![](https://pathology.ubc.ca/files/2022/12/Yemin-Wang1.png)
Wang, Yemin
PhD
Academic Rank(s): Assistant Professor, Dept of Pathology & Laboratory Medicine | Senior Research Scientist, Ovarian Cancer Research Centre and Vancouver Prostate Centre, Vancouver Coastal Health Research Institute
Affiliation(s): Vancouver Coastal Health Research Institute, BC Cancer Research Institute
Research and Scholarly Interests: ovarian and endometrial cancer; DICER1 syndrome; cancer cell of origin; cancer models; therapeutic vulnerability; genomics; oncogenic signaling; cancer metabolism
Dr. Wang obtained his PhD degree in Experimental Medicine at the University of British Columbia in 2009, studying the roles of ING family proteins in melanoma pathogenesis. He then pursued postdoctoral studies at the Fred Hutchison Cancer Research Centre in Seattle, exploring the role of microRNAs in DNA damaging response and chemoresistance. In 2012, he joined the laboratory of Dr. David Huntsman lab at BC Cancer Research Centre as postdoctoral fellows of Canadian Institutes of Health Research and Michael Smith Foundation for Health Research to study how genetic mutations in microRNA biogenesis gene DICER1 drive rare ovarian cancer development. Dr. Wang is currently a senior research scientist in the Ovarian Cancer Research (OVCARE) Center and Vancouver Prostate Centre at Vancouver Coastal Health Research Institute. His lab studies how genetic mutations drives the development and progression of rare aggressive ovarian and endometrial cancers to inform targeted therapeutics.
Academic Background
- Postdoctoral Fellow, University of British Columbia/BC Cancer, Vancouver BC (2012-2015)
- Postdoctoral Fellow, Fred Hutchinson Cancer Research Centre, Seattle WA (2009-2011)
- Ph.D. (Experimental Medicine), University of British Columbia, Canada (2009)
- M.Sc. (Botany), Nanjing University, China, 2003
- BSc. (Biology). Nanjing University, China, 2001
Awards and Recognition
- UBC Science Co-op Supervisor Recognition Award. UBC (2024)
- North Family Health Research Award. VGH & UBC foundation and OVCARE (2020-2023)
- UBC Science Co-op Supervisor Recognition Award, UBC (2019)
- Jeremy Jass Prize for Research Excellence in Pathology (2016), Journal of Pathology (2017)
- Postdoctoral fellowship, Michael Smith Foundation for health research (2012-2014)
- Postdoctoral fellowship, Canadian Institute of Health Research (2010-2013)
- Trainee Rising Star, Vancouver Coast Health Research Institute (2008) Terry Fox Foundation PhD Studentship, National Cancer Institute of Canada (2007-2009)
- Roman M. Babicki Fellowship in Medical Res, UBC (2006-2007)
Publications
Link to Dr. Yemin Wang’s Google Scholar Profile.
Selected Publications
- Chae Young Shin, Bengul Gokbayrak, Valerie L Tao, Noorah Almadani, Eunice Li, Rebecca Ho, Felix KF Kommoss, Jutta Huvila, Derek Chiu, Samuel Leung, Basile Tessier Cloutier, Jessica N. McAlpine, David G. Huntsman, C. Blake Gilks, Lien Hoang, Yemin Wang. Molecular subtypes and SWI/SNF protein expression in dedifferentiated/undifferentiated endometrial carcinoma. Histopathology, 2025 Jan 15 doi: 10.1111/his.15411. Online ahead of print. PMID: 39811899.
- Wang Y*, Chen SY, Ta M, Senz J, Tao LV, Thornton S, Tamvada N, Yang W, Moscovitz Y, Li E, Guo J, Shen C, Douglas JM, El-Naggar AM, Kommoss FKF, Underhill TM, Singh N, Gilks CB, Morin GB, Huntsman DG*. Bi-allelic mutations of Dicer1 in the gynecologic tract of mouse drives lineage specific development of DICER1 syndrome-associated cancer. Cancer Research. 2023 Nov 1; 83 (21): 3517-3528. doi: 10.1158/0008-5472.CAN-22-3620. PMID: 37494476 * co-corresponding
- Zhu X*, Fu Z*, Chen SY*, Ong D, Aceto G, Ho R, Steinberger J, Monast A, Pilon V, Li E, Ta M, Ching K, Adams B, Negri GL, Choiniere L, Fu L, Pavlakis K, Pirrotte P, Avizonis DZ, Trent J, Weissman BE, Klein Geltink RI, Morin GB, Park M, Huntsman DG, Foulkes WF, Wang Y§, Huang S§. Alanine supplementation exploits glutamine dependency induced by SMARCA4/2-loss. Nat Comm, 2023 May 20;14(1):2894. doi: 10.1038/s41467-023-38594-3. PMID: 37210563. §Co-corresponding
- Karnezis AN, Chen SY, Chow C, Yang W, Hendricks WPD, Ramos P, Briones N, Mes-Masson AM, Bosse T, Gilks CB, Trent JM, Weissman B, Huntsman DG, Wang Y. Re-assigning the histologic identities of COV434 and TOV-112D ovarian cancer cell lines. Gynecol Oncol. 2021 Feb: 160(2):568-578. doi:10.1016/j.ygyno.2020.12.004. Epub ahead of print. 2020 Dec 13PMID: 33328126.
- Wang Y*, Tao VL, Shin CY, Salamanca C, Chen SY, Chow C, Köbel M, Ben-Neriah S, Farnell D, Steidl C, Mcalpine JN, Gilks CB, Huntsman DG. Establishment and characterization of VOA1066 cells: An undifferentiated endometrial carcinoma cell line. PLoS One. 2020 Oct 14;15(10):e0240412. doi:10.1371/journal.pone.0240412. PMID: 33052929; PMCID: PMC7556492. §Co-corresponding
- Wang Y, Hoang L, Ji JX, Huntsman DG. SWI/SNF Complex Mutations in Gynecologic Cancers: Molecular Mechanisms and Models. Annu Rev Pathol. 2020 Jan 24;15:467-492. doi:10.1146/annurev-pathmechdis-012418-012917. PMID: 31977292; PMCID: PMC6986318.
- Karnezis AN*, Wang Y*, Keul J, Tessier-Cloutier B, Magrill J, Kommoss S, Senz J, Yang W, Proctor L, Schmidt D, Clement PB, Gilks CB, Huntsman DG, Kommoss F. DICER1 and FOXL2 Mutation Status Correlates With Clinicopathologic Features in Ovarian Sertoli-Leydig Cell Tumors. Am J Surg Pathol. 2019 May;43(5):628-638. doi:10.1097/PAS.0000000000001232. PMID: 30986800. *co-1st author
- Wang Y*, Chen SY, Colborne S, Lambert G, Shin CY, Santos ND, Orlando KA, Lang JD, Hendricks WPD, Bally MB, Karnezis AN, Hass R, Underhill TM, Morin GB, Trent JM, Weissman BE, Huntsman DG. Histone Deacetylase Inhibitors Synergize with Catalytic Inhibitors of EZH2 to Exhibit Antitumor Activity in Small Cell Carcinoma of the Ovary, Hypercalcemic Type. Mol Cancer Ther. 2018 Dec;17(12):2767-2779. doi: 10.1158/1535-7163.MCT-18-0348. Epub 2018 Sep 19. PMID: 30232145; PMCID: PMC6279577. * §Co-corresponding
- Wang Y*, Karnezis AN*, Magrill J, Tessier-Cloutier B, Lum A, Senz J, Gilks CB, McCluggage WG, Huntsman DG, Kommoss F. DICER1 hot-spot mutations in ovarian gynandroblastoma. *co-1st author Histopathology. 2018 Aug;73(2):306-313. doi:10.1111/his.13630. Epub 2018 Jun 5. PMID: 29660837.
- Wang Y, Chen SY, Karnezis AN, Colborne S, Santos ND, Lang JD, Hendricks WP, Orlando KA, Yap D, Kommoss F, Bally MB, Morin GB, Trent JM, Weissman BE, Huntsman DG. The histone methyltransferase EZH2 is a therapeutic target in small cell carcinoma of the ovary, hypercalcaemic type. J Pathol. 2017 Jul;242(3):371-383. doi: 10.1002/path.4912. Epub 2017 Jun 2. PMID: 28444909; PMCID: PMC6857704.
- Wang Y, Chen J, Yang W, Mo F, Senz J, Yap D, Anglesio MS, Gilks B, Morin GB, Huntsman DG. The oncogenic roles of DICER1 RNase IIIb domain mutations in ovarian Sertoli-Leydig cell tumors. Neoplasia. 2015 Aug;17(8):650-60. doi:10.1016/j.neo.2015.08.003. PMID: 26408257; PMCID: PMC4674484.
- Karnezis AN*, Wang Y*, Ramos P, Hendricks WP, Oliva E, D’Angelo E, Prat J, Nucci MR, Nielsen TO, Chow C, Leung S, Kommoss F, Kommoss S, Silva A, Ronnett BM, Rabban JT, Bowtell DD, Weissman BE, Trent JM, Gilks CB, Huntsman DG. Dual loss of the SWI/SNF complex ATPases SMARCA4/BRG1 and SMARCA2/BRM is highly sensitive and specific for small cell carcinoma of the ovary, hypercalcaemic type. J Pathol. 2016 Feb;238(3):389-400. doi: 10.1002/path.4633. Epub 2015 Dec 21. PMID: 26356327; PMCID: PMC4832362. *co-1st author
- Wang Y*, Huang JW, Castella M, Huntsman DG, Taniguchi T. p53 is positively regulated by miR-542-3p. Cancer Res. 2014 Jun 15;74(12):3218-27. doi:10.1158/0008-5472.CAN-13-1706. Epub 2014 Apr 24. PMID: 24762395; PMCID:PMC4058365. * §Co-corresponding
Research Interest
- Ovarian and endometrial cancer
- DICER1 syndrome
- Cancer cell of origin
- Cancer models
- Therapeutic vulnerability
- Genomics
- Oncogenic signaling
- Cancer metabolism
Research Program
The overarching theme of my research program is to dissect mechanisms by which genetic and epigenetic events drive malignant transformation and subsequent progression to a poorly differentiated and highly aggressive state that inform the development of prevention and targeted therapeutics. Two major types of cancers we study include SWI/SNF-mutant cancers and DICER1 syndrome-associated cancers.
The SWI/SNF chromatin remodeling complex members are mutated in ~25% of all human cancers, ranking it among the most highly mutated protein complexes in cancer. The understanding of their role in cancer initiation and progression is incomplete. Studies from the past decade have identified gynecologic cancer, particularly ovarian and endometrial cancers, as great models to study the roles of SWI/SNF complexes in tumorigenesis. SWI/SNF mutations can occur at different stages of gynecologic cancer development and may function as either a driver event, a transformation-permissive event or a progression event. These includes a) inactivating mutations of SMARCA4, occur as a germline event and function as a classic tumor suppressor and key driver in small cell carcinoma of the ovary, hypercalcemic type (SCCOHT); b) ARID1A inactivating mutations occur as a transformation-permissive event in the development of endometriosis-associated ovarian and endometrial cancers; and c) inactivation of SMARCA4, SMARCB1 mutations or ARID1A/ARID1B dual inactivating mutations in dedifferentiated/undifferentiated cancer of ovary and endometrium (DD/UDEC) as cancer progression events. However, the context-specific roles of SWI/SNF mutations in the initiation and progression of ovarian and endometrial cancers is far from being fully understood. Since most SWI/SNF-mutant cancers are highly aggressive and most of these genetic alterations result in protein loss that is not directly targetable, identifying druggable vulnerabilities specific to SWI/SNF deficiencies remains an unmet clinical need.
DICER1 tumor predisposition syndrome (DTPS) is an autosomal dominant tumor predisposition syndrome caused by heterozygous germline loss of function pathogenic sequence variants in the DICER1 gene, which encodes a microRNA (miRNA) processing enzyme. Key cancer sites are lung, brain, gynecologic tract, kidney and thyroid. Most DTPS cancers are sarcomas; the high-grade DICER1 sarcomas have poor outcomes and are challenging to treat: biology-informed novel treatment options are much needed. It has been proposed that the histologic similarities of DICER1-sarcomas, regardless of their anatomic sites, implies biological relatedness and the potential for generalizable therapeutic solutions. In DTPS, a hypomorphic missense mutation restricted to the DICER1 RNase IIIb domain is the usual second event in the tumors. These focal hotspot mutations change metal-binding residues essential for RNase IIIb endonuclease activity, resulting in RNase IIIb-defective proteins as the only expressed form of DICER1 in DTPS cancer. It is unknown how selective loss of RNase IIIb activity drives oncogenesis and how to treat them.
My research will utilize patient samples and genetically engineered mouse models along with their derivative cell lines and organoids as well as leading-edge methods including genome editing, genomic, single cell omics, proteomics, functional genomics and drug screening to interrogate the underlying mechanisms supporting tumorigenesis in lethal gynecologic cancers and DICER1 sarcomas to uncover therapeutic vulnerabilities to inform the development of novel therapeutic strategies for managing the hard-to-treat cancer types.
Clinical Service
Current Projects In My Lab Include
Teaching Interest
- Mechanisms and models of cancer