Carol Lange, PhD

Professor of Medicine, Division of Hematology, Oncology and Transplantation

Carol Lange

Contact Info

Office Phone 612-626-0621

Lab Phone 612-624-1971

Mailing Address:
Cancer and Cardiovascular Research Building
University of Minnesota
2231 6th Street SE
1st Floor Mailroom CCRB
2812A (Campus Delivery Code)
Minneapolis, MN 55455

Administrative Assistant Name
Marilyn Lingard

Administrative Phone

Administrative Email

Administrative Fax Number

Professor of Medicine, Division of Hematology, Oncology and Transplantation

Program Leader, Cell Signaling, Masonic Cancer Center (MCC)

Professor, Department of Pharmacology

Co-Director/Program Lead, Cellular Mechanisms Program, Masonic Cancer Center, Microbiology, Immunology and Cancer Biology (MICaB) Ph.D. Graduate Program

PhD, University of Colorado School of Pharmacy, Boulder, CO (1991)


Dr. Lange is a Professor in the Departments of Medicine and Pharmacology at the University of Minnesota. She received her Ph.D. from the University of Colorado School of Pharmacy in 1991. She holds memberships in The Endocrine Society (Full Member) and Women in Endocrinology. Dr. Lange serves as teaching faculty in the U of MN Department of Pharmacology Graduate Program, Microbiology, Immunology, and Cancer Biology Graduate Program and MD/PhD Combined Program. She has served on several NIH Study Sections including Biochemical Endocrinology and Metabolic Physiology.

Professional Associations

  • Member, American Society for Blood and Marrow Transplantation 2008-present
  • Director, Cancer Biology Training Grant (T32), Masonic Cancer Center, University of Minnesota (2010-present)
  • Director, Cell Signaling Program, Masonic Cancer Center, University of Minnesota
  • Tickle Family Land Grant Endowed Chair (2009-present)
  • Associate Editor, Hormones and Cancer
  • Scientific Editor, Endocrine Related Cancer


Research Summary/Interests

"CHANGE: My research program in the areas of breast and ovarian cancer is focused on the integrated actions of growth factor- or stress-activated protein kinases and steroid hormone receptors (SRs). We have made critical contributions to the understanding of mechanisms of ligand-independent SR action and their role in cancer progression. Estrogen receptor ? (ER) and progesterone receptors (PRs) are context-dependent transcription factors that are essential for development of the breast and reproductive tract. Altered sex hormone levels contribute to cancer risk in these tissues and drive early tumor progression. The presence of abnormally activated ERs and imbalanced/activated PR isoforms in tumors can dramatically influence response to endocrine or other therapies. All SRs can rapidly activate cytoplasmic protein kinases and act as “growth factor sensors.” In this role, SRs are heavily phosphorylated by mitogenic protein kinases (MAPKs, AKT, CDKs) that are frequently elevated and activated in breast and reproductive tract cancers. Phosphorylation of SRs alters their binding partners and promoter selection and influences cancer cell fate/plasticity by regulating genes that specify proliferative, pro-survival, and cancer stem cell programs via expression of both autocrine and paracrine factors. Identifying the essential pathways and partners will enable the targeting of multiple signaling molecules in addition to SRs, which is predicted to halt cancer progression, prevent recurrence, and increase patient survival."