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Joan S. Lewis-Wambi, PhD

Joan Lewis-Wambi portrait
Associate Professor, Cancer Biology

Program Director, Graduate Program Director, SOM-Kansas City, Cancer Biology

Professional Background

Joan Lewis-Wambi, Ph.D., is an Associate Professor (tenured) and the Director of Graduate Studies in the Department of Cancer Biology at KUMC. Dr. Lewis-Wambi received her Ph.D. in Cancer Biology in May 2002 from Rutgers University and she completed her post-doctoral training at Northwestern University (2002-2004) and at Fox Chase Cancer Center (2005-2008). Dr. Lewis-Wambi has worked in the breast cancer field for over 15 years with expertise in estrogen receptor signaling, endocrine therapy resistance, triple negative breast cancer, and cancer health disparities. The focus of her lab is to understand the mechanism(s) by which breast cancer cells and breast tumors develop resistance to endocrine therapies and to develop alternative therapies for breast cancer patients. She utilizes unique human breast cancer cell lines, animal models, and clinical breast cancer samples to uncover the molecular underpinnings that drive the development of resistance in breast cancer patients. Additionally, her lab also studies triple negative breast cancer (TNBC) and inflammatory breast cancer (IBC) which are two aggressive and lethal subtypes of breast cancer that are difficult to diagnose and treat and disproportionately affect African American (AA) women compared to other ethnic groups. She has discovered a novel marker called interferon induced transmembrane protein 1 (IFITM1) that plays a critical role in promoting the aggressiveness of TNBC in African American patients. Dr. Lewis-Wambi has published ~45 research articles and she has received several honors and awards including, NIH Young Investigator Award, Avon Scholar, Susan G. Komen Scholar, WIMS-AAMC Scholar Award, and the KUMC Rising Star Scholar. Her research has been funded by grants from NIH, ACS, and the Department of Defense-BCRP.

Education and Training
  • PhD, Cancer Biology, Rutgers University, New Brunswick, NJ
  • BS, Biochemistry, Rutgers University, New Brunswick, NJ
  • Post Doctoral Fellowship, Breast Cancer and endocrine resistance, Nothwestern University, Chicago, IL
  • Post Doctoral Fellowship, Breast cancer and endocrine resistance, Fox Chase Cancer Center, Philadelphia, PA
Professional Affiliations
  • American Association for Cancer Research, Member, 1996 - 2018



Role for Type 1 Interferon Signaling in Promoting Endocrine Resistance in Breast Cancer
Despite the benefits of endocrine therapies such as tamoxifen and aromatase inhibitors in treating estrogen receptor alpha (ERa)-positive breast cancer, many tumors eventually become resistant. Identifying the underlying cellular and molecular mechanisms responsible for endocrine resistance remains a critical and immediate need. Our laboratory is interested in identifying novel pathways of endocrine-resistance in breast cancer and using that knowledge to help develop alternative treatment options for patients with endocrine resistant and metastatic disease. We have identified a novel role for the interferon alpha (IFNa) signaling pathway in promoting aromatase inhibitor resistance in ER-positive breast cancer. Indeed, our lab has shown that Al-resistant breast cancer cells and resistant tumors secrete elevated levels of IFNa which upregulates JAK/STAT signaling to promote constitutive activation of IFNa-stimulated genes (ISGs) and drive cell survival. One ISG is IFITMI (interferon-induced transmembrane protein 1) which is overexpressed in AI-resistant cells and resistant tumors and its loss leads to cell death through activation of p21Waf1. The long-term goal of this project is to understand the role of type 1 interferon signaling in endocrine resistance and the impact of the microenvironment on this process. Type 1 IFNs are cytokines that regulate antiviral responses through activation of the JAK-STAT signaling pathway, however, their impact on epithelial-stromal interactions in the tumor microenvironment and their potential contribution to the development of Al-resistance through crosstalk with the ERa signaling pathway are not known.

Molecular underpinnings of Triple Negative and Inflammatory Breast Cancer
Dr. Lewis-Wambi’s lab also studies triple negative breast cancer (TNBC) and inflammatory breast cancer (IBC) which are two aggressive and lethal subtypes of breast cancer that are difficult to diagnose and treat and disproportionately affect African American (AA) women compared to other ethnic groups. Her lab has identified a novel marker called interferon induced transmembrane protein 1 (IFITM1) that appears to be highly expressed in TNBC tumors and TNBC cell lines derived from AA patients but not expressed in TNBC tumors from Caucasian patients and its overexpression enhances the aggressive phenotype of TNBC cells in culture. Her research efforts are focused on characterizing the role of IFITM1, in the pathobiology and progression of TNBC in African American patients and assess whether targeting IFITM1 has therapeutic benefits in vivo and whether it can serve as a novel diagnostic marker of cancer progression and metastasis.

  • Provance, Olivia , Geanes, Eric , Lui, Asona , Roy, Anuradha, Holloran, Sean, Gunewardena, Sumedha, Hagan, Christy, Weir, Scott, Lewis-Wambi, Joan. 2021. Disrupting interferon-alpha and NF-kappaB crosstalk suppresses IFITM1 expression attenuating triple-negative breast cancer progression. Cancer Letters, 514, 12-29.
  • Provance, Olivia, Lewis-Wambi, Joan. 2019. Deciphering the role of interferon alpha signaling and microenvironment crosstalk in inflammatory breast cancer. Breast Cancer Research, 21.
  • Escher, Taylor, Geanes, Eric , Walter, Katherine , Tawfik, Ossama, Hagan, Christy, Lewis-Wambi, Joan. 2019. Interaction between MUC1 and STAT1 drives IFITM1 overexpression in aromatase inhibitor-resistant breast cancer cells and mediates estrogen-induced apoptosis. Molecular Cancer Research, 17, 1180-1194.
  • Lui, Asona, Geanes, Eric, Ogony, Joshua, Behbod, Fariba, Marquess, Jordan, Kelli, Valdez, Jewell, William, Tawfik, Ossama, Lewis-Wambi, Joan. 2017. IFITM1 suppression blocks proliferation and invasion of aromatase inhibitor-resistant breast cancer in vivo by JAK/ STAT-mediated induction of p21. Cancer Letters, 399, 29-43.
  • Ogony, Joshua, Choi, Hye., Joung, Lui, Asona, Cristofanilli, Massimo, Lewis-Wambi, Joan. 2016. Interferon-induced transmembrane protein 1 (IFITM1) overexpression enhances the aggressive phenotype of SUM149 inflammatory breast cancer cells in a signal transducer and activator of transcription 2 (STAT2)-dependent manner. BREAST CANCER RESEARCH, 18
  • Lui, Asona, New, Jacob, Ogony, Joshua, Thomas, Sufi, Lewis-Wambi, Joan. 2016. Everolimus downregulates estrogen receptor and induces autophagy in aromatase inhibitor-resistant breast cancer cells. BMC CANCER, 16
  • Hayes, Erin., L., Lewis-Wambi, Joan., S.. 2015. Mechanisms of endocrine resistance in breast cancer: an overview of the proposed roles of noncoding RNA. BREAST CANCER RESEARCH, 17
  • Choi, Hye., Joung, Lui, Asona, Ogony, Joshua, Jan, Rifat, Sims, Peter., J., Lewis-Wambi, Joan. 2015. Targeting interferon response genes sensitizes aromatase inhibitor resistant breast cancer cells to estrogen-induced cell death. BREAST CANCER RESEARCH, 17
  • Jan, Rifat, Huang, Min, Lewis-Wambi, Joan. 2012. Loss of pigment epithelium-derived factor: a novel mechanism for the development of endocrine resistance in breast cancer. BREAST CANCER RESEARCH, 14 (6)
  • Ariazi, Eric., A., Lewis-Wambi, Joan., S., Gill, Shaun., D., Pyle, Jennifer., R., Ariazi, Jennifer., L., Kim, Helen., R., Sharma, Catherine G. N., Cordera, Fernando, Shupp, Heather., A., Li, Tianyu, Jordan, V.., Craig. 2006. Emerging principles for the development of resistance to antihormonal therapy: Implications for the clinical utility of fulvestrant. JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 102 (1-5), 128-138