Email

sjhan@bcm.edu

Positions

Associate Professor

Mol & Cell Biology-Mol.Regulation
Dan L. Duncan Cancer Center and Center for Reproductive Medicine
Baylor College of Medicine
Houston, TX US

Member

Dan L Duncan Comprehensive Cancer Center
Baylor College of Medicine
Houston, Texas United States

Member

Center for Drug Discovery
Baylor College of Medicine

Member

Therapeutic Innovative Center
Baylor College of Medicine

Co-Director

Center for Coregulator Research
Baylor College of Medicine
Houston, Texas United States

Addresses

BCM-Michael DeBakey Center (Office)

Room: BCMM-M711A
Houston, TX 77030
United States

Lab (Lab)

BCM-Micheal DeBakey Center
Room: BCMM-M711
Houston, TX 77030
United States

Education

Post-Doctoral Fellowship at Samsung Biomedical Reserach Institute

03/1997 - Seoul, South Korea

PhD from Seoul National University

02/1997 - Seoul, South Korea

Post-Doctoral Fellowship at Baylor College Of Medicine

06/2000 - Houston, Texas United States

Certifications

Medical Degree

BCM

Professional Interests

• Pathogenic Role of Steroid Receptor Coactivator and Nuclear Receptor in Women's Reproductive Disease

Professional Statement

As an estrogen-dependent pro-inflammatory disease, endometriosis is defined as the colonization and growth of endometrial tissues at anatomic sites outside of the uterine cavity, primarily on the pelvic peritoneum and ovaries. Up to 5-10% of reproductive-aged women worldwide suffer chronically from endometriosis symptoms, such as pelvic pain and infertility. Due to the severe chronic morbidity associated with this gynecological disorder, our study has attempted to identify the distinguishing molecular features of endometriotic lesions and endometrial dysfunction to develop more effective prognostic, diagnostic, and treatment strategies for the clinical management of this debilitating disease and the amelioration of endometriosis-associated infertility.

Tregs are essential in restraining immune responses for immune homeostasis. SRC-3 is a pleiotropic coactivator, the second-most highly expressed transcriptional coactivator in Tregs, and a suspect in Treg function. Our study showed that the disruption of SRC-3 expression in Tregs leads to 'complete lifetime eradication' of tumors in aggressive syngeneic breast cancer mouse models because deletion of SRC-3 alters the expression of a wide range of key genes involved in efferent and afferent Treg signaling. SRC-3KO Tregs confer this long-lasting protection against cancer recurrence in mice without an apparent systemic autoimmune pathological phenotype. Therefore, our team will develop the SRC-3 deleted Tregs cell therapy as a novel and efficient future treatment for eliminating tumor growth and recurrence without the autoimmune side-effects that typically accompany immune checkpoint modulators.

Websites

Videos

Selected Publications

• Han SJ, Jung SY , Wu S., Hawkins SM, Park, MJ, Kyo S., Qin J, Lydon JP, Tsai, S.Y., Tsai, M-J., DeMayo FJ, O'Malley BW. "Estrogen Receptor β modulate apoptosis complaex and the inflammasome to drive the pathogensis of endometriosis." Cell. 2015;163(4):960-74. Pubmed PMID: 26544941
• Han SJ, Hawkins SM, Begum K, Jung SY, Kovanci E, Qin J, Lydon JP, Demayo FJ, O'Malley BW "A new isoform of steroid receptor coactivator-1 is crucial for pathogenic progression of endometriosis.." Nat Med. 2012 Jun 3; Pubmed PMID: 22660634
• Han SJ, Lee JE, Cho YJ, Park MJ, O'Malley BW. "Genomic Function of Estrogen Receptor β in Endometriosis." Endocrinology. 2019 Nov;160 Pubmed PMID: 31504401
• Park Y, Cho YJ, Sung N, Park MJ, Guan X, Gibbons WE, O'Malley BW, Han SJ. "Oleuropein suppresses endometriosis progression and improves the fertility of mice with endometriosis." J Biomed Sci. 2022 Nov 22;29 Pubmed PMID: 36419064

Funding

The Genomic Function of Estrogen Receptor Beta in Endometriosis - #R01 HD098059-01A1

(03/06/2020 - 12/31/2024) Grant funding from NICHD

The major goals of this project are to define how the specific ER-beta mediated gene network modulate antiapoptosis, epithelial-mesenchymal transition and angiogenesis of endometriotic lesions for the progression of endometriosis.

Development of SRC-3 gene disrupted Tregs for adoptive cell therapy to treat cancer through the modulation of inherent tumor-immune system defenses

(09/01/2022 - 08/31/2024) Grant funding from CoRegen Inc

The main goal of this project is to develop a new immunotherapy using SRC-3 deleted regulatory T cells to eradicate cancer without adverse effects.