Dr. Richmond received her Bachelor of Science degree from Northeast Louisiana University, her Master of Natural Sciences degree from Louisiana State University and her Ph.D. in Developmental Biology at Emory University in 1979. She conducted postdoctoral research in Tumor Biology at Emory, and then joined the faculty there, rising to the rank of associate professor of Medicine before moving to Vanderbilt in 1989 as tenured associate professor of Cell Biology and Medicine and as a research career scientist at the U.S. Department of Veterans Affairs Nashville campus. She was promoted to full professor in 1995, and she was appointed professor and vice chair of the Department of Cancer Biology in 2000.
Dr. Richmond is internationally known for her research on chemokines, small “chemotactic” proteins that attract inflammatory cells. She was the first to demonstrate that a chemokine can regulate tumor growth. Her early research involved purification and sequencing of one of the first known chemokines, CXCL1, and her lab played a major role in characterization of the role of its receptor, CXCR2, in leukocyte trafficking, inflammation, angiogenesis, wound healing and tumor progression. She and her colleagues helped elucidate the role that inhibitor of kappa-beta kinaseβ (IKKβ), an activator of the transcription factor NF-κB, plays in chemokine expression and melanoma cell survival, suggesting that IKKβ may be a potential target for melanoma therapy. They also have shown that targeting the NF-kB/IL-6/STAT3 pathway is a rational strategy for treating angiosarcoma.
Dr. Richmond’s body of work — more than 164 publications cited by other scientists more than 10,000 times – has shed light on how the inflammatory process, combined with other genetic and environmental factors, contributes to tumor progression and metastasis. A goal of her research is the advancement of “personalized cancer therapy” — determining which genes are mutated or amplified in individual tumors and delivering drugs that specifically inhibit the activity of those genes. Antagonizing chemokine receptors may provide new therapeutic options. Toward that end, she and her colleagues are working to learn more about the effects of therapy on the tumor microenvironment, including the development of drug resistance.
The Richmond laboratory currently investigates the intracellular signals that are important in the tumor microenvironment and in the pre-metastatic niche to reduce the establishment of metastatic lesions. Recently, following basic discoveries on the pathways involved in melanoma progression, her group developed translational studies using patient derived xenograft models to explore new therapeutic approaches for melanoma. They demonstrated that combining aurora kinase A inhibitors with MDM2 antagonists markedly inhibit melanoma tumor growth, using patient derived xenograft models as well as immunocompetent mouse models. They have also shown that while targeted deletion of IKKβ in melanoma cells blocks mutant Ras mediated transformation, targeted deletion of IKKβ in myeloid cells leads to enhanced tumor growth and metastasis for melanoma tumors. Surprisingly, we have shown that systemic inhibition of NF-κB inhibits growth of mutant Ras driven melanoma tumors. She now plans to extend initial studies combining Aurora Kinase and MDM2 inhibitors to evaluate an even more promising combination therapy, CDK4/6 inhibitors and MDM2 antagonists. They will develop animal models and utilize in vitro and in vivo imaging techniques to characterize the mechanism by which antagonists of cell cycle combined with reagents that enhance apoptosis may synergize to improve treatment for cancer. Her laboratory has worked to determine how inflammatory signals from tumors induce the chronic and elevated expression of chemokines and/or their receptors to recruit leukocytes that enhance or inhibit tumorigenesis and metastasis. They are experienced in the characterization of leukocyte interaction with the tumor microenvironment and in identification of subsets of these cells within the tumor using FACS. Moreover, we are currently characterizing the role of a number of small molecule inhibitors that affect melanoma tumor growth and metastasis using patient derived xenografts. She and her group recently determined the role of CXCR4 in mediating estrogen independent growth and metastasis of breast cancer and have shown that inhibition of CXCR2 and CXCR4 can alter the leukocyte composition of the pre-metastatic niche. She has an outstanding group of collaborators and access to phenomenal infrastructure for acquiring patients, obtaining informed consent, tissue collection, patient follow-up, and access to patients in clinical trials.
Dr. Richmond also is deeply committed to education. She has mentored more than 50 undergraduates, graduate students and postdoctoral fellows. She served as assistant dean of Biomedical Research Education and Training from 2005 to 2010, organized the first Chemokine and Chemokine Gordon Research Conference, which remains enormously popular, and is the current past president of the Society for Leukocyte Biology.