Matthew Oser, MD, PhD

Matthew Oser, MD, PhD

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Matthew Oser, MD, PhD

Dr. Oser received his MD and PhD degrees from Albert Einstein College of Medicine in 2011. He received internal medicine training at Brigham and Women’s Hospital and his medical oncology fellowship training at Dana-Farber/Harvard Cancer Center. He is currently an Assistant Professor of Medicine at Dana-Farber Cancer Institute and Harvard Medical School where he runs a research laboratory focused on small cell lung cancer and is a medical oncologist.



Assistant Professor of Medicine, Harvard Medical School

Clinical Interests

Thoracic oncology

Board Certification

  • Internal Medicine, 2014
  • Medical Oncology
    , 2016


  • Dana-Farber/Harvard Cancer Center


  • Brigham and Women's Hospital

Medical School

  • Albert Einstein College of Medicine

Recent Awards

  • Damon Runyon Clinical Investigator Award (2019)


    Identification of Novel Dependencies in Small Cell Lung Cancer (SCLC) that are a Consequence of Loss of Function Mutations in Tumor Suppressor Genes or from SCLCs Neuroendocrine Differentiation State
    Although small cell lung cancer (SCLC) is initially highly responsive to chemotherapy, the disease recurs in nearly all patients in less than a year. At recurrence, there are no approved targeted therapies. Genomic sequencing of human SCLCs has shown that SCLCs have no actionable mutations and that nearly all SCLCs harbor loss of function (LOF) mutations in the tumor suppressor genes RB1 and TP53, while ~25% of SCLCs harbor LOF mutations in NOTCH.  Furthermore, sustained expression of neural/neuroendocrine lineage transcription factors ASCL1 and NEUROD1 are required for SCLC survival. However, ASCL1 and NEUROD1 are transcriptions factors and therefore are not directly druggable.
    The Oser laboratory utilizes CRISPR-Cas9 screening approaches to identify new SCLC therapeutic targets that are either required for sustained expression of the neural/neuroendocrine lineage transcription factors ASCL1 and NEUROD1, or that are required for SCLC survival as a consequence of LOF mutations in tumor suppressor genes (i.e. are synthetic lethal interactors with SCLC tumor suppressor genes). In addition, we utilize a novel genetically-engineered mouse model of SCLC developed using CRISPR-Cas9 to study the consequences of inactivating novel candidate therapeutic targets during SCLC tumorigenesis. Ultimately, the Oser laboratory seeks to discover new targeted therapies for SCLC patients that function as synthetic lethal interactors with SCLC tumor suppressor genes or that function to block neuroendocrine differentiation.


      • KDM6A epigenetically regulates subtype plasticity in small cell lung cancer. Nat Cell Biol. 2023 09; 25(9):1346-1358. View in: Pubmed

      • Regulation of neuroendocrine plasticity by the RNA-binding protein ZFP36L1. Nat Commun. 2022 08 25; 13(1):4998. View in: Pubmed

      • Plasticity in the Absence of NOTCH Uncovers a RUNX2-Dependent Pathway in Small Cell Lung Cancer. Cancer Res. 2022 01 15; 82(2):248-263. View in: Pubmed

      • Intrinsic Immunogenicity of Small Cell Lung Carcinoma Revealed by Its Cellular Plasticity. Cancer Discov. 2021 08; 11(8):1952-1969. View in: Pubmed

      • Targeting oncoproteins with a positive selection assay for protein degraders. Sci Adv. 2021 02; 7(6). View in: Pubmed

      • New Approaches to SCLC Therapy: From the Laboratory to the Clinic. J Thorac Oncol. 2020 04; 15(4):520-540. View in: Pubmed

      • CDK7 Inhibition Potentiates Genome Instability Triggering Anti-tumor Immunity in Small Cell Lung Cancer. Cancer Cell. 2020 01 13; 37(1):37-54.e9. View in: Pubmed

      • The KDM5A/RBP2 histone demethylase represses NOTCH signaling to sustain neuroendocrine differentiation and promote small cell lung cancer tumorigenesis. Genes Dev. 2019 12 01; 33(23-24):1718-1738. View in: Pubmed

      • Cyclin D-CDK4 relieves cooperative repression of proliferation and cell cycle gene expression by DREAM and RB. Oncogene. 2019 06; 38(25):4962-4976. View in: Pubmed

      • Deubiquitinases Maintain Protein Homeostasis and Survival of Cancer Cells upon Glutathione Depletion. Cell Metab. 2019 05 07; 29(5):1166-1181.e6. View in: Pubmed

      • Cells Lacking the RB1 Tumor Suppressor Gene Are Hyperdependent on Aurora B Kinase for Survival. Cancer Discov. 2019 02; 9(2):230-247. View in: Pubmed

      • Autochthonous tumors driven by Rb1 loss have an ongoing requirement for the RBP2 histone demethylase. Proc Natl Acad Sci U S A. 2018 04 17; 115(16):E3741-E3748. View in: Pubmed

      • Small-Cell Neuroendocrine Tumors: Cell State Trumps the Oncogenic Driver. Clin Cancer Res. 2018 04 15; 24(8):1775-1776. View in: Pubmed

      • Peptidic degron in EID1 is recognized by an SCF E3 ligase complex containing the orphan F-box protein FBXO21. Proc Natl Acad Sci U S A. 2015 Dec 15; 112(50):15372-7. View in: Pubmed

      • Transformation from NSCLC to SCLC: when did it happen? - Authors' reply. Lancet Oncol. 2015 Jul; 16(7):e309-10. View in: Pubmed

      • Transformation from non-small-cell lung cancer to small-cell lung cancer: molecular drivers and cells of origin. Lancet Oncol. 2015 Apr; 16(4):e165-72. View in: Pubmed

      • A severe photosensitivity dermatitis caused by crizotinib. J Thorac Oncol. 2014 Jul; 9(7):e51-e53. View in: Pubmed

      • Cortactin phosphorylation regulates cell invasion through a pH-dependent pathway. J Cell Biol. 2011 Nov 28; 195(5):903-20. View in: Pubmed

      • A novel spatiotemporal RhoC activation pathway locally regulates cofilin activity at invadopodia. Curr Biol. 2011 Apr 26; 21(8):635-44. View in: Pubmed

      • An EGFR-Src-Arg-cortactin pathway mediates functional maturation of invadopodia and breast cancer cell invasion. Cancer Res. 2011 Mar 01; 71(5):1730-41. View in: Pubmed

      • Specific tyrosine phosphorylation sites on cortactin regulate Nck1-dependent actin polymerization in invadopodia. J Cell Sci. 2010 Nov 01; 123(Pt 21):3662-73. View in: Pubmed

      • Nck1 and Grb2 localization patterns can distinguish invadopodia from podosomes. Eur J Cell Biol. 2011 Feb-Mar; 90(2-3):181-8. View in: Pubmed

      • The cofilin activity cycle in lamellipodia and invadopodia. J Cell Biochem. 2009 Dec 15; 108(6):1252-62. View in: Pubmed

      • Cortactin regulates cofilin and N-WASp activities to control the stages of invadopodium assembly and maturation. J Cell Biol. 2009 Aug 24; 186(4):571-87. View in: Pubmed

      • N-WASP and cortactin are involved in invadopodium-dependent chemotaxis to EGF in breast tumor cells. Cell Motil Cytoskeleton. 2009 Jun; 66(6):303-16. View in: Pubmed

      • A Mena invasion isoform potentiates EGF-induced carcinoma cell invasion and metastasis. Dev Cell. 2008 Dec; 15(6):813-28. View in: Pubmed

      • Polycomb group protein ezh2 controls actin polymerization and cell signaling. Cell. 2005 May 06; 121(3):425-36. View in: Pubmed


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      Dana-Farber Cancer Institute, Longwood Center (LC4202)

      360 Longwood Ave Boston, MA 02215
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      Dana-Farber Cancer Institute, Longwood Center (LC4202)

      Location Avtar

      Dana-Farber Cancer Institute, Longwood Center (LC4202)

      360 Longwood Ave Boston, MA 02215
      Get Direction
      42.339, -71.1078