David M. Feldser, Ph.D.
Assistant Professor of Cancer Biology
Department: Cancer Biology
Graduate Group Affiliations
Contact information
421 Curie Blvd.
713 BRB II/III
Philadelphia, PA 19104-6160
713 BRB II/III
Philadelphia, PA 19104-6160
Office: 215-898-9203
Fax: 215-573-6735
Lab: 215-746-1452
Fax: 215-573-6735
Lab: 215-746-1452
Email:
dfeldser@upenn.edu
dfeldser@upenn.edu
Publications
Links
Search PubMed for articles
AFCRI website
Department of Cancer Biology faculty page
Feldser Lab website
Search PubMed for articles
AFCRI website
Department of Cancer Biology faculty page
Feldser Lab website
Education:
B.S. (Biochemistry and Molecular Biology)
Juniata College, 1998.
Ph.D. (Human Genetics and Molecular Biology)
Johns Hopkins University School of Medicine, 2007.
Permanent linkB.S. (Biochemistry and Molecular Biology)
Juniata College, 1998.
Ph.D. (Human Genetics and Molecular Biology)
Johns Hopkins University School of Medicine, 2007.
Description of Research Expertise
Research Interests- Mechanisms of tumor-suppressor gene action
- Role of the immune system in tumor suppression
- Genome engineering in the mouse
- Chemical genetic strategies to modulate tumor suppression
Key Words: mouse modeling, tumor suppressors, tumor immunology, tumor microenvironment, lung cancer
Current Research In The Feldser Laboratory
The Feldser lab uses genetically engineered mouse models to study tumor progression and metastasis of common forms of human cancer. These models faithfully recapitulate many aspects of the histopathological progression of their human counterparts. Tumors initiate as lesions within the appropriate tissue microenvironment from single cells due to induced activation of latent oncogenes and/or deletion of key tumor suppressor genes. These lesions evolve through multiple cellular states toward malignant and metastatic disease. Our research is dedicated to deconstructing the multistep process of tumorigenesis. The major emphasis of our laboratory is to uncover the pathways that are disabled by mutational inactivation of tumor-suppressor genes as well as those pathways stimulated by aberrant oncogene activation. We focus on mouse models in order to employ novel genetic tools to regulate gene function in developing cancerous lesions as well as to track cancer growth and dissemination via bioluminescent and fluorescent techniques. We couple cellular, genomic and biochemical analyses to our powerful in vivo tools to discern the mechanics of tumor progression and metastasis with the goal of identifying new therapeutic strategies to eradicate malignant cells.
Rotation Projects
- Studies of the physiological role of p53, Rb, and Kras in lung cancer
- Oncogene signal amplification in tumor initiation and progression
- Validation of novel methods to regulate gene function in the mouse
- Characterization of chemical regulators of tumor suppressors
Please contact Dr. Feldser to discuss specific rotation projects.
Selected Publications
Feldser David M: The p53 tumor suppressor orchestrates a novel tumor immune surveillance pathway that requires natural killer cells. Cold Spring Harbor: Mechanisms and Models of Cancer 2012.Xue Wen, Meylan Etienne, Oliver Trudy G, Feldser David M, Winslow Monte M, Bronson Roderick, Jacks Tyler: Response and resistance to NF-κB inhibitors in mouse models of lung adenocarcinoma. Cancer Discovery 1(3): 236-47, Aug 2011.
Winslow Monte M, Dayton Talya L, Verhaak Roel G W, Kim-Kiselak Caroline, Snyder Eric L, Feldser David M, Hubbard Diana D, DuPage Michel J, Whittaker Charles A, Hoersch Sebastian, Yoon Stephanie, Crowley Denise, Bronson Roderick T, Chiang Derek Y, Meyerson Matthew, Jacks Tyler: Suppression of lung adenocarcinoma progression by Nkx2-1. Nature 473(7345): 101-4, May 2011.
Feldser David M: Uncovering p53 Tumor-Suppressor Mechanisms in Lung Adenocarcinoma. Salk Institute: Mechanisms and Models of Cancer 2011.
Feldser David M, Kostova Kamena K, Winslow Monte M, Taylor Sarah E, Cashman Chris, Whittaker Charles A, Sanchez-Rivera Francisco J, Resnick Rebecca, Bronson Roderick, Hemann Michael T, Jacks Tyler: Stage-specific sensitivity to p53 restoration during lung cancer progression. Nature 468(7323): 572-5, Nov 2010.
Huarte Maite, Guttman Mitchell, Feldser David, Garber Manuel, Koziol Magdalena J, Kenzelmann-Broz Daniela, Khalil Ahmad M, Zuk Or, Amit Ido, Rabani Michal, Attardi Laura D, Regev Aviv, Lander Eric S, Jacks Tyler, Rinn John L: A large intergenic noncoding RNA induced by p53 mediates global gene repression in the p53 response. Cell 142(3): 409-19, Aug 2010.
Feldser David M: Experimental restoration of tumor suppressor function identifies a context specific sensitivity to p53 in non-small cell lung cancer. Cold Spring Harbor: Mechanisms and Models of Cancer 2010.
Meylan Etienne, Dooley Alison L, Feldser David M, Shen Lynn, Turk Erin, Ouyang Chensi, Jacks Tyler: Requirement for NF-kappaB signalling in a mouse model of lung adenocarcinoma. Nature 462(7269): 104-7, Nov 2009.
Guttman Mitchell, Amit Ido, Garber Manuel, French Courtney, Lin Michael F, Feldser David, Huarte Maite, Zuk Or, Carey Bryce W, Cassady John P, Cabili Moran N, Jaenisch Rudolf, Mikkelsen Tarjei S, Jacks Tyler, Hacohen Nir, Bernstein Bradley E, Kellis Manolis, Regev Aviv, Rinn John L, Lander Eric S: Chromatin signature reveals over a thousand highly conserved large non-coding RNAs in mammals. Nature 458(7235): 223-7, Mar 2009.
Godar Samuel, Ince Tan A, Bell George W, Feldser David, Donaher Joana Liu, Bergh Jonas, Liu Anne, Miu Kevin, Watnick Randolph S, Reinhardt Ferenc, McAllister Sandra S, Jacks Tyler, Weinberg Robert A: Growth-inhibitory and tumor- suppressive functions of p53 depend on its repression of CD44 expression. Cell 134(1): 62-73, Jul 2008.

