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About

Ramon E. Parsons, MD, PhD, is Director of The Tisch Cancer Institute (TCI) and Dean for Cancer Research at the Icahn School of Medicine at Mount Sinai. He is also the Ward-Coleman Chair in Cancer Research, Director of the Mount Sinai Tisch Cancer Center, and Chair of the Department of Oncological Sciences at Icahn Mount Sinai. In 2017, Dr. Parsons was appointed Director of The Tisch Cancer Institute—a National Cancer Institute-designated cancer center—after serving as Deputy Director and Co-Leader of the Cancer Mechanisms program. Dr. Parsons joined Icahn Mount Sinai in 2013. Previously, he was on the faculty of the departments of Pathology and Medicine at Columbia University. He was named Assistant Professor in 1995 and later became the Avon Foundation Chair for Breast Cancer Research in 2002. He was named Professor in 2007 and Leader of its Breast Cancer Program at the Herbert Irving Comprehensive Cancer Center in 2005. Dr. Parsons is a member of the National Academy of Medicine, American Society for Clinical Investigation, American College of Physicians. He was Chair of the AACR Special conferences committee for two terms from 2011-2017, which initiated and planned more than 75 scientific meetings on different cancer-related topics. Dr. Parsons maintains an active laboratory and has received multiple awards for his research, including the 2011 American Association for Cancer Research (AACR) Outstanding Investigator Award for Breast Cancer Research. He is internationally recognized as an expert in the fields of cancer genetics and signal transduction with an emphasis on tumor suppressor genes including PTEN. Ramon Parsons, MD, PhD., grew up in Washington, DC, and graduated from Columbia College, Columbia University in 1983.  Dr. Parsons then attended the State University of New York at  Stony Brook where he received his M.D. and Ph.D. degrees in 1992.  Dr. Parsons continued his education at Johns Hopkins University  School of Medicine as a postdoctoral fellow with Bert Vogelstein.  There, he and his colleagues discovered that inactivation of DNA mismatch repair genes cause hereditary colorectal cancer. At Columbia University Medical Center, his research laboratory identified the PTEN tumor suppressor gene, which he showed is inactivated in a wide variety of cancers and cancer predisposition syndromes. He has been a leader in establishing the importance of PTEN and the PI3K pathway for cancer using a combination of genetic, biochemical, human tissue, metabolic, and systems biology approach. In 2013, he joined the faculty at the Icahn School of Medicine at Mount Sinai as Ward-Coleman Professor in Cancer Research, Chairman of the Department of Oncological Sciences and co-Leader of the Cancer Mechanisms Program of the Tisch Cancer Institute. In 2016, he was selected as an Icahn Scholar and as the Deputy Director of the Tisch Cancer Institute. Recently, Dr. Parsons was appointed Director of the Tisch Cancer Institute, ISMMS, and Director of Mount Sinai Cancer, MSHS. Prior to joining the faculty at ISMMS, Dr. Parsons was the Avon Professor of Pathology and Medicine and Leader of the Breast Cancer Program of the Herbert Irving Cancer Center at Columbia University Medical Center. Dr. Parsons is a member of the American Society for Clinical Investigation and the American Association of Physicians. He is also a recipient of the 2011 American Association for Cancer Research Outstanding Investigator Award for Breast Cancer Research. He served as Chair of the Special Conferences Committee at the AACR from 2011-2017. Dr. Parsons was inducted into the Johns Hopkins University Society of Scholars in 2015 and, elected to the National Academy of Medicine in 2017.

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Skills

Experience

Organization
Director of Tisch Cancer Institute & Mount Sinai Cancer

Icahn School of Medicine at Mount Sinai

Mar-2013 to Present

Publication

  • dott image February, 1996

Analysis of mismatch repair genes in hereditary non–polyposis colorectal cancer patients

Hereditary non–polyposis colorectal cancer (HNPCC) is an autosomal dominant disorder characterized by the early onset of colorectal cancer and linked to germline defects in at least four m...

  • dott image December, 1995

Microsatellite Instability and Mutations of the Transforming Growth Factor β Type II Receptor Gene in Colorectal Cancer1

The TGFβ type II receptor (RII) was found to be mutated within a polyadenine tract in 100 of 111 (90%) colorectal cancers with microsatellite instability. Other polyadenine tracts of simila...

  • dott image December, 1995

A Transforming Growth Factor β Receptor Type II Gene Mutation Common in Colon and Gastric but Rare in Endometrial Cancers with Microsatellite Instabi...

We have recently demonstrated that mutation of the transforming growth factor-β (TGF-β) receptor type II (RII) gene is characteristic of colon cancers exhibiting microsatellite instability...

  • dott image March, 1995

The Molecular Basis of Turcot's Syndrome

Background Turcot's syndrome is characterized clinically by the concurrence of a primary brain tumor and multiple colorectal adenomas. We attempted to define the syndrome at the molecular l...

  • dott image January, 1995

Mismatch repair gene defects in sporadic colorectal cancers with microsatellite instability

Microsatellite instability has been observed in both sporadic and hereditary forms of colorectal cancer. In the hereditary form, this instability is generally due to germline mutations in mi...

  • dott image September, 1994

hMSH2 Mutations in Hereditary Nonpolyposis Colorectal Cancer Kindreds1

It has recently been shown that hereditary nonpolyposis colorectal cancer (HNPCC) is caused by hereditable defects in DNA mismatch repair genes. However, the fraction of HNPCC due to defects...

  • dott image December, 1993

Mutations of a mutS homolog in hereditary nonpolyposis colorectal cancer

Recent studies have shown that a locus responsible for hereditary nonpolyposis colorectal cancer (HNPCC) is on chromosome 2p and that tumors developing in these patients contain alterations ...

  • dott image December, 1993

Hypermutability and mismatch repair deficiency in RER+ tumor cells

A subset of sporadic colorectal tumors and most tumors developing in hereditary nonpolyposis colorectal cancer patients display frequent alterations in microsatellite sequences. Such tumors ...

  • dott image November, 1993

WAF1, a potential mediator of p53 tumor suppression

The ability of p53 to activate transcription from specific sequences suggests that genes induced by p53 may mediate its biological role as a tumor suppressor. Using a subtractive hybridizati...