David M. Feldser

faculty photo
Assistant Professor of Cancer Biology
Department: Cancer Biology
Graduate Group Affiliations

Contact information
751 BRB II/III
Department of Cancer Biology
Abramson Family Cancer Research Institute
421 Curie Blvd.
Philadelphia, PA 19104-6160
Office: 215-898-9203
Fax: 215-573-6735
Lab: 215-746-1452
Education:
B.S. (Biochemistry and Molecular Biology)
Juniata College, 1998.
Ph.D. (Human Genetics and Molecular Biology)
Johns Hopkins University School of Medicine, 2007.
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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.

Lab Members
Graduate Students:
Brian Lauderback
David Walter

Postdoctoral Fellows:
Michelle Cicchini
Travis Yates

Research Technician:
Camila Robles-Oteiza

Undergraduate Student:
Walter Wang

Administrative contact:
Carrie Kitzmiller
754 BRB II/III
kitzmill@upennn.edu
215-898-8532

Selected Publications

Li Y, Park AI, Mou H, Colpan C, Bizhanova A, Akama-Garren E, Joshi N, Hendrickson EA, Feldser D, Yin H, Anderson DG, Jacks T, Weng Z, Xue W: A versatile reporter system for CRISPR-mediated chromosomal rearrangements. Genome Biology 16(111): 1-11, 2015.

Yates T, Robles-Oteiza C, Cicchini M, Lauderback B, Feldser DM: XTR: A recombinase-based system for regulating gene function in a conditional and reversible manner. Salk Institute: Mechanisms and Models of Cancer 2015.

Yates T, Robles-Oteiza C, Wang W, Feldser DM: XTR: A recombinase-based system for regulating gene function in a conditional and reversible manner. AACR: Fourth International Conference on Frontiers in Basic Cancer Research 2015.

Robles-Oteiza C, Taylor S, Yates T, Cicchini M, Lauderback B, Cashman CR, Burds AA, Winslow MM, Jacks T, Feldser DM: Recombinase-based conditional and reversible gene regulation via XTR alleles. Nature Communications 6(8783): 1-9, 2015.

Chiou SH, Kim-Kiselak C, Risca V, Heimann M, Chuang CH, Burds A, Greenleaf W, Jacks T, Feldser DM, Winslow MM: A conditional system to specifically link disruption of protein-coding function with reporter expression in mice. Cell Reports 7(6): 2078-2086, 2014.

Feldser DM: The p53 tumor suppressor activates a tumor immune surveillance pathway that requires natural killer cells. Salk Institute: Mechanisms and Models of Cancer 2013.

Feldser DM: 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.

Feldser DM: Uncovering p53 Tumor-Suppressor Mechanisms in Lung Adenocarcinoma. Salk Institute: Mechanisms and Models of Cancer 2011.

Winslow MM, Dayton TL, Verhaak RGW, Kim-Kiselak C, Snyder EL, Feldser DM, Hubbard DD, DuPage MJ, Whittaker CA, Hoersch S, Yoon S, Crowley D, Bronson RT, Chiang DY, Meyerson M, Jacks T: Suppression of lung adenocarcinoma progression by Nkx2-1. Nature 473(7345): 101-104, 2011.

Xue W, Meylan E, Oliver TG, Feldser DM, Winslow MM, Bronson R, Jacks T: Response and resistance to NF-κB inhibitors in mouse models of lung adenocarcinoma. Cancer Discovery 1(3): 236-247, 2011.

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Last updated: 04/15/2016
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