Monte Winslow

Monte M. Winslow, PhD, Associate Professor, Departments of Genetics and Pathology, Stanford University School of Medicine

Research Description: Dr. Winslow’s group focuses on understanding the mechanisms that drive cancer development, progression, metastasis, and therapy response. The goal of their research is to develop and use genomic methods and in vivo mouse models to uncover the molecular and cellular changes that underlie cancer progression and development. Pancreatic cancer, one focus of his group, has been linked to pancreatogenic diabetes (type 3c: T3cD). His group has a strong track record of developing novel cancer modeling approaches that enable more rapid and quantitative analyses or cancer progression as well as for translational studies. In fact, throughout his career, Dr. Winslow has successfully developed multiple novel methods to assess gene function in vivo. His group has developed methods for somatic CRISPR/Cas9-mediated genome editing and used these models to induce both gain- and loss-of-function alleles. This can be adapted to several organ systems. Together with Seung Kim, they also have a long history of generating mouse models for diabetes studies, including mouse models with somatic CRISPR/Cas9-mediated genome editing. They have used these models to induce gain and loss of function alleles specifically in the pancreas to investigate disease biology across many organs and disease types, including diabetes (Chiou et al 2015). With Kim’s group, Winslow is also exploring the hypothesis that type 3c diabetes may reflect a paraneoplastic syndrome from pancreatic metaplasia leading to ectopic expression of the ‘decretin’ hormone Neuromedin U (NMU). Winslow is also developing methodology for molecular barcoding in the pancreas through a P01 grant with Drs. Habtezion, Engleman, Nolan, Park and others. This award focuses on deciphering, stem-cell and cell-of-origin, genetic and immune mechanisms regulating the earliest stages of pancreas cancer development, when T3cD typically manifests.

Selected relevant publications (Stanford DRC Members in BOLD):

  1. Han K, Pierce SE, Li A, Spees K, Anderson GR, Seoane JA, Lo YH, Dubreuil M, Olivas M, Kamber RA, Wainberg M, Kostyrko K, Kelly MR, Yousefi M, Simpkins SW, Yao D, Lee K, Kuo CJ, Jackson PK, Sweet-Cordero A, Kundaje A, Gentles AJ, Curtis C, Winslow MM, Bassik MC. CRISPR screens in cancer spheroids identify 3D growth-specific vulnerabilities. Nature. 2020 Apr;580(7801):136-141. doi: 10.1038/s41586-020-2099-x. PMID: 32238925; PMCID: PMC7368463. 

  2. Tang R, Murray CW, Linde IL, Kramer NJ, Lyu Z, Tsai MK, Chen LC, Cai H, Gitler AD, Engleman E, Lee W, Winslow MM. A versatile system to record cell-cell interactions. Elife. 2020 Oct 7;9:e61080. doi: 10.7554/eLife.61080. PMID: 33025906; PMCID: PMC7682987.  

  3. Winters IP, Chiou SH, Paulk NK, McFarland CD, Lalgudi PV, Ma RK, Lisowski L, Connolly AJ, Petrov DA, Kay MA, Winslow MM. Multiplexed in vivo homology-directed repair and tumor barcoding enables parallel quantification of Kras variant oncogenicity. Nat Commun. 2017 Dec 12;8(1):2053. doi: 10.1038/s41467-017-01519-y. PMID: 29233960; PMCID: PMC5727199.