Positions
- Richard E. Buller Professor
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Mol & Cell Biology
ÌÇÐÄÊÓƵ of Medicine
Houston, TX, US
- Professor
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Obstetrics & Gynecology
ÌÇÐÄÊÓƵ of Medicine
Houston, Texas, United States
- Co-Director
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Center for Coregulator Research
ÌÇÐÄÊÓƵ of Medicine
Houston, Texas, United States
- Faculty Member
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Center for Drug Discovery
ÌÇÐÄÊÓƵ of Medicine
Houston, Texas, United States
- Faculty Member
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Dan L Duncan Comprehensive Cancer Center
ÌÇÐÄÊÓƵ of Medicine
Houston, Texas, United States
- Faculty Member
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Therapeutic Innovative Center
ÌÇÐÄÊÓƵ of Medicine
Houston, Texas, United States
Addresses
- BCM-Michael DeBakey Center (Office)
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Room: BCMM-M804A1
HOUSTON, TX, 77030
United States
Phone: (713) 798-6276
sjhan@bcm.edu
- Lab (Lab)
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BCM-Micheal DeBakey Center
Room: BCMM-M805 and M807
HOUSTON, TX, 77030
United States
Phone: (713) 798-6276
sjhan@bcm.edu
Education
- Postdoctoral Fellowship at Samsung Biomedical Reserach Institute
- 03/1997 - Seoul, South Korea
- PhD from Seoul National University
- 02/1997 - Seoul, South Korea
- Postdoctoral Fellowship at ÌÇÐÄÊÓƵ Of Medicine
- 06/2000 - Houston, Texas, United States
- MSc from Seoul National University
- 01/1993 - Gwanak-Gu, Seoul, South Korea
Certifications
- Medical Degree
- ÌÇÐÄÊÓƵ of Medicine
Honors & Awards
- Investigator-Initiated Research Award (2024)
- Department of Defense's Office
- Mike Hogg Research Award (2016)
- Mike Hogg Research Foundation
- NURSA (Nuclear Receptor Signaling Atlas) Research Award (2017)
- National Institute of Diabetes and Digestive and Kidney Diseases
- Cozzarelli Prize Award (2024)
- National Academy of Sciences
- Richard and Catherin Buller Endowed Professorship (2024)
- ÌÇÐÄÊÓƵ of Medicine
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.
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.
Videos
Selected Publications
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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.. " " Cell. 2015 ; 163 (4) : 960-74.
Pubmed PMID: . -
Han SJ, Hawkins SM, Begum K, Jung SY, Kovanci E, Qin J, Lydon JP, Demayo FJ, O'Malley BW. " " Nat Med. 2012 Jun 3;
Pubmed PMID: . -
Park Y, Cho YJ, Sung N, Park MJ, Guan X, Gibbons WE, O'Malley BW, Han SJ.. " " J Biomed Sci. 2022 Nov 22; 29
Pubmed PMID: . -
Han SJ, Sung N, Wang J, O'Malley BW, Lonard DM.. " " Breast Cancer Res.. 2022 Oct 31; 24
Pubmed PMID: .
Funding
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The Genomic Function of Estrogen Receptor Beta in Endometriosis
#R01 HD098059-01A1 - 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.
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Development of SRC-3 gene disrupted Tregs for adoptive cell therapy to treat cancer through the modulation of inherent tumor-immune system defenses
- 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.
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Defining the Critical Module to Cooperatively Control the Estrogen/Growth Factor/Immunity Signaling in Endometriosis Progression
#HT9425-24-1-0254 - Grant funding from Department of Defense Office of the Congressionally Directed Medical Research Programs
- Endometriosis is a complex disease because aberrant estrogen and growth factor signaling, and immune dysregulation are closely associated for the endometriosis progression. Therefore, what is the key modulator to cooperatively coordinate estrogen/growth factor/immunity axis for the endometriosis progression is the $64 question to understand the nature of the molecular pathogenesis of endometriosis. Unfortunately, this question still needs to be answered. Here, we propose that Hepatocyte Growth Factor activates MET receptor tyrosine kinase (MET) in endometriotic lesions and then directly phosphorylates the Y99 site of Estrogen Receptor beta (ERβ), stimulating its transcriptional activity. The activated MET/ERβ directly elevates the Programmed Death-Ligand 1 (PD-L1) in endometriotic lesions and then generate an endometriotic immune microenvironment to enhance endometriosis progression. Thus, anti-PD-L1 antibody immunotherapy changes the endometriotic immune microenvironment to suppress endometriosis progression and relieve endometriosis-associated symptoms, such as pain and infertility.
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