Research > Faculty By Division > Szeman Ruby Chan, PhD
|Research Instructor, Pathology and Immunology|
Room 8607, BJCIH Building
Office: (314) 362-8128
Lab: (314) 362-8746
|Breast cancer is the second deadliest cancer for women in the United States. Approximately 80% of all newly diagnosed cases are classified as estrogen receptor-alpha-positive (ER-alpha+). However, 40 – 60% of these patients do not benefit from standard-of-care endocrine treatment. Therefore, understanding the natural progression of ER-alpha+ breast cancer is critical to the identification of alternative therapeutic targets for this most common subtype of breast cancer. Therefore, our research interests focus on understanding the cellular and molecular mechanisms by which ER-alpha+ mammary tumors originate and evolve with the goals of uncovering and validating novel and effective therapeutic modalities that will benefit breast cancer patients who do not respond to hormone therapy.
Our research centers on the surprising finding that aged STAT1-/- female mice spontaneously develop ER-alpha+ / progesterone receptors-positive (PR+) mammary gland adenocarcinomas. These tumors not only resemble human ER-alpha+ / PR+ breast cancers because of the presence of steroid hormone receptors, they also display similar pathological progression and dependency on steroid hormones. In addition, the transcriptional program of STAT1-/- mammary tumors closely overlaps with that of human ER-alpha+ breast cancers. Together, these findings indicate that STAT1-/- mammary tumors represent an unprecedented preclinical model for human ER-alpha+ breast cancer.
Our research interests now focus in two areas: (1) the role of STAT1 in suppressing mammary tumor development and (2) development of novel anti-cancer treatment that aims at targeting the dysregulated pathways in the tumor cells.
|Service to the University|
|2011 - Present||Discussion Group Facilitator, Bio 5068|
|Chan SR, Rickert C, Vermi W, Sheehan KCF, Arthur C, Allen JA, White JM, Archambault J, Lonardi S, McDevitt TM, Bhattacharya D, Lorenzi MV, Allred DC, Schreiber RD. Dysregulated STAT1-SOCS1 control of JAK2 promotes mammary luminal progenitor cell survival and drives ER alpha+ tumorigenesis. Cell Death Differ, 2013 Abstract|
|Chan SR, Vermi W, Luo J, Lucini L, Rickert C, Fowler AM, Lonardi S, Arthur C, Young LJT, Levy DE, Welch MJ, Cardiff RD, Schreiber RD. STAT1-deficient mice spontaneously develop estrogen receptor alpha-positive luminal mammary carcinomas. Breast Cancer Research,14:R16, 2012 Abstract|
|Fowler AM, Chan SR, Sharp TL, Fettig NM, Zhou D, Dence CS, Carlson KE, Jeyakumar M, Katzenellenbogen JA, Schreiber RD, Welch MJ. MicroPET imaging of steroid hormone receptors predicts tumor response to endocrine therapy using a preclinical model of breast cancer. J Nucl Med, 53:1-8, 2012 Abstract|