News and Events
December 1, 2011
Tumor-Targeting Compound Points the Way to New Personalized Cancer Treatments
One major obstacle in the fight against cancer is that anticancer drugs often affect normal cells in addition to tumor cells, resulting in significant side effects. Yet research into development of less harmful treatments geared toward the targeting of specific cancer-causing mechanisms is hampered by lack of knowledge of the molecular pathways that drive cancers in individual patients.
"A major goal of cancer research is to replace chemotherapy with drugs that correct specific molecular pathways disrupted by cancer," says Dr. Ari Melnick, one of the study's lead investigators and director of the Raymond and Beverly Sackler Center for Biomedical and Physical Sciences and associate professor of medicine at Weill Cornell Medical College. "But looking for mutations isn't always the way to find the most important factors that are keeping cancer cells alive."
Through a collaboration among Weill Cornell Medical College, the Sloan-Kettering Institute at Memorial Sloan-Kettering Cancer Center and the National Cancer Institute (NCI), a team of scientists has now reported that a tumor-targeting compound called PU-H71 can reveal with great accuracy the set of altered pathways that contribute to malignancy. Because the drug specifically binds to abnormal protein complexes in cancer cells, it could lead to the development of more targeted and effective therapies that produce fewer side effects. These findings were recently published in the journal Nature Chemical Biology.
"The holy grail in the field was to develop some way to figure out what factors keep cancer cells alive, regardless of whether they have mutations," says Dr. Melnick. "In this paper, we present a method to do just that."
Through nearly a decade of research, PU-H71 was discovered and refined in the laboratory of Dr. Gabriela Chiosis, associate member of the Molecular Pharmacology and Chemistry Program at the Sloan-Kettering Institute and an associate attending chemist of Memorial Hospital, Memorial-Sloan Kettering Cancer Center. Dr. Chiosis, who is the senior investigator in this new study, reported initial findings about the drug five years ago. The compound was designed to inhibit heat shock protein 90 (Hsp90), which helps other proteins fold into the correct three-dimensional shape and function properly.
Hsp90 plays an essential role in the ability of cells to tolerate stress. The altered growth and metabolism of tumors induce a high degree of stress in these cells. To cope with this stress, tumor cells produce a special form of Hsp90 that is tuned to specially protect those proteins required for their growth and survival. Because this tumor/stress form of Hsp90 regulates many pathways that go awry in cancer, it is a more promising drug target than current targets that play a role in only a single pathway, Dr. Chiosis says. Importantly, PU-H71 specifically suppresses the cancer form of Hsp90 but has little effect on Hsp90 in normal cells.
Several years ago, Dr. Chiosis partnered with Dr. Melnick to examine the effectiveness of PU-H71 in treating breast cancer and lymphomas, and they have previously reported that the drug has dramatic antitumor effects without being toxic to animals. As a result of the drug's success in fighting these two aggressive types of cancer, the research team received approval from the National Cancer Institute to carry out clinical trials. Patients are currently being recruited for the first trial, which will test the drug's safety in treating a variety of tumor types, and subsequent clinical trials are being planned for patients with lymphomas, breast cancer, chemotherapy-resistant leukemia and other specific types of cancer.
In their new study Dr. Chiosis, Dr. Melnick, and collaborators demonstrated that because PU-H71 binds to tumor-Hsp90, and tumor-Hsp90 binds to proteins that are required for tumor survival, it is possible to use PU-H71 as a method to "fish out" entire networks of abnormal proteins in tumor cells in an unbiased fashion, which has not been possible up until now. Importantly, many or even most of the genes encoding proteins that maintain tumor cell survival are not mutated in tumors. Hence genetic screening would not be able to detect these networks, Dr. Melnick says. "The value of this method is that it's the first time you can go and probe the functional proteome, or the whole set of proteins that are important to maintaining the tumor." This strategy opens up new avenues for understanding in greater detail the molecular basis of cancer and identifying novel drug targets.
For example, in chronic myeloid leukemia cells, the PU-H71 drug preferentially binds to the Hsp90 complex containing Bcr-Abl, an abnormal protein that is overactive in these cells, rather than to Hsp90 associated with the normal protein Abl. Similar findings were observed in other tumor types, with PU-H71-Hsp90 complexes protecting only the tumor-associated proteins.
The researchers then used PU-H71 and proteomic analyses to identify all of the abnormal proteins bound to Hsp90 in chronic myeloid leukemia cells and built networks of these proteins using bioinformatics analyses. They found that these proteins are part of signaling pathways involved in cell death, growth and division. Bcr-Abl is known to use many of these pathways to propagate abnormal signaling in this type of cancer cell. The researchers experimentally confirmed that proteins from these pathways are crucial for cancer cell growth, division and survival, suggesting that their approach can be used to accurately identify Bcr-Abl-related protein networks. Moreover, the same experiments identified many proteins not previously known to drive chronic myeloid leukemia cells. One example of such a protein was CARM1, a regulator of gene expression, which the investigators showed maintains survival of these tumor cells.
Importantly, this PU-H71 cancer proteome method can also be used to identify networks of abnormal proteins in the cells from individual patients, paving the way to personalized therapies that target multiple pathways. "No two tumors are exactly alike, and we don't really know what is driving cancer in one patient versus the other," the researchers say. "If you can use this method to identify in a given individual the factors that are maintaining that patient's particular cancer, then you could develop targeted drugs that hit these specific factors — in effect, designing personalized therapy for individual patients."
Based on these findings, Dr. Melnick and Dr. Chiosis recently received a multi-investigator collaborative grant from the National Cancer Institute to use this new PU-H71 proteome method to identify the proteins that maintain the survival of lymphoma cells. This funding is an example of how collaboration between investigators and institutions can synergistically accelerate the pace of biomedical research.
Study collaborators include Kamalika Moulick, James Ahn, Anna Rodina, Erica Gomes DaGama, Eloisi Caldas-Lopes, Fabiana Perna, Ly Vu, Xinyang Zhao, Danuta Zatorska, Tony Taldone, Mary Alpaugh, Stephen Nimer, Peter Smith-Jones, Nagavarakishore Pillarsetty, Thomas Ku, Jason Lewis, Steven Larson, Ross Levine and Hediye Erdjument-Bromage of Memorial Sloan-Kettering Cancer Center in New York City; Hongliang Zong, Leandro Cerchietti, Katerina Hatzi, Steven Gross and Monica Guzman of Weill Cornell Medical College; and Kristin Beebe and Len Neckers of the National Cancer Institute in Bethesda, Md.
This work was supported in part by the National Cancer Institute, Leukemia and Lymphoma Society, the Breast Cancer Research Fund, the SPORE Pilot Award and Research and Therapeutics Program in Prostate Cancer, the Hirshberg Foundation for Pancreatic Cancer Research, the Byrne Fund and the V Foundation for Cancer Research.
November 17, 2011
Researchers Discover Achilles' Heel in Lethal Form of Prostate Cancer
Weill Cornell Scientists Say This Vulnerability Can Be Attacked by a Targeted Drug Already in Clinical Trials to Treat Other Types of Cancers NEW YORK (Nov. 17, 2011) -- An international team of researchers led by clinicians at Weill Cornell Medical College have discovered a genetic Achilles' heel in an aggressive type of prostate cancer -- a vulnerability they say can be attacked by a targeted drug that is already in clinical trials to treat other types of cancers.
In today's issue of Cancer Discovery, the researchers report that the investigational drug had a dramatic response in animal models of neuroendocrine prostate cancer, and so provides the first hope of an effective human therapy for this lethal cancer. While fewer than 2 percent of prostate tumors in men are initially classified as neuroendocrine, many common adenocarcinoma prostate cancers change their biology during hormone therapy and morph into this aggressive subtype.
The study is the largest in-depth analysis of neuroendocrine prostate cancer yet undertaken, and the findings "are very exciting, because our bench-to-bedside approach identified a new molecular target for a subtype of prostate cancer for which a drug is now available," says the study's senior investigator, Dr. Mark A. Rubin, a professor of pathology and laboratory medicine at Weill Cornell Medical College and a pathologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
The finding is especially important because many men are now being treated with new, highly potent androgen suppression therapy, which these researchers believe will significantly increase the risk of future development of neuroendocrine tumors. Androgen is the fuel that feeds adenocarcinoma prostate cancers -- the most common kind of prostate cancer -- and androgen suppression therapy effectively destroys cancer cells that depend on this hormone. But the treatment does not touch neuroendocrine cells that may have been part of the tumor mix, and those untreatable cells now have room to grow and spread, the researchers say.
Although most of the approximately 30,000 men who die of advanced prostate cancer each year had been treated with androgen suppression therapy, it is impossible to know how many of them developed neuroendocrine tumors because patients are not usually biopsied at that stage in their disease, the researchers say. Studies to define changing biology in prostate cancer are only now starting.
"Still, there is evidence to suggest that androgen suppression results in a more aggressive cancer in a growing number of men, and now, with this study, we may have a way to treat these patients," says the study's lead investigator, Dr. Himisha Beltran, assistant professor of medicine at Weill Cornell Medical College and a medical oncologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
The Weill Cornell researchers undertook the study to see if they could find a way to target neuroendocrine tumors, which is considered an orphan disease among other types of prostate cancer. They used a next-generation sequence analysis to study the transcriptome -- the RNA messages that tumors produce -- of neuroendocrine tumors compared to adenocarcinoma prostate cancers.
A series of analyses using prostate cancer samples gathered by researchers from the U.S. and Europe concluded that the majority of neuroendocrine prostate cancers significantly overexpressed AURKA and MYCN genes, and 40 percent of these tumors also had extra copies of these genes. Surprisingly, they also found that a smaller subset of prostate adenocarcinomas also overexpressed these genes, and 5 percent had extra copies. "This may represent a high-risk population that could potentially benefit from screening and early intervention," says Dr. Beltran.
The AURKA gene produces aurora A kinase that plays an important role in cell growth, and some studies have suggested it is an oncogene, says Dr. Rubin. Overproduction of AURKA protein has been identified in colon, pancreatic, breast, liver, head and neck cancers, as well as other tumor types. MYCN encodes a transcription factor that is involved in nervous system development and works to turn on other genes. Alterations in the MYCN gene have not previously been seen in prostate cancer.
In neuroendocrine prostate cancer, the AURKA and MYCN mutations need to work together to promote cancer development, Dr. Rubin says. The kind of lethal interaction has also been found in neuroblastoma, a pediatric brain cancer. But the very good news, he adds, is that aurora kinase inhibitors have been developed and are being tested in a variety of cancers.
This study demonstrated that the aurora kinase inhibitor PHA-739358 worked against human neuroendocrine prostate cells in the laboratory, and that it had a dramatic response in animal models of neuroendocrine prostate cancer. It shrank large tumors to very small sizes in a short period of time, compared to untreated mice. There was also significantly enhanced sensitivity of neuroendocrine prostate cancer compared to prostate adenocarcinoma, Dr. Rubin says. While PHA-739358 was studied in prostate cancer without success, the researchers suspect that few of the patients who participated had neuroendocrine prostate tumors. Dr. Beltran is preparing a clinical trial to test an aurora kinase inhibitor in prostate cancer patients whose tumors contain neuroendocrine cancer cells or similar molecular alterations involving AURKA and MYCN.
"Not only are we eager to test the drug in patients diagnosed with neuroendocrine prostate cancer, we hope to develop biomarkers that can help us screen patients for these cells before the cancer advances," says Dr. Beltran.
Working with the Weill Cornell researchers on the study were researchers from Yale University, the University of British Columbia, the University of Pittsburgh School of Medicine, the University of Michigan, Howard Hughes Medical Institute, and INSERM, a French biomedical research institution.
"This is a great example of team science," Dr. Rubin says. "The study was only possible because a number of investigators from the U.S. and Europe sent us rare samples of this lethal cancer."
"The Prostate Cancer Foundation was pleased to provide support for this research," states Dr. Howard Soule, chief science officer at the Prostate Cancer Foundation. "This work is highly focused on our Foundation goal to eliminate lethal prostate cancer. We congratulate this team for generating findings that will be rapidly translated into patient treatment."
Other contributing Weill Cornell researchers include David S. Rickman, Kyung Park, Sung Suk Chae, Theresa Y. MacDonald, Karen L. Sheikh, Stéphane Terry, Scott T. Tagawa, Francesca Demichelis and David M. Nanus.
The research was sponsored by the Ann and William Bresnan Foundation, the Prostate Cancer Foundation, the NCI Early Detection Research Network, and the Department of Defense.
September 26, 2011
NIH Awards $5.5 Million Grant to Weill Cornell for Research Into Preventing Spina Bifida
The National Institutes of Health (NIH) has awarded a five-year, $5.5 million Transformative Research Project (T-R01) Award to fund research into risk factors for spina bifida and related congenital defects in which an area of the affected baby's spine or brain is not fully enclosed.The research will be led by Dr. Margaret Elizabeth Ross and Dr. Christopher E. Mason at Weill Cornell Medical College. Dr. Ross is the director of the Laboratory of Neurogenetics and Development and professor and vice chair for research in the Department of Neurology and Neuroscience, and Dr. Mason is an assistant professor of computational genomics in the Department of Physiology and Biophysics and at the HRH Prince Alwaleed Bin Talal Bin Abdulaziz Alsaud Institute for Computational Biomedicine. They will work in collaboration with Dr. Richard H. Finnell of the University of Texas at Austin.The award to Dr. Ross and Dr. Mason is among 79 awards totaling $143.8 million that were recently announced by the NIH. It is also one of only 17 given in the transformative research category in 2011. According to the NIH: "The Common Fund's NIH Director's Transformative Research Award initiative, formerly known as the Transformative Research Project (TR01), is created specifically to support exceptionally innovative and/or unconventional research projects that have the potential to create or overturn fundamental paradigms."Spina bifida and other serious neural tube defects (NTDs) develop from a complex interaction between genetic and environmental factors in which the environment influences how the fetus' genetic blueprint is read during development. One critical influence is the addition of methyl groups to DNA that can make it less likely that the modified, methylated gene will be used to make the protein it encodes. The Weill Cornell study seeks to identify which among all the genes in the cell are modified by folic acid levels, and how those patterns can be used to assess individual risk for having a child with spina bifida, or other serious NTDs. They will compare DNA from patients with NTDs with DNA from healthy patients with the ultimate goal of developing more individually targeted and more effective prevention strategies.The U.S. Public Health Service recommends that all women capable of becoming pregnant should consume folic acid to reduce their risk for having a pregnancy affected by spina bifida and other NTDs. Folic acid is in most multivitamins and many foods, including vegetables like broccoli and spinach, and fruits and juices such as orange juice. Some foods also have folic acid added to them, like certain breakfast cereals and other bread and grain products. Research at Weill Cornell will address questions of how folic acid protects against neural tube defects, how the need for folic acid varies with the genetic makeup of an individual, and whether there are alternative supplements, perhaps working elsewhere in the same pathway as folic acid, that would more effectively promote healthy birth outcomes by providing a patient-specific genetic test before pregnancy begins.In addition to the Weill Cornell award, three research scientists at Cornell University in Ithaca received a five-year Transformative Research Projects Award (T-R01) of approximately $3.04 million to fight cancer by targeting the regulation of metabolic enzymes. Drs. Richard A. Cerione, professor of pharmacology in the Department of Molecular Medicine, College of Veterinary Medicine, and professor of chemistry and chemical biology in the College of Arts and Sciences; Hening Lin, assistant professor of chemistry and chemical biology; and Robert S. Weiss, associate professor of molecular genetics in the College of Veterinary Medicine, are working on the project, "Succinylation and Malonylation as Novel Protein Modifications in Cancer." The research will focus on a new set of regulatory modifications that occur on proteins and which appear to be important to cancer progression, explain the researchers."More specifically, we believe that these modifications help to activate proteins that are responsible for meeting the hefty energy requirements of cancer cells. Thus, if we can block these modifications and the activation of the metabolic proteins, the cancer cells will not be able to meet their energy needs and hopefully die," says Dr. Cerione.
September 9, 2011
Register Now for Our Upcoming Open House for Prospective Students
Join us on Saturday, October 22, 2011 for a prospective student open house. You will have a chance to hear from faculty and current student representatives about the programs we offer. Come get your questions answered and learn how you fit in at WCGS!
The event will be held in the Weill Auditorium (2nd floor) at the Weill Cornell Medical College (1300 York Ave, at 69th). The schedule for the day is as follows:
11:30 am - 12:00 pm Registration
12:00 pm - 12:30 pm Program Presentation
12:30 pm - 3:00 pm Meet representatives from our PhD Programs of Study:
Biochemistry and Structural Biology
Cell and Developmental Biology
Immunology and Microbial Pathogenesis
Molecular Biology
Neuroscience
Pharmacology
Physiology, Biophysics and Molecular Biology
Register online now
Click here for a PDF version of the open house schedule.
August 31, 2011
Weill Cornell–Led Study Looks at Delayed Gratification in Adults First Tested With Marshmallows and Cookies as Pre-Schoolers. Researchers Find Aptitude for Delaying Gratification Is Consistent From Childhood Into Adulthood
NEW YORK (Aug. 31, 2011) — A landmark study in the late 1960s and early 1970s used marshmallows and cookies to assess the ability of preschool children to delay gratification. If they held off on the temptation to eat a treat, they were rewarded with more treats later. Some of the children resisted, others didn't.
A newly published follow-up revisits some of the same children, now adults, revealing that these differences remain: Those better at delaying gratification as children remained so as adults; likewise, those who wanted their cookie right away as children were more likely to seek instant gratification as adults. Furthermore, brain imaging showed key differences between the two groups in two areas: the prefrontal cortex and the ventral striatum. The findings are published in the Aug. 29 edition of the Proceedings of the National Academy of Sciences.
"This is the first time we have located the specific brain areas related to delayed gratification. This could have major implications in the treatment of obesity and addictions," says lead author Dr. B.J. Casey, director of the Sackler Institute for Developmental Psychobiology at Weill Cornell Medical College and the Sackler Professor of Developmental Psychobiology.
In the current study, Dr. Casey and her co-investigators recruited 59 adults who participated as young children in the original study and represented either extreme of the delayed-gratification spectrum — high delayers and low delayers. Because marshmallows and cookies can be less rewarding to adults, the researchers substituted two tests. In the first, participants looked at a screen displaying a series of faces and were asked to signal only when a face of one gender was shown. This "cool" test revealed no significant differences between the two groups. A second, "hot" test used emotional cues such as a happy or frightened face. These results were much more varied and revealed that aptitude for delayed gratification was consistent from childhood into adulthood.
"In this test, a happy face took the place of the marshmallow. The positive social cue interfered with the low delayer's ability to suppress his or her actions," explains Dr. Casey.
The second test was then repeated while the participant's brain was scanned using functional magnetic resonance imaging (fMRI). The results showed that the brain's prefrontal cortex was more active for high delayers and the ventral striatum — an area linked to addictions — was more active in low delayers.
The original marshmallows and cookies study was led by Dr. Walter Mischel, a co-author of the current study and the Niven Professor of Humane Letters at Columbia University.
Additional authors include Leah H. Somerville, Theresa Teslovich and Nicholas Franklin of Weill Cornell Medical College; Vivian Zayas of Cornell University, Ithaca, N.Y.; Gary Glover and Ian H. Gotlib of Stanford University; Ozlem Ayduk of the University of California, Berkeley; Mary Askren, John Jonides and Marc G. Berman of the University of Michigan, Ann Arbor; and Yuichi Shoda and Nicole L. Wilson of the University of Washington, Seattle. Funding for this multi-site study was provided by the National Institutes of Health (PI: Yuichi Shoda).
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August 5, 2011
Summer Academy 2011
From July 5 - August 4, 2011, 16 students from Manhattan Comprehensive Night and Day High School (MCNDHS) participated in a four week intensive program designed to expose the students to the basic concepts of molecular biology. The students attended lectures and preformed experiments under the guidance of Weill Cornell PhD students.
The program provides an interactive setting, which gives the students a more informative experience than they would otherwise receive in their normal high school classes.
On the final day of class, Dr. Randi Silver, Associate Dean of the Weill Cornell Graduate School of Medical Sciences addressed the students and stressed the importance of participating in programs such as the Summer Academy saying "When applying to college, you have to incorporate all of your academic experiences from high school into your applications and participating in our program not only provides you with vital lab experience, but it shows your initiative to explore subjects on an in-depth level before you get to college."
Outreach Director Dr. Xiaoai Chen informed the students that they are encouraged to come back and visit; previous students have returned during the summer and informed current students about what they can expect in college while pursuing a career in science and how the Sumer Academy played an important role in choosing their careers.
Associate Dean Francoise Freyre talked to the students about the Access Summer Research Program at Weill Cornell as well as the importance of exploring other scientific enrichment programs.
"If you want a Ph.D. I strongly encourage you to participate in summer programs. They will provide you with the necessary research experience to pursue a graduate level degree," she said.
July 25, 2011
Weill Cornell Graduate Student Attends Lindau Nobel Laureate Meeting
A Weill Cornell Ph.D. students was among the 3% of 20,000 applicants chosen to meet in June with Nobel Laureate scientists from around the world. Armen Kherlopian, a fourth-year student in the Physiology, Biophysics and Systems Biology program, attended the 61st annual Lindau Nobel Laureate Meeting from June 26th to July 1st along with close to 600 other students. The meeting gives young scientists the opportunity to spend a week engaging in in-depth discussions with 23 Nobel Laureates.
Armen, a member of Dr. David Christini's laboratory, works on the interface of high performance computing and biological applications. Speaking of his experience at the meeting Armen said that "Attending the Lindau Nobel Laureates and Students meeting was both personally and scientifically enriching." Armen reflected that "It was a distinct honor to have the chance to speak with a number of Nobel Laureates in small groups and on-on-one. I considered it a privilege to represent my school and country at the meeting"
May 23, 2011
Congratulations to the Class of 2011!
The 2011 Weill Cornell Graduate School of Medical Sciences' commencement ceremony, shared with the Medical College, honored 150 graduating MS (90) and PhD (60) students in Carnegie Hall on May 23.
Cornell University President David Skorton's address to the graduates was followed by Dean of the Graduate School Dr. David Hajjar’s introduction of the graduate student speaker Jason Gray.
Following the conferral of degrees, Dr. Hajjar presented the Distinguished Alumnus Award to Dr. Kathleen W. Scotto, MD/PhD ('83). Dr. Scotto is the Vice President of Research and Interim Dean of the Graduate School of Biomedical Sciences at the University of Medicine and Dentistry of New Jersey.
A reception to honor the graduates followed the ceremony.
Congratulations to our 2011 graduates!
May 23, 2011
Pharmacology Professor's Investigative Drug Shuts Down Aggressive Form of Leukemia That Affects Children
Dr. Ari Melnick, professor of pharmacology at Weill Cornell Graduate School and his colleagues at the University of California, San Francisco have been able to overcome resistance of a form of leukemia to targeted therapy, demonstrating complete eradication of the cancer in cell and animal studies. To read the full article click here.
May 20, 2011
Students Honored at Convocation Ceremony
This year's convocation ceremony was held on May 20 in Uris Auditorium
After presenting faculty member Dr. Heidi Stuhlman with the award for Excellence in Teaching and Mentoring, Dean of the Graduate School Dr. David Hajjar along with Associate Dean Dr. Randi Silver gave special recognition to the winners of the Vincent du Vigneaud awards and the Julian R. Rachele prize.
The list of this year’s winners is as follows:
2011 Vincent du Vigneaud Awards of Excellence
Poster Presentation:
Hao-Wei Wang, “Activation of Macrophages by IL-4 and Other Cytokines: Priming for Protumoral
Functions.” (Professor Johanna Joyce)
Oral Presentation:
Mark Lundquist, “Regulation of Nuclear Actin Pools by MICAL2.” (Professor Samie R. Jaffrey)
2011 Vincent du Vigneaud First-Year Award
Amy Jia Wang, “Determining the Role of HSP90 Subcellular Localization in HSP90 Inhibitor Resistance
in Glioblastoma.” (Professor Gabriela Chiosis)
2011 Vincent du Vigneaud Second-Year Award
Rachel Niec, “Development and Function of Peripherally Induced Regulatory T Cells.”
(Professor Alexander Rudensky)
2011 Julian R. Rachele Prize
Eduardo F. Gallo,“Neuronal Nitric Oxide Contributes to Neuroplasticity-Associated Protein Expression
through cGMP, Protein Kinase G, and Extracellular Signal-Regulated Kinase.” Journal of
Neuroscience 31(19):6947-6955, May 11, 2011 (Professor Constantino Iadecola)
Polloneal Ocbina,“Complex interactions between genes controlling trafficking in primary cilia.” Nature
Genetics, published online May 8, 2011(Professor Kathryn V. Anderson)
May 4, 2011
Weill Cornell's Dr. Carl Nathan Elected a Member of the National Academy of Sciences
NEW YORK (May 4, 2011) -- Weill Cornell Graduate School Professor of Microbiology and Immunology and of Medicine Dr. Carl Nathan was elected a member of the National Academy of Sciences (NAS) for his excellence in scientific research. Membership in the NAS is one of the highest honors given to a scientist in the United States. Dr. Nathan, chairman of the department of microbiology and immunology, the R.A. Rees Pritchett Professor of Microbiology, and the director of the Abby and Howard P. Milstein Program in Chemical Biology and Infectious Diseases at Weill Cornell Medical College, will be inducted into the Academy next April during its 149th annual meeting in Washington, D.C.
This year, Dr. Nathan has been elected along with 71 others. There are currently just over 2,000 active NAS members. More than 180 living Academy members have won Nobel Prizes.
One of today's pre-eminent immunologists, Dr. Nathan studies host-pathogen interactions along with an interdisciplinary team that seeks to bring immunology, microbiology, biochemistry, structural biology and chemical biology to bear on tuberculosis. Dr. Nathan received a medical degree from Harvard Medical School in Cambridge, Mass. He joined the Weill Cornell faculty in 1985 and was elected to the Institute of Medicine, another branch of the National Academies, in 1998.
"Dr. Nathan's pioneering work in immunology, microbiology, infectious disease and global health has long been a source of pride for Weill Cornell," says Dr. Antonio M. Gotto Jr., the Stephen and Suzanne Weiss Dean of Weill Cornell Medical College. "We are extremely proud that Dr. Nathan has been recognized with this honor."
"Each one of Dr. Nathan's many unique research contributions has significantly deepened our understanding of the immune system and its interaction with pathogens. In particular, his investigations into the mechanisms of tuberculosis have the potential to overcome the problem of antibiotic drug resistance and transform the way the disease is treated," says Dr. David P. Hajjar, the Frank H.T. Rhodes Distinguished Professor of Cardiovascular Biology and Genetics and dean of the Weill Cornell Graduate School of Medical Sciences.
Tuberculosis is a major cause of death around the world, with as many as one-third of the world's population infected with the bacterium, among whom about 9.4 million develop the disease each year and 1.7 million succumb, mainly in developing countries.
"This honor belongs to all of us and to those I've been so privileged to work with in years past," says Dr. Nathan, acknowledging his current and former labmates and collaborators, as well as the support of Weill Cornell's leadership.
The National Academy of Sciences is a private, nonprofit honorific society of distinguished scholars engaged in scientific and engineering research, dedicated to the furthering of science and technology and to their use for the general welfare. Established in 1863, the National Academy of Sciences has served to "investigate, examine, experiment and report upon any subject of science or art" whenever called upon to do so by any department of the government. For more information, or for the full list of newly elected members, visit www.nasonline.org/site/PageServer.
February 23, 2011
Dr. David P. Hajjar Named to Fulbright Scholars Program
Dean of the Weill Cornell Graduate School of Medical Sciences, Dr. David P. Hajjar has been named to the Fulbright Specialist Program by the Fulbright Commission. Dr. Hajjar is only the second Weill Cornell faculty member to be named to this scholarship program.
As part of this prestigious honor, Dr. Hajjar will work in Qatar with Dr. Javaid Sheikh, dean of Weill Cornell Medical College-Qatar and Dr. Kassim Ali Shaaban, dean of the College of Arts and Sciences of Qatar University in an effort to develop collaborative opportunities between Weill Cornell Medical College-Qatar and Qatar University.
Click here to read the complete article featured on the Weill Cornell Medical College website.
