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Sarah J. Hill, MD, PhD

Sarah J. Hill, MD, PhD

Medical Oncology/Molecular and Cellular
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Biography

Sarah J. Hill, MD, PhD

Dr. Sarah Hill, M.D./Ph.D., is a physician scientist in the Department of Medical Oncology and Division of Molecular and Cellular Oncology at Dana-Farber Cancer Institute focused on understanding the role of BRCA1 in breast and ovarian tumor suppression, tumor biology, and therapeutic sensitivity and resistance.  She completed her A.B. at Harvard College, her Ph.D. at Harvard University in the laboratory of Dr. David Livingston at Dana-Farber Cancer Institute, and her M.D. at Harvard Medical School in the Harvard-MIT HST program.  She is also a Rhodes Scholar and completed an M.Sc. in biochemistry at Oxford University. Upon graduation from the Harvard M.D./Ph.D. program, she completed a brief residency. She joined the faculty at Dana-Farber as an independent investigator immediately upon completion of her residency without any post-doctoral training and won an NIH Early Independence Award with the support of her Ph.D. mentor Dr. Livingston. 

Researcher

Physician

Assistant Professor of Medicine, Dana-Farber Cancer Institute and Harvard Medical School

Clinical Interests

Breast cancer, Ovarian cancer, Women’s Cancers

Recent Awards

  • ASCI Young Physician Scientist Award 2023
  • AACR Annual Meeting NextGen Star Award 2022
  • AACR Cancer Research Early Career Award 2021
  • NIH Director’s Early Independence DP5 Award 2020
  • Rhodes Scholarship 2005
  • Henderson Prize 2005

Research

    View Dr. Hill’s Research

    The mission of the Hill Lab is to develop a deep mechanistic understanding of breast, ovarian, and endometrial cancer development and tumor biology which we will harness to make these cancers more manageable diseases for all patients through the development of effective methods of detection, prevention, and treatment.

    In pursuit of this mission, the Hill lab focuses on understanding the role of the BRCA1 tumor suppressor and cell cycle checkpoints in basic molecular and cellular biology and in breast, ovarian, and endometrial carcinogenesis and tumor biology.

    We utilize molecular/cellular biology and fluorescence microscopy techniques in breast, ovarian, and endometrial cancer cell lines, patient-derived normal and cancer organoids, and mouse models.

    Research Departments

    Support my research

    Research Website

    https://hilllab.dana-farber.org/

    Publications

      View Dr. Hill's Publications

      • Germline and Somatic Fumarate Hydratase Testing in Atypical Uterine Leiomyomata. Cancer Prev Res (Phila). 2024 May 02; 17(5):201-208. View in: Pubmed

      • Sialyl-Tn serves as a potential therapeutic target for ovarian cancer. J Ovarian Res. 2024 Apr 02; 17(1):71. View in: Pubmed

      • Targeting Galectin 3 illuminates its contributions to the pathology of uterine serous carcinoma. Br J Cancer. 2024 May; 130(9):1463-1476. View in: Pubmed

      • The ORFIUS complex regulates ORC2 localization at replication origins. NAR Cancer. 2024 Mar; 6(1):zcae003. View in: Pubmed

      • Endometrial Cancer Risk Among Germline BRCA1/2 Pathogenic Variant Carriers: Review of Our Current Understanding and Next Steps. JCO Precis Oncol. 2023 Sep; 7:e2300290. View in: Pubmed

      • Discovery of antibodies and cognate surface targets for ovarian cancer by surface profiling. Proc Natl Acad Sci U S A. 2023 01 03; 120(1):e2206751120. View in: Pubmed

      • Enhanced Efficacy of Aurora Kinase Inhibitors in G2/M Checkpoint Deficient TP53 Mutant Uterine Carcinomas Is Linked to the Summation of LKB1-AKT-p53 Interactions. Cancers (Basel). 2021 May 03; 13(9). View in: Pubmed

      • Enhanced Efficacy of Simultaneous PD-1 and PD-L1 Immune Checkpoint Blockade in High-Grade Serous Ovarian Cancer. Cancer Res. 2021 01 01; 81(1):158-173. View in: Pubmed

      • Exploiting the Prevalence of Homologous Recombination Deficiencies in High-Grade Serous Ovarian Cancer. Cancers (Basel). 2020 May 11; 12(5). View in: Pubmed

      • Two familial ALS proteins function in prevention/repair of transcription-associated DNA damage. Proc Natl Acad Sci U S A. 2016 11 29; 113(48):E7701-E7709. View in: Pubmed

      • BRCA1 recruitment to transcriptional pause sites is required for R-loop-driven DNA damage repair. Mol Cell. 2015 Feb 19; 57(4):636-647. View in: Pubmed

      • Systematic screening reveals a role for BRCA1 in the response to transcription-associated DNA damage. Genes Dev. 2014 Sep 01; 28(17):1957-75. View in: Pubmed

      • BRCA1 pathway function in basal-like breast cancer cells. Mol Cell Biol. 2014 Oct; 34(20):3828-42. View in: Pubmed

      • BRCA1 is required for postreplication repair after UV-induced DNA damage. Mol Cell. 2011 Oct 21; 44(2):235-51. View in: Pubmed

      • BMI1 is recruited to DNA breaks and contributes to DNA damage-induced H2A ubiquitination and repair. Mol Cell Biol. 2011 May; 31(10):1972-82. View in: Pubmed

      Locations

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      Dana-Farber Cancer Institute

      450 Brookline Ave. 1410C Dana Boston, MA 02215
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      Dana-Farber Cancer Institute

      Location Avtar

      Dana-Farber Cancer Institute

      450 Brookline Ave. 1410C Dana Boston, MA 02215
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      42.3374, -71.1082

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