Monte Winslow

Monte M. Winslow, PhD, Assistant 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. 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. Together with Seung Kim, they also have a long history of generating mouse models for diabetes studies, including seminal work published in 2006 on NFAT/Calcineurin signaling regulation of pancreas development and islet b-cell function (Heit et al 2006: Arron et al 2006). Recently with Kim they developed mouse models with somatic CRISPR/Cas9-mediated genome editing and used these models to induce gain and loss of function alleles specifically in the pancreas which could represent important methods to investigate disease biology across many organs and disease types, including diabetes (Chiou et al 2015). These methods seem poised to change the magnitude of what is possible in genetically engineered mouse models of human cancer. With Kim’s group, Winslow is also exploring the hypothesis that type 3c diabetes (pancreatogenic diabetes) may reflect a paraneoplastic syndrome from pancreatic metaplasia leading to ectopic expression of the ‘decretin’ hormone Neuromedin U (NMU).

Selected relevant publications (Stanford DRC Members in BOLD):

1.     Chiou S-H, Winters IP, Wang J, Naranjo S, Dudgeon C, Tamburini FB, Brady JJ, Yang D, Grüner BM, Chuang C-H, Caswell DR, Zeng H, Chu P, Kim GE, Carpizo DR, Kim SK, Winslow MM (2015). Pancreatic cancer modeling using retrograde viral vector delivery and in vivo CRISPR/Cas9-mediated somatic genome editing. Genes and Development 29: 1576-85.

2.     Arron J*, Winslow MM*, Polleri A*, Chang CP, Wu H, Gao X, Neilson JR, Chen L, Heit JJ, Kim SK, Yamasaki N, Miyakawa T, Franke U, Graef IA*, and Crabtree GR. (2006) NFAT dysregulation by increased dosage of DSCR1 and DYRK1A on Chromosome 21. Nature 441: 595-600. *Contributed equally

3.     Winslow MM, Pan M, Starbuck M, Gallo EM, Deng L, Karsenty G, and Crabtree GR. (2006) Calcineurin/NFAT signaling in osteoblasts regulates bone mass. Developmental Cell 10: 771-782.

4.     Heit JJ, Apelqvist AA, Gu X, Winslow MM, Neilson JR, Crabtree GR, and Kim SK. (2006) Calcineurin/NFAT signalling regulates pancreatic ß-cell growth and function. Nature 443: 345-349.