Event Detail (Archived)

Cancer Initiation and Maintenance Genes

  • This event already took place in January 2014
  • Caspary Auditorium

Event Details

Type
Friday Lecture Series
Speaker(s)
Scott Lowe, Ph.D., chair, Geoffrey Beene Cancer Research Center, Memorial Sloan-Kettering Cancer Center; investigator, Howard Hughes Medical Institute
Speaker bio(s)

Cancer arises through an evolutionary process whereby normal cells acquire mutations that erode growth controls, leading to the inappropriate expansion of aberrantly proliferating cells. Such mutations can involve activation of oncogenes or inactivation of tumor-suppressor genes, each contributing one or more new capabilities to the developing cancer cell. However, cancer is not an inevitable consequence of oncogenic mutations; instead, cells acquiring such mutations can be eliminated or kept in check by innate tumor-suppressor programs that can be activated in these damaged cells. Dr. Lowe's laboratory studies tumor-suppressor networks controlling apoptosis and senescence and how their disruption influences malignant behavior. They previously showed that apoptosis and cellular senescence are potent barriers to oncogene-driven tumorigenesis and that each contributes to the antitumor action of many chemotherapeutic drugs. Thus, not only do mutations that disrupt apoptosis and senescence promote tumor progression but, depending on the particular lesion, they can also reduce the efficacy of cancer therapy. To facilitate this research, Dr. Lowe's lab has recently developed new mouse cancer models based on the genetic manipulation of stem and progenitor cells ex vivo, followed by transplantation of the altered cells into the appropriate organ of syngeneic recipient mice. This approach allows the scientists to rapidly study the impact of many genes and gene combinations on tumorigenesis in a "mosaic" setting where tumor-initiating cells are embedded in normal tissues. Furthermore, the lab has developed powerful methods for using RNA interference to suppress gene function in vivo in either a stable and reversible manner. Current efforts in the laboratory strive to integrate mosaic mouse models, RNA interference and cancer genomics to identify new components of tumor suppressor gene networks and characterize their impact on tumorigenesis and treatment response. In addition, the lab is optimizing and implementing new RNAi-based methods to identify tumor maintenance genes whose inhibition causes cancer regressions.
 
Dr. Lowe completed his graduate studies at the Massachusetts Institute of Technology under the supervision of Dr. H. Earl Ruley, and received his Ph.D. for research on the role of the p53 tumor suppressor in oncogenic transformation, apoptosis and chemosensitivity. After a brief postdoctoral position in the MIT Center for Cancer Research, Dr. Lowe initiated independent research at Cold Spring Harbor Laboratory as a Cold Spring Harbor Laboratory Fellow and then a member of the faculty. Dr. Lowe's research has made important contributions to our understanding of the p53 tumor suppressor pathway, as well as the processes of multi-step carcinogenesis, cellular senescence and tumor-cell drug resistance. Dr. Lowe's work has been recognized by several awards, including a Sydney Kimmel Foundation Scholar Award, a Rita Allen Foundation Scholar Award, the AACR Outstanding Investigator Award, the Paul Marks Prize for Cancer Research, the Kunio Yagi Medal and the Alfred G. Knudsen Award.

Open to
Public
Reception
Refreshments, 3:15 p.m. - 3:45 p.m., Abby Lounge
Contact
Linda Hanssler
Phone
(212) 327-7714
Sponsor
Linda Hanssler
(212) 327-7714
lhanssler@rockefeller.edu
Readings
http://librarynews.rockefeller.edu/?p=3281