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Home
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Primary Faculty
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Michelle M. Williams, PhD
Michelle M. Williams, PhD
Assistant Professor
Assembly Building, 5051 Centre Avenue
2nd Floor, Office: 2047
Pittsburgh, PA 15213
mmw178@pitt.edu
Phone: 412-383-2434
Education
BS (Biochemistry), Allegheny College, Meadville, PA, 2012
PhD (Cancer Biology), Vanderbilt University, Nashville, TN, 2017
Postdoctoral Training (Pathology/Cancer Biology and Immunology), University of Colorado, Aurora, CO, 2024
Research Details
Publications
Research Areas
Cancer Genomics
Cancer Pharmacology
Drug Discovery
Signal Transduction
The FDA approval of immunotherapies for metastatic triple-negative breast cancer suggests that stimulating an anti-tumor immune response may be an effective way to limit metastatic progression. These immunotherapies reactivate cytotoxic T cells, an immune cell type that is suppressed during tumor progression and cannot effectively target and kill tumor cells. However, liver metastases from several different tumor types have the poorest response to immunotherapy, possibly because liver metastases express the lowest levels of the molecules (PD-L1) and cells (T cells) that these immunotherapies target. Little is known about what regulates this site-specific therapy resistance in liver metastases. One strategy to increase response rates in metastatic breast cancer is to enhance our understanding of the interactions between metastatic breast cancer cells and the liver microenvironment. The
goal
of my research program is to address these gaps in knowledge and identify rational approaches to induce an anti-tumor immune response at this deadly metastatic site.
Current studies in the lab focus on the impact of tumor cell heme metabolism on the liver metastatic microenvironment by addressing the questions:
Does tumor cell heme metabolism support progression and treatment resistance in breast cancer liver metastases by promoting suppressive T cell activity?
Is the function of tissue resident immune cells, particularly liver resident macrophages or Kupffer cells, impacted by tumor cell secreted heme metabolites?
Can heme metabolism alter the global metabolic profile of breast cancer cells to support survival in the glycolytically active liver?
For more information please visit:
www.williamslabpitt.com
Journal Articles
Williams MM
, Hafeez SA, Christenson JL, O’NeillKI, Hammond NG and Richer JK. Reversing an oncogenic epithelial-to-mesenchymal transition program in breast cancer reveals actionable immune suppressive pathways.
Pharmaceuticals. Nov
2021.
Williams MM
, Christenson JL, O’Neill KI, Hafeez SA, Ihle CL, Spoelstra NS, Slansky JE and Richer JK. MicroRNA-200c restoration reveals a cytokine profile to enhance M1 macrophage polarization in breast cancers.
npj Breast Cancer
. May 2021.
Arnesen S, Blanchard Z,
Williams MM
, Berrett K, Li Z, Oesterreich S, Richer JK and Gertz J. Estrogen receptor alpha mutations in breast cancer cells cause gene expression changes through constant activity and through secondary effects.
Can Res
. February 2021
Rogers TJ, Christenson JL, Greene LI, O’Neil KI,
Williams MM
, Gordon MA, Nemkov T, D’Alessandro A, Degala GD, Shin J, Tan AC, Cittelly DM, Lambert JR and Richer JK. Modulation of epithelial to mesenchymal transition by miR200c alters tryptophan catabolism and a program of immune suppression in triple negative breast cancer.
MCR
.
January 2019.
Williams MM
, Lee L, Hicks DJ, Morrison-Joly MM, Ellion D, Rahman B, McKernan C, Sanchez V, Balko JM, Stricker T, Estrada V and Cook RS. Mcl-1, a key survival factor in breast cancers, correlates inversely with sensitivity to combined Bcl-2/Bcl-xL inhibition.
Mol Can Res
. March 2017.