Kevin Roarty, Ph.D.
Breast cancer is not one disease, but rather a heterogeneous one comprised of diversities that range from the clinical stage down to the molecular level. In an attempt to explain this heterogeneity, the cancer stem cell theory explains that there is a subset of tumor cells with stem-like properties, termed cancer stem cells or tumor-initiating cells, which drive tumor initiation, progression, and recurrence. Like normal stem cells, these cells have the abilities to self-renew and to differentiate, albeit in an uncontrolled manner, leading to the production of all cell types within a tumor. Most importantly, an increasing number of reports about cancer stem cells demonstrate the intrinsic abilities of these cell populations to resist conventional chemotherapeutic and radiation therapies. The identification of key regulators of self-renewal and differentiation networks thus becomes critically important to gain better insight into normal breast biology, as well as for defining new targets for cancer therapy.
The Wnt/ß-catenin signaling pathway is implicated in the control of various stem cell populations in multiple tissues, and aberrant activation of this pathway is linked with many cancers, including breast cancer. Of interest, there are alternative Wnt signaling routes, known as ß-catenin independent or non-canonical Wnt outputs, which can signal via alternative mechanisms, and in some cases, antagonize the Wnt/ß-catenin pathway. My research focuses on unraveling components of ß-catenin-independent Wnt signaling in normal breast biology and breast cancer. Further investigation of noncanonical Wnt components will provide valuable insight into the interplay of ß-catenin-dependent and independent signaling, the effects on stem cell dynamics, and ultimately the therapeutic implications of this interaction.
- Joined Lab: October 2008
- Position: Postdoctoral Fellow
- Degrees: BS, Virginia Tech, 2001, MS, University of Alabama at Birmingham, 2003, & Ph.D., University of Alabama at Birmingham, 2008
- Awards: Department of Defense BCRP Postdoctoral Fellowship (2010-2013)
Roarty K, Baxley SE, Crowley MR, Frost AR, Serra R. Loss of TGF-beta or Wnt5a results in an increase in Wnt/beta-catenin activity and redirects mammary tumour phenotype. Breast Cancer Research. 2009;11(2):R19. Epub 2009 Apr 3. *Comment in: Breast Cancer Research. 2009;11(3):103.
Roarty K, and Serra R. (2007). Wnt5a is required for proper mammary gland development and TGF-ß-mediated inhibition of ductal growth. Development. 2007. 134(21):3929-39.
Johnson E, Nicola T, Roarty K, Yoder BK, Haycraft CJ, and Serra, R. A role for cilia in the regulation of mouse ovarian function. Dev Dyn. 2008. 237(8):2053-2060.
Brantley EC, Nabors LB, Gillespie GY, Choi YH, Palmer CA, Harrison K, Roarty K, Benveniste EN. Loss of PIAS3 Expression in Glioblastoma Multiforme Tumors: Implications for STAT-3 Activation and Gene Expression. Clin Cancer Res. 2008 Aug 1;14(15):4694-704.
Hongwei Qin, Lanfang Wang, Charles Ol. Elson, Sandrine A. Niyongere, Sun Jung Lee, Etty N. Benveniste, Craig L. Maynard, Casey T. Weaver, Kevin Roarty, Rosa A. Serra, And Yingzi Cong. TGF-beta promotes TH17 cell development through inhibition of SOCS3.
Kidwell DA, Kidwell JD, Shinohara F, Harper C, Roarty K, Bernadt K, McCaulley RA, Smith FP. (2003). Comparison of daily urine, sweat, and skin swabs among cocaine users. Forensic Science International. 2003. 133(1-2):63-78.