر E6 و  E7ابا امکان عود این بیماری خبر دادند. این محقین عنوان نمودند که این آزمایش را می توان با هزینه کم در بیشتر آزمایشگاههای تشخیص طبی انجام داد.

 

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نتایج امیدوار کننده در درمان سرطان پیشرفته مثانه یا نیولوماب

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در کنگره انکولوژی آمریکا اعلام شد

داروی نیولوماب که برای درمان لنفوم هوچکین،  ملانوما, سرطان کلیه ،  سرطان ریه, و برخی سرطان های دیگر توسط FDA تایید شده است می تواند در درمان سرطان مثانه پیشرفته مورد استفاده قرار گیرد.

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مطالعه حیوانات کلید حل مشکل سرطان در انسان

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حیوانات می توانند کلید حل معمای ایمنی سرطان در انسان باشند. در حیوانات و انسان، سیستم ایمنی بدن در برخی موارد به طور موثر سلول های تومور را می کشد، در حالی که در موارد دیگر سلول های سرطانی فرار می کنند. بر خلاف باور عمومی، سرطان در برخی موارد واگیر دار است. برای مثال نوعی جانور کیسه دار در استرالیا به که اندازه سگ های کوچک است به دلیل نوعی سرطان مسری در آستانه انقراض است. به طور مشابه، سگ ها نیز می توانند سرطان مسری مبتلا شوند.  اما معمولا به شکل خود به خود بر آن غلبه می کنند. پس از آن، این سگ ها در برابر سرطان مقاوم می شوند. این موضوع  سرنخ جذابی در مورد نقش سیستم ایمنی بدن در سرطان را در اختیار ما قرار می دهد. بر خلاف نظر و اعتقاد عمومی، کوسه ها نیز به سرطان مبتلا می شوند. در انسان، یک فرم غیر معمول از کوتاهی قد به نام سندرم لارون که تقریبا به صورت کامل در برابر سرطان مقاوم است.  در یک مورد عجیب یک کرم لوله ای در روده یک بیمار مبتلا به سرطان شد که “سرطان”، در سراسر بدن بیمار منتقل گردید. در مورد فوق العاده درمان به ظاهر معجزه آسا از یکی از بیماران به نام دانیل، که ملانوم متاستاتیک پیشرفت داشت اتفاق افتاد. در این بیمارسرطان بسیار تهاجمی به کبد و استخوان دانیال گسترش یافته بود، و به نظر میرسید که تنها چند ماه از زندگی او باقی مانده است. دانیل از یک تومور در استخوان ران (استخوان ران) خود رنج می برد در این حالت جهت کاهش درد موضعی و کوچک شدن تومور، برای وی رادیوتراپی انجام می شود اما سه ماه بعد، سی تی اسکن هیچ ردی از سرطان در بدن وی نشان نمی دهد.این پدیده نادر به نام اثر abscopalنامیده می شود، که در آن درمان موضعی نه تنها به کوچک شدن تومورمنجر می شود  بلکه تومورهای دور را نیز از بین می برد.  به نظر می رسد تابش محلی به نحوی محرک سیستم ایمنی بدن دانیال برای حمله به سرطان در سراسر بدن او بوده است. “این پدیده abscopal نشان دهنده یک مثال از توانایی سیستم ایمنی بدن برای غلبه بر سرطان حتی در  موارد بسیار پیشرفته باشد.” دکتر ویلز می نویسد. تلاشهای اولیه برای مبارزه با سرطان با سلول های بنیادی ناامید کننده بود. درمان تقویت سیستم ایمنی بدن راه جدی برای درمان سرطان است. دوره تردید در روش های سلول درمانی پایان یافته است.

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درمان جدید سرطان: قطع شاهراه تغذیه سلول های سرطانی

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محققین موفق به کشف شاهراهی در مسیر تغذیه سول های سرطانی شده اند که از آن طریق سلول های سرطانی به اسید آمینه گلوتامین دست می یابند. از طریق مسدود کردن این شاهراه ، می توان سلول سرطانی را از انرژی لازم برای ادامه زندگی محروم کرد. نکته مهم آن است که سلول های سالم از گلوتامین به این منظور استفاده نمی کنند.

تاکنون ۹۱۷ نوع سرطان شناسایی شده است و برای هر کدام گاها درمان های مختلف وجود دارد و نهایتا اکثر موارد نیز منجر بروز مقاومت می شود.  اما این شیوه درمانی  امکان دور زدن را برای سلول سرطانی مشکل می کند. از طرفی این شیوه درمانی منجر به ریزش مو نیز نمی شود.

جزییات این تحقیق در مجله Journal of Biological Chemistry چاپ شده است.

 

 

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يك جهش ژنتيكي جديد عامل پاركينسون كشف شد 

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Using a novel method, Whitehead Institute researchers have determined how a non-coding mutation identified in genome-wide association studies (GWAS) can contribute to sporadic Parkinson’s disease (PD). The approach could be used to analyze GWAS results for other sporadic diseases with genetic causes, such as multiple sclerosis, diabetes, and cancer.

“This is really the first time we’ve gone from risk variants highlighted by GWAS to a mechanistic and molecular understanding–right down to the nucleotide–of how a mutation can contribute to the risk of developing disease,” says Whitehead Founding Member Rudolf Jaenisch, who is also a professor of biology at MIT.

About 90% of PD cases are sporadic; that is, caused by complex interactions between environmental and common genetic risk factors. Because scientists have had difficulty analyzing these interactions, most research has focused on rare familial forms of the disease. GWAS, which identify common mutations that increase the risk to develop a particular condition, have been used to study sporadic PD, and other complex conditions, with limited success.

GWAS are akin to genomic treasure maps bearing hundreds or thousands of X’s marking the general locations of mutations that could be risk factors for a given condition. However, GWAS do not reveal the specific locations of potentially pathogenic mutations, nor do they indicate how an X on a genomic map contributes, if at all, to a disease. For example, in sporadic PD, multiple GWAS point to the alpha-synuclein gene (SNCA) as one of the strongest risk loci in patients’ genomes, yet GWAS contain little information regarding the mechanism of how this gene is dysregulated in sporadic PD patients.

To see if distant gene regulatory elements on the same chromosome carrying SNCA could affect cellular levels of alpha-synuclein, a team of researchers led by Frank Soldner, a senior researcher in the Jaenisch lab, investigated two GWAS-flagged risk variants located in a putative SNCA enhancer. Their results are described online in the journal Nature.

The team used clustered regularly-interspaced short palindromic repeats (CRISPR)/Cas9 to edit the mutations into isogenic human pluripotent stem cells. By altering the genetic variant on only one chromosome, the other chromosome remains unchanged and acts as an internal control. This method allows the scientists to measure very subtle effects with very high confidence, while eliminating the effect of any genetic or epigenetic modifications and cell culture related variations that could occur during the experiment.

“Our method addresses an essential shortcoming of GWAS–using the correlations produced by GWAS, you cannot distinguish the effect between two variants that are very close together in the genome,” says Soldner, who is the lead author of the Nature paper. “Such physical proximity means that they will always co-segregate during inheritance, which is why we had to do what we did–modify and analyze each variant independently while keeping the rest of the genome completely constant.”

After differentiating the cells into neurons, the scientists noted the changes in SNCA expression. Although one of the mutations has no effect, the other, which switches one nucleotide from an A to a G, slightly but significantly boosts alpha-synuclein production. When compared to the enhanced alpha-synuclein production in the familial form of the disease, the modest effect created by the A to G mutation would be sufficient over a lifetime to increase the risk of PD, according to Soldner.

To see how the mutation affects alpha-synuclein production, the researchers identified two transcription factors that bind to the enhancer that carries this mutation. When the enhancer is not mutated, the transcription factors bind to it, which suppresses SNCA. If the enhancer has the G mutation, the transcription factors are unable to bind to the enhancer, and SNCA is activated.

Most genetic conditions are sporadic and caused by a combination of mutations.

Jaenisch says that the method that identified the single point mutation in SNCA’s enhancer could be used to pinpoint additional pathogenic genes for sporadic PD and sift through the GWAS hits for other diseases, including Alzheimer’s disease, cancer, diabetes, and multiple sclerosis.

حمله به سلول هاي سرطاني با لنفوسيت هاي مهندسي شده

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IMAGE: Dr. Philip Greenberg, head of immunology and a member of the Clinical Research Division at Seattle’s Fred Hutchinson Cancer Research Center and a leader in cancer immunology, will describe how… view more

Credit: Fred Hutch News Service

SEATTLE AND NEW ORLEANS – Dr. Philip Greenberg, head of immunology and a member of the Clinical Research Division at Seattle’s Fred Hutchinson Cancer Research Center and a leader in cancer immunology, will describe how he and colleagues are genetically engineering T cells to seek out cancer cells, penetrate their defenses and kill them.

In a presentation at the American Association for Cancer Research Annual Meeting 2016 in New Orleans, he also will provide a preview of next-generation strategies and upcoming clinical trials for a variety of cancers. The presentation will be from 10:55 to 11:20 a.m. CDT April 20 as part of a symposium on the function of T cells and their therapeutic application in cancer.

T cells are white blood cells that attack abnormal cells in our bodies, including those infected by viruses and other foreign invaders. T cells can also target cancer cells, but they sometimes fail to recognize cancer cells as the enemy. Many cancer cells produce proteins that suppress nearby T cell activity, rendering the immune response futile.

Among Greenberg’s topics will be:

  • Research to discover antigens that are good targets for T cell receptors (TCRs). For example, an appropriate target would be plentiful in tumor cells but absent or nearly so in normal tissues. As will be discussed, WT1 is a targetable tumor antigen for leukemia and potentially some other cancers. T cell receptors are molecules on the surfaces of T cells that are responsible for recognizing and binding to antigens.
  • Preliminary data from a clinical trial for patients with acute myeloid leukemia (AML) in which T cells are being engineered with a receptor selected for its ability to target the WT1 antigen.
  • Other current or planned trials using TCR-engineered T cells to target tumors. These include non-small cell lung cancer and mesothelioma, pancreatic cancer, high-grade serous ovarian cancer and additional studies on AML.
  • An update on a mesothelioma study in which three patients with advanced, treatment-resistant disease have received the experimental T cell therapy. One now has stable disease and one has experienced significant tumor regression.
  • Next-generation strategies, which include designing better, more targeted synthetic T cell receptors and manipulating other factors, such as elements of the tumor environment, to improve antitumor activity.
  • Engineering T cells to treat solid tumors. Mouse studies using pancreatic cancer as a model are providing numerous insights. Among them: T cell therapy using TCR-engineered T cells induces tumor cell death, but this is only temporary as the tumor ultimately turns the T cells off. However, anti-tumor activity can be sustained by administering multiple infusions, and if repeated every two weeks the infusions significantly prolong survival in mice. This strategy is in the process of being translated to human clinical trials.

Greenberg is a founder of and consultant to Juno Therapeutics. He is a stockholder in the company and he receives grant and research support from it. Juno Therapeutics was initially formed on technology from researchers at Fred Hutch, Memorial Sloan Kettering Cancer Center and Seattle Children’s Research Institute to commercialize promising immunotherapies.

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Editor’s note: For researcher bios, photos and more, please visit fredhutch.org/media.

At Fred Hutchinson Cancer Research Center, home to three Nobel laureates, interdisciplinary teams of world-renowned scientists seek new and innovative ways to prevent, diagnose and treat cancer, HIV/AIDS and other life-threatening diseases. Fred Hutch’s pioneering work in bone marrow transplantation led to the development of immunotherapy, which harnesses the power of the immune system to treat cancer with minimal side effects. An independent, nonprofit research institute based in Seattle, Fred Hutch houses the nation’s first and largest cancer prevention research program, as well as the clinical coordinating center of the Women’s Health Initiative and the international headquarters of the HIV Vaccine Trials Network. Private contributions are essential for enabling Fred Hutch scientists to explore novel research opportunities that lead to important medical breakthroughs. For more information visit fredhutch.org or follow Fred Hutch on Facebook, Twitter or YouTube.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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جهش در ژن هاي  عامل سرطان سينه در زنهايي كه تخمك هاي كمتري دارند بيشتر ديده مي شود

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Researchers have discovered a link between the BRCA1 gene mutation and lower levels of a hormone that is an indicator of the number of eggs left in a woman’s ovaries, according to research published today (Wednesday) in Human Reproduction [1], one of the world’s leading reproductive medicine journals.

In the first large study looking at BRCA1 and BRCA2 genetic mutations and levels of anti-Müllerian hormone (AMH) in women who carry the mutated genes, the group of international researchers found that carrying the BRCA1 mutation was associated with AMH concentrations that were, on average, 25% lower than those in non-carriers. The effect was not seen in women with the BRCA2 mutation.

Professor Kelly-Anne Phillips, a consultant medical oncologist at the Peter MacCallum Cancer Centre in East Melbourne (Victoria, Australia) and the first author of the study, said: “This means that women in their mid-30s, who carry the BRCA1 mutation, have, on average, ovarian reserves similar to those of non-carriers who are two years older.”

Although AMH is a reliable marker of ovarian reserve, Prof Phillips said: “It’s important to remember that AMH is only one indicator of a woman’s potential fertility, the ability to conceive and carry a baby to full term is affected by many other factors as well, including egg quality and whether the fallopian tubes are unobstructed, neither of which are measured by AMH. Women with low AMH levels can sometimes still have a baby and, conversely, women with high AMH levels are sometimes unable to do so.

“However, our findings suggest that women carrying the BRCA1 mutation should try to avoid delaying pregnancy until their late 30s or 40s when fertility is reduced anyway because of their age. For women trying to conceive in their 20s, any difference in ovarian reserve between BRCA1 mutation carriers and non-carriers is unlikely to be of clinical significance.”

Women who carry the BRCA1 and BRCA2 gene mutations have a higher risk of cancers in the breast, ovaries, fallopian tubes and peritoneum. The risk increases with age and is generally higher for those with the BRCA1 mutation than with the BRCA2 mutation. The mutations are rare in the general population – about 0.1% for BRCA1 and 0.2% for BRCA2 – although they can be more prevalent in certain groups, such as Ashkenazi Jews. As mutation carriers enter their early 40s they are usually advised to have their ovaries and fallopian tubes removed in order to minimise their cancer risk (as these cancers are hard to detect in their early stages when they are easier to treat). For this reason, many women who know they are carriers try to have their children when they are younger. However, until now, there has been little good-quality evidence about the effects of these genetic mutations on non-cancer-related conditions such as fertility.

Prof Phillips and colleagues from research centres in Australia and Scotland (UK), analysed AMH levels from 693 women, aged between 25-45 years (average age was 35), who had no personal history of cancer but who had enrolled into the Australian and New Zealand Kathleen Cuningham Foundation Consortium for research into Familial Breast Cancer (kConFab) study between 1997 and 2012. A total of 172 women were carriers and 216 women non-carriers from families carrying the BRCA1 mutations, and 147 carriers and 158 non-carriers were from families with the BRCA2 mutations. The women retained both ovaries and were not pregnant or breast-feeding at the time that blood was taken from them. The researchers adjusted their results to take account of age, oral contraceptive use, body mass index and smoking.

In addition to BRCA1 mutations carriers having 25% lower AMH concentrations, on average, than non-carriers, they were also more likely to have AMH concentrations that placed them in the lowest quarter when the women were divided into four groups according to the AMH levels. This was not seen in BRCA2 mutation carriers.

In their Human Reproduction paper, the authors say that a possible mechanism for the link between the BRCA1 mutation and ovarian reserve may be the role played by both the mutations in DNA repair – inefficient DNA repair has been shown to contribute to the aging of a woman’s eggs. BRCA1 and BRCA2 are both integral to mending breaks that occur in both strands of the DNA helix.

“BRCA2 has a more limited role in double-strand DNA break repair compared with BRCA1 and BRCA2 mutation carriers tend to develop fewer cancers and at a later age, compared with BRCA1 mutation carriers,” explained Prof Phillips. “So it is credible that any effect of mutation status on ovarian reserve would be more pronounced in BRCA1 mutation carriers. There may be a lesser effect in BRCA2 mutation carriers as well, but our study did not have adequate power to detect it.”

The researchers say that their findings also raise the hypothesis that BRCA1 mutations carriers may have a higher than average risk of chemotherapy-induced menopause. “The hypothesis is that if BRCA1 mutation carriers have lower ovarian reserve than their non-carrier counterparts when they start chemotherapy for cancer treatment, the carriers may be more likely to develop menopause associated with the chemotherapy. However, this is just a hypothesis at this stage and requires further research,” she concluded.

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[۱] “Anti-Müllerian hormone serum concentrations of women with germline BRCA1 or BRCA2 mutations”, by Kelly-Anne Phillips et al. Human Reproduction journal. doi:10.1093/humrep/dew044

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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ارتباط سرطان لوزالمعده با يك باكتري دهان

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The presence of certain bacteria in the mouth may reveal increased risk for pancreatic cancer and enable earlier, more precise treatment. This is the main finding of a study led by researchers at NYU Langone Medical Center and its Laura and Isaac Perlmutter Cancer Center to be presented April 19 in New Orleans at the annual meeting of the American Association for Cancer Research.

Pancreatic cancer patients are known to be susceptible to gum disease, cavities, and poor oral health in general, say the study authors. That vulnerability led the research team to search for direct links between the makeup of bacteria driving oral disease and subsequent development of pancreatic cancer, a disease that often escapes early diagnosis and causes 40,000 US deaths annually.

“Our study offers the first direct evidence that specific changes in the microbial mix in the mouth — the oral microbiome — represent a likely risk factor for pancreatic cancer along with older age, male gender, smoking, African-American race, and a family history of the disease,” says senior investigator and epidemiologist Jiyoung Ahn, PhD.

Specifically, researchers found that men and women whose oral microbiomes included Porphyromonas gingivalis had an overall 59 percent greater risk of developing pancreatic cancer than those whose microbiomes did not contain the bacterium. Similarly, oral microbiomes containing Aggregatibacter actinomycetemcomitans were at least 50 percent more likely overall to develop the disease. Doctoral student and study lead investigator XiaoZhou Fan, MS, says both types of bacteria have been tied in the past to such diseases as periodontitis, or inflammation of the gums.

“These bacterial changes in the mouth could potentially show us who is most at risk of developing pancreatic cancer,” adds Ahn, an associate professor at NYU Langone and associate director of population sciences at the Perlmutter Cancer Center.

In another study published last month, Ahn and her colleagues showed that cigarette smoking was linked to dramatic, although reversible, changes in the amount and mix of bacteria in the oral microbiome. But she cautions that further research is needed to determine if there is any cause-and-effect relationship, or how or whether such smoking-related changes alter the immune system or otherwise trigger cancer-causing activities in the pancreas.

For the new study, researchers compared bacterial contents in mouthwash samples from 361 American men and women who developed pancreatic cancer with samples from 371 people of similar age, gender, and ethnic origin who did not. All were initially healthy and participating in larger ongoing cancer-risk studies led by the National Cancer Institute (NCI) and the American Cancer Society. Mouthwash samples were obtained at the beginning of each investigation, after which participants were monitored for nearly a decade to determine who got cancer.

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Funding support for the study, which took two years to complete, was provided by NCI grants R01 CA159036, U01 CA182370, R01 CA164964, R03 CA159414, R21 CA183887, and P30 CA016087.

Besides Ahn and Fan, other NYU Langone scientists involved in this research were Alexander Alekseyenko, PhD; Jing Wu, PhD; George Miller, MD; and Richard Hayes, DDS, PhD. Additional research support was provided by Mark Purdue, PhD; Christian Abnet, PhD; and Rachel Stolzenberg-Solomon, PhD, at the NCI in Bethesda, Md.; Eric Jacobs, PhD; and Susan Gapstur, PhD, at the American Cancer Society in Atlanta, Ga.; as well as by Jacque Ravel, PhD, at the University of Maryland in Baltimore.

Media Inquiries:

David March
Phone: 212-404-3528
david.march@nyumc.org

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