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David M. Feldser, Ph.D.
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Associate Professor of Cancer Biology
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Department: Cancer Biology
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Graduate Group Affiliations
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- Immunology 6b
- Cell and Molecular Biology e
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Contact information
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421 Curie Blvd.
16 756 BRB II/III
25 Department of Cancer Biology
51 Abramson Family Cancer Research Institute
Philadelphia, PA 19104-6160
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16 756 BRB II/III
25 Department of Cancer Biology
51 Abramson Family Cancer Research Institute
Philadelphia, PA 19104-6160
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Office: 215-898-9203
32 Fax: 215-746-5525
32 Lab: 215-746-1452
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32 Fax: 215-746-5525
32 Lab: 215-746-1452
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Email:
dfeldser@upenn.edu
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dfeldser@upenn.edu
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Publications
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Education:
21 9 B.S. 2f (Biochemistry and Molecular Biology) c
28 Juniata College, 1998.
21 a Ph.D. 31 (Human Genetics and Molecular Biology) c
44 Johns Hopkins University School of Medicine, 2007.
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21 9 B.S. 2f (Biochemistry and Molecular Biology) c
28 Juniata College, 1998.
21 a Ph.D. 31 (Human Genetics and Molecular Biology) c
44 Johns Hopkins University School of Medicine, 2007.
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Links
a1 Search PubMed for articles
54 AFCRI website
8b Department of Cancer Biology faculty page
58 Feldser Lab website
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Permanent linka1 Search PubMed for articles
54 AFCRI website
8b Department of Cancer Biology faculty page
58 Feldser Lab website
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34 - Cyclophilin-assisted programmed cell death
30 - Genotype-dependent immune surveillance
2d - Regulation of cell state plasticity
22 - Cancer gene dependencies
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72 Key Words: mouse modeling, tumor suppressors, tumor immunology, tumor microenvironment, lung cancer
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3a Current Research In The Feldser Laboratory
4fc 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.
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20 Rotation Projects
235 The Feldser Lab is seeking a thesis student to study a novel form of cell death that is induced by the p53 tumor suppressor. Our preliminary data demonstrate that reintroduction of p53 in small cell lung cancer induces a massive increase in ER-phagy, a directed autophagy program that recycles the endoplasmic reticulum, ultimately leading to cell swelling and necrosis. The thesis student would elucidate the molecular determinants of this new cell death program. Experimental platforms will involve in vivo mouse models and in vitro cell culture systems.
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49 Please contact Dr. Feldser to discuss specific rotation projects.
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1a Lab Members
18 Postdocs:
39 Maria Solares, Ph.D. Penn State University
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21 Graduate Students:
1e Keren Adler, CB (2018)
21 Amy Gladstein, G&E (2019)
1f Katie Doerig, CB (2019)
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23 Research Specialist:
18 Maggie Robertson
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19 Undergrad:
15 Faaiz Quaisar
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28 Administrative Assistant:
50 Lesley Moreno Ljmoreno@upenn.edu
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Description of Research Expertise
2a Research Interests34 - Cyclophilin-assisted programmed cell death
30 - Genotype-dependent immune surveillance
2d - Regulation of cell state plasticity
22 - Cancer gene dependencies
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72 Key Words: mouse modeling, tumor suppressors, tumor immunology, tumor microenvironment, lung cancer
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3a Current Research In The Feldser Laboratory
4fc 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.
8
20 Rotation Projects
235 The Feldser Lab is seeking a thesis student to study a novel form of cell death that is induced by the p53 tumor suppressor. Our preliminary data demonstrate that reintroduction of p53 in small cell lung cancer induces a massive increase in ER-phagy, a directed autophagy program that recycles the endoplasmic reticulum, ultimately leading to cell swelling and necrosis. The thesis student would elucidate the molecular determinants of this new cell death program. Experimental platforms will involve in vivo mouse models and in vitro cell culture systems.
8
49 Please contact Dr. Feldser to discuss specific rotation projects.
8
1a Lab Members
18 Postdocs:
39 Maria Solares, Ph.D. Penn State University
8
21 Graduate Students:
1e Keren Adler, CB (2018)
21 Amy Gladstein, G&E (2019)
1f Katie Doerig, CB (2019)
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23 Research Specialist:
18 Maggie Robertson
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19 Undergrad:
15 Faaiz Quaisar
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28 Administrative Assistant:
50 Lesley Moreno Ljmoreno@upenn.edu
e 29
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1cb Acosta J, Li Q, Freeburg NF, Murali N, Indeglia A, Grothusen GP, Cicchini M, Mai H, Gladstein AC, Adler KM, Doerig KR, Li J, Ruiz-Torres M, Manning KL, Stanger BZ, Busino L, Murphy M, Wan L, Feldser DM: p53 restoration in small cell lung cancer identifies a latent cyclophilin-dependent necrosis mechanism. Nature Communications 14(1): 4403, 2023 Notes: doi: 10.1038/s41467-023-40161-9.
117 Walter DM, Gladstein AC, Doerig KR, Natesan R, Baskaran SG, Gudiel AA, Adler KM, Acosta JO, Wallace DC, Asangani IA, Feldser DM: Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 71 signaling. Communications Biology 6(1): 255, 2023 Notes: doi: 10.1038/s42003-023-04618-3.
102 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.
14c 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.
104 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.
c6 Acosta J, Wang W, and Feldser DM: Off and Back-On Again: A Tumor Suppressor's Tale. Oncogene 2018 Notes: Epub ahead of print.
16b 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.
10f 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.
11b 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.
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Selected Publications
14e Freeburg NF, Peterson N, Ruiz DA, Gladstein AC, Feldser DM: Metastatic Competency and Tumor Spheroid Formation Are Independent Cell States Governed by RB in Lung Adenocarcinoma. Cancer Res Commun 3(10): 1992-2002, 2023 Notes: doi: 10.1158/2767-9764.CRC-23-0172.1cb Acosta J, Li Q, Freeburg NF, Murali N, Indeglia A, Grothusen GP, Cicchini M, Mai H, Gladstein AC, Adler KM, Doerig KR, Li J, Ruiz-Torres M, Manning KL, Stanger BZ, Busino L, Murphy M, Wan L, Feldser DM: p53 restoration in small cell lung cancer identifies a latent cyclophilin-dependent necrosis mechanism. Nature Communications 14(1): 4403, 2023 Notes: doi: 10.1038/s41467-023-40161-9.
117 Walter DM, Gladstein AC, Doerig KR, Natesan R, Baskaran SG, Gudiel AA, Adler KM, Acosta JO, Wallace DC, Asangani IA, Feldser DM: Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 71 signaling. Communications Biology 6(1): 255, 2023 Notes: doi: 10.1038/s42003-023-04618-3.
102 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.
14c 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.
104 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.
c6 Acosta J, Wang W, and Feldser DM: Off and Back-On Again: A Tumor Suppressor's Tale. Oncogene 2018 Notes: Epub ahead of print.
16b 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.
10f 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.
11b 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.
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