Faculty

David M. Feldser, Ph.D.

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

Contact information
421 Curie Blvd.
709 BRB II/III
Department of Cancer Biology
Abramson Family Cancer Research Institute
Philadelphia, PA 19104-6160
Office: 215-898-9203
Fax: 215-746-5525
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
- Genome engineering in the mouse
- Role of the immune system in 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
Rotation students are typically paired with an established member of the lab to carryout their rotation project. While progress on the project and technical competency is expected, the major goal of the rotation is to determine whether the student is a good fit for the lab. Establishing strong working relationships with each lab member is key. Rotation students will meet formally with Dr. Feldser each week but are encouraged to 'stop by' often. At the end of the rotation period, the student will present a synopsis of the project's results at the Feldser Lab Group Meeting.

Current projects for the 2021-2022 academic year are:
1- Investigate the intersection of chromatin regulation and metabolic control in lung cancer
2- Investigate a novel p53-regulated (non-apoptotic) cell death mechanism in lung cancer
3- Investigate cell state plasticity during tumor evolution and in response to therapy
4- Investigate the concept of an immunogenicity threshold and its impact on immunoediting and immune checkpoint therapy

Please contact Dr. Feldser to discuss specific rotation projects.

Lab Members
Graduate Students:
Jonuelle Acosta, CB (2016)
Trip Freeburg, CB (2017)
Keren Adler, CB (2018)
Amy Gladstein, G&E (2019)
Katie Doerig, CB (2019)


Administrative contact:
Ashley Hughes
757 BRB II/III
ashughes@upenn.edu
215-898-8532

Selected Publications

Kharbanda A, Walter DM, Gudiel AA, Schek N, Feldser DM, and Witze ES: Blocking EGFR palmitoylation suppresses PI3K signaling and mutant KRAS lung tumorigenesis. Science Signaling 13(621), 2020.

Lin JH, Huffman AP, Wattenberg MM, Walter DM, Carpenter EL, Feldser DM, Beatty GL, Furth EE, Vonderheide RN: Type 1 conventional dendritic cells are systemically dysregulated early in pancreatic carcinogenesis. Journal of Experimental Medicine 217(8), 2020.

Garg R, Cooke M, Benavides F, Abba MC, Cicchini M, Feldser DM, Kazanietz MG: PKC epsilon is required for KRAS-driven lung tumorigenesis. Cancer Research 2020 Notes: Epub ahead of print.

Tsang T, Posimo JM, Guidiel A, Cicchini M, Feldser DM, Brady D: Copper is an essential regulator of the autophagic kinases ULK1/2 to drive lung adenocarcinoma. Nat Cell Biology 22(4): 412-424, 2020 Notes: Epub 2020 Mar 16.

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.

Stokes 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, 2019.

Acosta J, Wang W, and Feldser DM: Off and Back-On Again: A Tumor Suppressor's Tale. Oncogene 2018 Notes: Epub ahead of print.

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.

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Last updated: 09/14/2021
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