Honors & Awards

  • Postdoctoral Fellowship, American Cancer Society (2022-2024)
  • Postdoctoral Fellowship, Tobacco-Related Disease Research Program (2020-2021)
  • Dean's Postdoctoral Fellowship, Stanford School of Medicine (2019-2020)
  • Graduate Fellowship, Ludwig Center for Molecular Oncology (2016-2017)
  • Presidential Fellowship, Massachusetts Institute of Technology (2012-2013)

Professional Education

  • Bachelor of Science, Georgetown University, Biology (2012)
  • Doctor of Philosophy, Massachusetts Institute of Technology (2019)
  • Ph.D., Massachusetts Institute of Technology, Biology (2019)
  • B.S., Georgetown University, Biology (2012)

Stanford Advisors

Lab Affiliations

All Publications

  • Dissecting metastasis using preclinical models and methods. Nature reviews. Cancer Hebert, J. D., Neal, J. W., Winslow, M. M. 2023


    Metastasis has long been understood to lead to the overwhelming majority of cancer-related deaths. However, our understanding of the metastatic process, and thus our ability to prevent or eliminate metastases, remains frustratingly limited. This is largely due to the complexity of metastasis, which is a multistep process that likely differs across cancer types and is greatly influenced by many aspects of the in vivo microenvironment. In this Review, we discuss the key variables to consider when designing assays to study metastasis: which source of metastatic cancer cells to use and where to introduce them into mice to address different questions of metastasis biology. We also examine methods that are being used to interrogate specific steps of the metastatic cascade in mouse models, as well as emerging techniques that may shed new light on previously inscrutable aspects of metastasis. Finally, we explore approaches for developing and using anti-metastatic therapies, and how mouse models can be used to test them.

    View details for DOI 10.1038/s41568-023-00568-4

    View details for PubMedID 37138029

    View details for PubMedCentralID 5308465

  • Multiplexed screens identify RAS paralogues HRAS and NRAS as suppressors of KRAS-driven lung cancer growth. Nature cell biology Tang, R., Shuldiner, E. G., Kelly, M., Murray, C. W., Hebert, J. D., Andrejka, L., Tsai, M. K., Hughes, N. W., Parker, M. I., Cai, H., Li, Y. C., Wahl, G. M., Dunbrack, R. L., Jackson, P. K., Petrov, D. A., Winslow, M. M. 2023


    Oncogenic KRAS mutations occur in approximately 30% of lung adenocarcinoma. Despite several decades of effort, oncogenic KRAS-driven lung cancer remains difficult to treat, and our understanding of the regulators of RAS signalling is incomplete. Here to uncover the impact of diverse KRAS-interacting proteins on lung cancer growth, we combined multiplexed somatic CRISPR/Cas9-based genome editing in genetically engineered mouse models with tumour barcoding and high-throughput barcode sequencing. Through a series of CRISPR/Cas9 screens in autochthonous lung cancer models, we show that HRAS and NRAS are suppressors of KRASG12D-driven tumour growth in vivo and confirm these effects in oncogenic KRAS-driven human lung cancer cell lines. Mechanistically, RAS paralogues interact with oncogenic KRAS, suppress KRAS-KRAS interactions, and reduce downstream ERK signalling. Furthermore, HRAS and NRAS mutations identified in oncogenic KRAS-driven human tumours partially abolished this effect. By comparing the tumour-suppressive effects of HRAS and NRAS in oncogenic KRAS- and oncogenic BRAF-driven lung cancer models, we confirm that RAS paralogues are specific suppressors of KRAS-driven lung cancer in vivo. Our study outlines a technological avenue to uncover positive and negative regulators of oncogenic KRAS-driven cancer in a multiplexed manner in vivo and highlights the role RAS paralogue imbalance in oncogenic KRAS-driven lung cancer.

    View details for DOI 10.1038/s41556-022-01049-w

    View details for PubMedID 36635501

  • Combinatorial Inactivation of Tumor Suppressors Efficiently Initiates Lung Adenocarcinoma with Therapeutic Vulnerabilities. Cancer research Yousefi, M., Boross, G., Weiss, C., Murray, C. W., Hebert, J. D., Cai, H., Ashkin, E. L., Karmakar, S., Andrejka, L., Chen, L., Wang, M., Tsai, M. K., Lin, W., Li, C., Yakhchalian, P., Colon, C. I., Chew, S., Chu, P., Swanton, C., Kunder, C. A., Petrov, D. A., Winslow, M. M. 2022; 82 (8): 1589-1602


    Lung cancer is the leading cause of cancer death worldwide, with lung adenocarcinoma being the most common subtype. Many oncogenes and tumor suppressor genes are altered in this cancer type, and the discovery of oncogene mutations has led to the development of targeted therapies that have improved clinical outcomes. However, a large fraction of lung adenocarcinomas lacks mutations in known oncogenes, and the genesis and treatment of these oncogene-negative tumors remain enigmatic. Here, we perform iterative in vivo functional screens using quantitative autochthonous mouse model systems to uncover the genetic and biochemical changes that enable efficient lung tumor initiation in the absence of oncogene alterations. Generation of hundreds of diverse combinations of tumor suppressor alterations demonstrates that inactivation of suppressors of the RAS and PI3K pathways drives the development of oncogene-negative lung adenocarcinoma. Human genomic data and histology identified RAS/MAPK and PI3K pathway activation as a common feature of an event in oncogene-negative human lung adenocarcinomas. These Onc-negativeRAS/PI3K tumors and related cell lines are vulnerable to pharmacologic inhibition of these signaling axes. These results transform our understanding of this prevalent yet understudied subtype of lung adenocarcinoma.SIGNIFICANCE: To address the large fraction of lung adenocarcinomas lacking mutations in proto-oncogenes for which targeted therapies are unavailable, this work uncovers driver pathways of oncogene-negative lung adenocarcinomas and demonstrates their therapeutic vulnerabilities.

    View details for DOI 10.1158/0008-5472.CAN-22-0059

    View details for PubMedID 35425962