David M. Feldser, Ph.D.
709 BRB II/III
Department of Cancer Biology
Abramson Family Cancer Research Institute
Philadelphia, PA 19104-6160
B.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 ExpertiseResearch 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.
- 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.
757 BRB II/III
Selected PublicationsStokes K, Acosta J, Lauderback B, Robles-Oteiza C, Cicchini M, and Feldser DM: Natural killer cells limit the clearance of senescent lung adenocarcinoma cells. Oncogenesis 8(4): 24, April 2019.
Walter DM, Yates TJ, Ruiz-Torres M, Kim-Kiselak C, Gudiel AA, Deshpande C, Wang WZ, Cicchini M, Stokes KL, Tobias JW, Buza E, Feldser DM: RB constrains lineage fidelity and multiple stages of tumour progression and metastasis. Nature 569(7756): 423-427, 2019.
Acosta J, Wang W, and Feldser DM: Off and Back-On Again: A Tumor Suppressor's Tale. Oncogene 2018 Notes: e-published before printing.
Feldser DM: Modeling Rb loss and pathway reactivation in lung adenocarcinoma. Fifth AACR-IASLC International Joint Conference: Lung Cancer Translational Science from the Bench to the Clinic 2018.
Cicchini M, Buza EL, Sagal KM, Gudiel AA, Durham AC, Feldser DM: Context-Dependent Effects of Amplified MAPK Signaling during Lung Adenocarcinoma Initiation and Progression. Cell Reports 18(8): 1958-1969, 2017.
Walter DM, Venancio OS, Buza EL, Tobias JW, Deshpande C, Gudiel AA, Kim-Kiselak C, Cicchini M, Yates TJ, Feldser DM: Systematic in vivo inactivation of chromatin regulating enzymes identifies Setd2 as a potent tumor suppressor in lung adenocarcinoma. Cancer Research 77(7): 1719-1729, 2017.
Feldser DM: Rb limits tumor progression and the onset metastatic disease states in lung adenocarcinoma by repressing Hmga2. The Fourth International Rb Meeting 2016.
Xue W, Li Y, Park A, Moue H, Cansu C, Bizhanova A, Akama-Garren E, Joshi J, Hendrickson E, Feldser DM, Yin, Anderson DG, Jacks T, Weng, Z: 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.