
Ann Richmond, Ph.D.
- Ingram Professor of Cancer Research
- Professor of Pharmacology
- Professor of Dermatology
Phone
432-B Preston Building
Nashville, TN 37232-6840
Ann Richmond, Ph.D.
- Ingram Professor of Cancer Research
- Professor of Pharmacology
- Professor of Dermatology
615-343-7777
ann.richmond@vanderbilt.edu
432-B Preston Building
Nashville, TN 37232-6840
Research Program
Departments/Affiliations
Profile
Ann Richmond, Ph.D., is an Ingram Professor of Cancer Research and Professor of Pharmacology and Dermatology at Vanderbilt University School of Medicine. A major question her lab is investigating is "What is the role of the inflammatory response in tumor progression". They are studying the role of proteins that promote the migration of inflammatory cells into tissues. These "chemotactic" proteins can educate leukocytes to either stimulate or inhibit tumor progression. These factors can also stimulate the growth of the tumor and recruit blood vessels into the tumor to provide a continuous supply of nutrients to feed tumor growth. They have tested how pharmaceutical drugs that shut down the inflammatory process and alter the expression of genes that recruit inflammatory cells into the tumor microenvironment effect tumor progression. They are also evaluating how to deliver therapies that teach the patient's leukocytes to fight the growth of the tumor and switch from a pro-tumorigenic to an anti-tumorigenic state.
They have learned that the inflammatory process, combined with other genetic and environmental factors, contributes to mutations in genes that regulate the growth of cells. Some of these mutations make the cells capable of continuous growth and enable the cancer cells to spread throughout the body and grow in distant organs. By determining what genes become mutated or amplified in each patient's tumor and then providing therapies that specifically inhibit the activity of that mutated or amplified gene, we can deliver "personalized cancer treatment" that addresses the problem in that persons specific cancer. This works so much better than the "one size fits all" approach often used previously in chemotherapy. Recently they have determined that inhibition of aurora kinases or cyclin dependent kinases 4 and 6 induce tumor cells to undergo senescence and when these kinases are inhibited while at the same time other drugs are added that activate the tumor suppressor p53 or the death receptor DR5, melanoma cells die and tumors regress. The Richmond Lab is also interested in evaluating how therapeutic agents that target driver mutations such as PI3K, RAS or BRAF affect the tumor microenvironment and the immune response to the tumor. They postulate that in some instances drug resistance comes in part due to deleterious effects of the therapy on the tumor microenvironment. Dr. Richmond collaborate with medical oncologists, surgical oncologists, bioengineers, cellular and molecular biologists, and scientists in pharmaceutical companies to address the scientific questions we are asking. This TEAM interaction enables us to optimize our studies to make important breakthroughs in tumor biology and tumor therapy.
Education
- Ph.D., Emory University, Atlanta, Georgia (1979)
- M.N.S., Louisiana State University, Baton Rouge, Louisiana (1972)
- B.S., Northeast Louisiana University, Monroe, Louisiana (1966)
Research Emphasis
chemokines, transcription, signal transduction, melanoma, breast cancer, vascular biology
Research Description
A major question we are trying to answer in my laboratory is "What is the role of the inflammatory response in tumor progression". We are studying the role of proteins that promote the migration of inflammatory cells into tissues. These "chemotactic" proteins can educate leukocytes to either stimulate or inhibit tumor progression. These factors can also stimulate the growth of the tumor and recruit blood vessels into the tumor to provide a continuous supply of nutrients to feed tumor growth. We have tested with a variety of pharmaceutical drugs that shut down the inflammatory process and alter the expression of genes that recruit inflammatory cells into the tumor microenvironment. We are also evaluating how to deliver therapies that teach the patient's leukocytes to fight the growth of the tumor and switch from a pro-tumorigenic to an anti-tumorigenic state.
We have also learned that this inflammatory process, combined with other genetic and environmental factors, contributes to mutations in genes that regulate the growth of cells. Some of these mutations make the cells capable of continuous growth and enable the cancer cells to spread throughout the body and grow in distant organs. By determining what genes become mutated or amplified in each patient's tumor and then providing therapies that specifically inhibit the activity of that mutated or amplified gene, we can deliver "personalized cancer treatment" that addresses the problem in that persons specific cancer. This works so much better than the "one size fits all" approach often used previously in chemotherapy. Recently we have determined that inhibition of aurora kinases induce tumor cells to undergo senescence and when we inhibit aurora kinases while at the same time activate the tumor suppressor p53 or the death receptor DR5, melanoma cells die and tumors regress. We are also interested in evaluating how therapeutic agents that target driver mutations such as PI3K, RAS or BRAF affect the tumor microenvironment and the immune response to the tumor. We postulate that in some instances drug resistance comes in part due to deleterious effects of the therapy on the tumor microenvironment. We collaborate with medical oncologists, surgical oncologists, bioengineers, cellular and molecular biologists, and scientists in pharmaceutical companies to address the scientific questions we are asking. This TEAM interaction enables us to optimize our studies to make important breakthroughs in tumor biology and tumor therapy. Our research is funded by the TVHS Department of Veterans Affairs, the National Cancer Institute, and the Department of Defense. I work with a wonderful group of postdoctoral fellows, students, and laboratory scientists who dedicate their lives to providing better treatments for cancer patients.
Publications
- Vilgelm AE, Saleh N, Shattuck-Brandt R, Riemenschneider K, Slesur L, Chen SC, Johnson CA, Yang J, Blevins A, Yan C, Johnson DB, Al-Rohil RN, Halilovic E, Kauffmann RM, Kelley M, Ayers GD, Richmond A. MDM2 antagonists overcome intrinsic resistance to CDK4/6 inhibition by inducing p21. Sci Transl Med. 2019 Aug 8/14/2019; 11(505): PMID: 31413145, PII: 11/505/eaav7171, DOI: 10.1126/scitranslmed.aav7171, ISSN: 1946-6242.
- Daniels AB, Froehler MT, Nunnally AH, Pierce JM, Bozic I, Stone CA, Santapuram PR, Tao YK, Boyd KL, Himmel LE, Chen SC, Du L, Friedman DL, Richmond A. Rabbit Model of Intra-Arterial Chemotherapy Toxicity Demonstrates Retinopathy and Vasculopathy Related to Drug and Dose, Not Procedure or Approach. Invest. Ophthalmol. Vis. Sci. 2019 Mar 3/1/2019; 60(4): 954-64. PMID: 30882851, PMCID: PMC6424472, PII: 2728304, DOI: 10.1167/iovs.18-25346, ISSN: 1552-5783.
- Vilgelm AE, Richmond A. Chemokines Modulate Immune Surveillance in Tumorigenesis, Metastasis, and Response to Immunotherapy. Front Immunol. 2019; 10: 333. PMID: 30873179, PMCID: PMC6400988, DOI: 10.3389/fimmu.2019.00333, ISSN: 1664-3224.
- Yang J, Kumar A, Vilgelm AE, Chen SC, Ayers GD, Novitskiy SV, Joyce S, Richmond A. Loss of CXCR4 in Myeloid Cells Enhances Antitumor Immunity and Reduces Melanoma Growth through NK Cell and FASL Mechanisms. Cancer Immunol Res [print-electronic]. 2018 Oct; 6(10): 1186-98. PMID: 30108045, PMCID: PMC6170679, PII: 2326-6066.CIR-18-0045, DOI: 10.1158/2326-6066.CIR-18-0045, ISSN: 2326-6074.
- Rogers M, Sobolik T, Schaffer DK, Samson PC, Johnson AC, Owens P, Codreanu SG, Sherrod SD, McLean JA, Wikswo JP, Richmond A. Engineered microfluidic bioreactor for examining the three-dimensional breast tumor microenvironment. Biomicrofluidics. 2018 May; 12(3): 34102. PMID: 29774083, PMCID: PMC5938175, PII: 002803BMF, PII: 1.5016433, DOI: 10.1063/1.5016433, ISSN: 1932-1058.
- Vilgelm AE, Cobb P, Malikayil K, Flaherty D, Andrew Johnson C, Raman D, Saleh N, Higgins B, Vara BA, Johnston JN, Johnson DB, Kelley MC, Chen SC, Ayers GD, Richmond A. MDM2 Antagonists Counteract Drug-Induced DNA Damage. EBioMedicine [print-electronic]. 2017 Oct; 24: 43-55. PMID: 29030058, PMCID: PMC5652019, PII: S2352-3964(17)30369-9, DOI: 10.1016/j.ebiom.2017.09.016, ISSN: 2352-3964.
- Pellom ST, Dudimah DF, Thounaojam MC, Uzhachenko RV, Singhal A, Richmond A, Shanker A. Bortezomib augments lymphocyte stimulatory cytokine signaling in the tumor microenvironment to sustain CD8+T cell antitumor function. Oncotarget. 2017 Jan 1/31/2017; 8(5): 8604-21. PMID: 28052005, PII: 14365, DOI: 10.18632/oncotarget.14365, ISSN: 1949-2553.
- Lavender N, Yang J, Chen SC, Sai J, Johnson CA, Owens P, Ayers GD, Richmond A. The Yin/Yan of CCL2: a minor role in neutrophil anti-tumor activity in vitro but a major role on the outgrowth of metastatic breast cancer lesions in the lung in vivo. BMC Cancer. 2017 Jan 1/31/2017; 17(1): 88. PMID: 28143493, PMCID: PMC5286656, PII: 10.1186/s12885-017-3074-2, DOI: 10.1186/s12885-017-3074-2, ISSN: 1471-2407.
- Sai J, Owens P, Novitskiy SV, Hawkins OE, Vilgelm AE, Yang J, Sobolik-Delmaire T, Lavender N, Johnson AC, McClain C, Ayers GD, Kelley MC, Sanders M, Mayer IA, Moses HL, Boothby M, Richmond A. PI3K Inhibition Reduces Mammary Tumor Growth and Facilitates Anti-tumor Immunity and Anti-PD1 Responses. Clin. Cancer Res [print-electronic]. 2016 Dec 12/21/2016; PMID: 28003307, PII: 1078-0432.CCR-16-2142, DOI: 10.1158/1078-0432.CCR-16-2142, ISSN: 1078-0432.
- Vilgelm AE, Johnson DB, Richmond A. Combinatorial approach to cancer immunotherapy: strength in numbers. J. Leukoc. Biol [print-electronic]. 2016 Aug; 100(2): 275-90. PMID: 27256570, PII: jlb.5RI0116-013RR, DOI: 10.1189/jlb.5RI0116-013RR, ISSN: 1938-3673.