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Article ; Online: Multiomic characterization of high-grade serous ovarian carcinoma: editorial commentary on recent application and consideration for future directions.

Jones, Tiffany Nicole / Shih, Ie-Ming / Wang, Tian-Li

2023 Volume 12, Issue 5, Page(s) 1368–1371

Language	English
Publishing date	2023-04-07
Publishing country	China
Document type	Editorial ; Comment
ZDB-ID	2901601-0
ISSN	2219-6803 ; 2218-676X
ISSN (online)	2219-6803
ISSN	2218-676X
DOI	10.21037/tcr-23-355
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Article ; Online: Serous tubal intra-epithelial carcinoma: what do we really know at this point?

Vang, Russell / Shih, Ie-Ming

Histopathology

2022 Volume 81, Issue 5, Page(s) 542–555

Abstract: Serous tubal intra-epithelial carcinoma (STIC) is the earliest morphologically recognisable step in the development of invasive high-grade serous carcinoma of the fallopian tube. Lesions occurring prior to STIC within the carcinogenic sequence for the ... ...

Abstract	Serous tubal intra-epithelial carcinoma (STIC) is the earliest morphologically recognisable step in the development of invasive high-grade serous carcinoma of the fallopian tube. Lesions occurring prior to STIC within the carcinogenic sequence for the pathogenesis of invasive high-grade serous carcinoma include the p53 signature and secretory cell outgrowth (SCOUT). Variable histological criteria have been used for diagnosing STIC, but a combination of morphology and immunohistochemistry for p53/Ki-67 improves interobserver agreement. Half of all carcinomas identified in risk-reducing salpingo-oophorectomy specimens are in the form of STIC; however, STIC also may be incidentally found on occasion in specimens from women at low or average risk of ovarian/tubal/peritoneal carcinoma. TP53 mutation is the earliest known DNA sequence alteration in STIC and almost all invasive high-grade serous carcinomas of the ovary and peritoneum. Data on the clinical behaviour of STIC are limited. While the short-term follow-up in the prior literature suggests a low risk of malignant progression, a more recent meta-analysis indicates a 10-year risk of 28%. STIC probably should be best regarded as a lesion with uncertain malignant potential at present, and future molecular analysis will help to classify those with higher risk of dissemination. This review provides an update on the current knowledge of STIC and related issues.
MeSH term(s)	Adenocarcinoma in Situ ; Carcinoma ; Carcinoma in Situ/pathology ; Carcinoma, Ovarian Epithelial ; Cystadenocarcinoma, Serous/pathology ; Fallopian Tube Neoplasms/pathology ; Female ; Humans ; Ki-67 Antigen ; Ovarian Neoplasms/pathology ; Tumor Suppressor Protein p53/analysis
Chemical Substances	Ki-67 Antigen ; Tumor Suppressor Protein p53
Language	English
Publishing date	2022-08-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	131914-0
ISSN	1365-2559 ; 0309-0167
ISSN (online)	1365-2559
ISSN	0309-0167
DOI	10.1111/his.14722
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Zs.A 1328: Show issues

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Article ; Online: ARID1A loss activates MAPK signaling via DUSP4 downregulation.

Mandal, Jayaprakash / Yu, Zheng-Cheng / Shih, Ie-Ming / Wang, Tian-Li

Journal of biomedical science

2023 Volume 30, Issue 1, Page(s) 94

Abstract: Background: ARID1A, a tumor suppressor gene encoding BAF250, a protein participating in chromatin remodeling, is frequently mutated in endometrium-related malignancies, including ovarian or uterine clear cell carcinoma (CCC) and endometrioid carcinoma ( ... ...

Abstract	Background: ARID1A, a tumor suppressor gene encoding BAF250, a protein participating in chromatin remodeling, is frequently mutated in endometrium-related malignancies, including ovarian or uterine clear cell carcinoma (CCC) and endometrioid carcinoma (EMCA). However, how ARID1A mutations alter downstream signaling to promote tumor development is yet to be established. Methods: We used RNA-sequencing (RNA-seq) to explore transcriptomic changes in isogenic human endometrial epithelial cells after deleting ARID1A. Chromatin immunoprecipitation sequencing (ChIP-seq) was employed to assess the active or repressive histone marks on DUSP4 promoter and regulatory regions. We validated our findings using genetically engineered murine endometroid carcinoma models, human endometroid carcinoma tissues, and in silico approaches. Results: RNA-seq revealed the downregulation of the MAPK phosphatase dual-specificity phosphatase 4 (DUSP4) in ARID1A-deficient cells. ChIP-seq demonstrated decreased histone acetylation marks (H3K27Ac, H3K9Ac) on DUSP4 regulatory regions as one of the causes for DUSP4 downregulation in ARID1A-deficient cells. Ectopic DUSP4 expression decreased cell proliferation, and pharmacologically inhibiting the MAPK pathway significantly mitigated tumor formation in vivo. Conclusions: Our findings suggest that ARID1A protein transcriptionally modulates DUSP4 expression by remodeling chromatin, subsequently inactivating the MAPK pathway, leading to tumor suppression. The ARID1A-DUSP4-MAPK axis may be further considered for developing targeted therapies against ARID1A-mutated cancers.
MeSH term(s)	Female ; Humans ; Mice ; Animals ; Down-Regulation ; Nuclear Proteins/genetics ; Carcinoma, Endometrioid/genetics ; Carcinoma, Endometrioid/metabolism ; Carcinoma, Endometrioid/pathology ; Mitogen-Activated Protein Kinase Phosphatases/genetics ; Mitogen-Activated Protein Kinase Phosphatases/metabolism ; Dual-Specificity Phosphatases/genetics ; Dual-Specificity Phosphatases/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	Nuclear Proteins ; Mitogen-Activated Protein Kinase Phosphatases (EC 3.1.3.16) ; Dual-Specificity Phosphatases (EC 3.1.3.48) ; DUSP4 protein, human (EC 3.1.3.48) ; ARID1A protein, human ; DNA-Binding Proteins ; Transcription Factors
Language	English
Publishing date	2023-12-09
Publishing country	England
Document type	Journal Article
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-023-00985-5
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Zs.A 4037: Show issues

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Article ; Online: ARID1A loss activates MAPK signaling via DUSP4 downregulation

Jayaprakash Mandal / Zheng-Cheng Yu / Ie-Ming Shih / Tian-Li Wang

Journal of Biomedical Science, Vol 30, Iss 1, Pp 1-

2023 Volume 14

Abstract: Abstract Background ARID1A, a tumor suppressor gene encoding BAF250, a protein participating in chromatin remodeling, is frequently mutated in endometrium-related malignancies, including ovarian or uterine clear cell carcinoma (CCC) and endometrioid ... ...

Abstract	Abstract Background ARID1A, a tumor suppressor gene encoding BAF250, a protein participating in chromatin remodeling, is frequently mutated in endometrium-related malignancies, including ovarian or uterine clear cell carcinoma (CCC) and endometrioid carcinoma (EMCA). However, how ARID1A mutations alter downstream signaling to promote tumor development is yet to be established. Methods We used RNA-sequencing (RNA-seq) to explore transcriptomic changes in isogenic human endometrial epithelial cells after deleting ARID1A. Chromatin immunoprecipitation sequencing (ChIP-seq) was employed to assess the active or repressive histone marks on DUSP4 promoter and regulatory regions. We validated our findings using genetically engineered murine endometroid carcinoma models, human endometroid carcinoma tissues, and in silico approaches. Results RNA-seq revealed the downregulation of the MAPK phosphatase dual-specificity phosphatase 4 (DUSP4) in ARID1A-deficient cells. ChIP-seq demonstrated decreased histone acetylation marks (H3K27Ac, H3K9Ac) on DUSP4 regulatory regions as one of the causes for DUSP4 downregulation in ARID1A-deficient cells. Ectopic DUSP4 expression decreased cell proliferation, and pharmacologically inhibiting the MAPK pathway significantly mitigated tumor formation in vivo. Conclusions Our findings suggest that ARID1A protein transcriptionally modulates DUSP4 expression by remodeling chromatin, subsequently inactivating the MAPK pathway, leading to tumor suppression. The ARID1A-DUSP4-MAPK axis may be further considered for developing targeted therapies against ARID1A-mutated cancers.
Keywords	ARID1A ; DUSP4 ; MAPK ; Chromatin remodeling ; Therapeutics ; Medicine ; R
Language	English
Publishing date	2023-12-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Follicular fluid has more to offer: Insulin-like growth factor axis on ovarian carcinogenesis.

Chu, Tiffany / Shih, Ie-Ming

EBioMedicine

2019 Volume 41, Page(s) 30–31

MeSH term(s)	Biomarkers ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Female ; Follicular Fluid/metabolism ; Humans ; Ovarian Neoplasms/diagnosis ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/metabolism ; Somatomedins/metabolism
Chemical Substances	Biomarkers ; Somatomedins
Language	English
Publishing date	2019-02-21
Publishing country	Netherlands
Document type	Letter
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2019.02.030
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Zs.A 7090: Show issues

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Article ; Online: Salpingectomy for ectopic pregnancy reduces ovarian cancer risk-a nation-wide study.

Yen, Ju-Chuan / Wu, Tzu-I / Stone, Rebecca / Wang, Tian-Li / Visvanathan, Kala / Chen, Li-Ying / Hsu, Min-Huei / Shih, Ie-Ming

JNCI cancer spectrum

2024

Abstract: Recent studies propose fallopian tubes as the tissue origin for many ovarian epithelial cancers. To further support this paradigm, we assessed whether salpingectomy for treating ectopic pregnancy had a protective effect using the Taiwan Longitudinal ... ...

Abstract	Recent studies propose fallopian tubes as the tissue origin for many ovarian epithelial cancers. To further support this paradigm, we assessed whether salpingectomy for treating ectopic pregnancy had a protective effect using the Taiwan Longitudinal National-Health-Research Database. We identified 316,882 women with surgical treatment for ectopic pregnancy and 3,168,820 age- and index-date-matched controls from 2000-2016. In a nested cohort, 91.5% of cases underwent unilateral salpingectomy, suggesting that most surgically managed patients have salpingectomy. Over a follow-up period of 17 years, the ovarian carcinoma incidence was 0.0069 (95%CI : 0.0060-0.0079) and 0.0089 (95%CI : 0.0086-0.0092) in the ectopic pregnancy and the control groups, respectively (p < .001). After adjusting the events to per 100-person years, the hazard ratio in the ectopic pregnancy group was 0.70 (95%CI : 0.61-0.80). The risk reduction occurred only in epithelial ovarian cancer (HR : 0.73, CI : 0.63-0.86) and not in non-epithelial subtypes. These findings show a decrease in ovarian carcinoma incidence following salpingectomy for treating ectopic pregnancy.
Language	English
Publishing date	2024-04-08
Publishing country	England
Document type	Journal Article
ISSN	2515-5091
ISSN (online)	2515-5091
DOI	10.1093/jncics/pkae027
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Article ; Online: Not All Peritoneal Implants Are Created Equal.

Varghese, Aaron / Shih, Ie-Ming

Gynecologic oncology

2019 Volume 156, Issue 1, Page(s) 1–2

MeSH term(s)	Adult ; Carcinoma, Ovarian Epithelial/genetics ; Carcinoma, Ovarian Epithelial/pathology ; Cystadenocarcinoma, Serous/genetics ; Cystadenocarcinoma, Serous/pathology ; Female ; Humans ; Middle Aged ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Peritoneal Neoplasms/genetics ; Peritoneal Neoplasms/pathology ; Peritoneal Neoplasms/secondary ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Young Adult
Chemical Substances	KRAS protein, human ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2019-12-12
Publishing country	United States
Document type	Editorial
ZDB-ID	801461-9
ISSN	1095-6859 ; 0090-8258
ISSN (online)	1095-6859
ISSN	0090-8258
DOI	10.1016/j.ygyno.2019.12.014
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Article ; Online: Treating ARID1A mutated cancers by harnessing synthetic lethality and DNA damage response.

Mandal, Jayaprakash / Mandal, Prativa / Wang, Tian-Li / Shih, Ie-Ming

Journal of biomedical science

2022 Volume 29, Issue 1, Page(s) 71

Abstract: Chromatin remodeling is an essential cellular process for organizing chromatin structure into either open or close configuration at specific chromatin locations by orchestrating and modifying histone complexes. This task is responsible for fundamental ... ...

Abstract	Chromatin remodeling is an essential cellular process for organizing chromatin structure into either open or close configuration at specific chromatin locations by orchestrating and modifying histone complexes. This task is responsible for fundamental cell physiology including transcription, DNA replication, methylation, and damage repair. Aberrations in this activity have emerged as epigenomic mechanisms in cancer development that increase tumor clonal fitness and adaptability amidst various selection pressures. Inactivating mutations in AT-rich interaction domain 1A (ARID1A), a gene encoding a large nuclear protein member belonging to the SWI/SNF chromatin remodeling complex, result in its loss of expression. ARID1A is the most commonly mutated chromatin remodeler gene, exhibiting the highest mutation frequency in endometrium-related uterine and ovarian carcinomas. As a tumor suppressor gene, ARID1A is essential for regulating cell cycle, facilitating DNA damage repair, and controlling expression of genes that are essential for maintaining cellular differentiation and homeostasis in non-transformed cells. Thus, ARID1A deficiency due to somatic mutations propels tumor progression and dissemination. The recent success of PARP inhibitors in treating homologous recombination DNA repair-deficient tumors has engendered keen interest in developing synthetic lethality-based therapeutic strategies for ARID1A-mutated neoplasms. In this review, we summarize recent advances in understanding the biology of ARID1A in cancer development, with special emphasis on its roles in DNA damage repair. We also discuss strategies to harness synthetic lethal mechanisms for future therapeutics against ARID1A-mutated cancers.
MeSH term(s)	Chromatin ; DNA Damage ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Female ; Histones ; Humans ; Nuclear Proteins/metabolism ; Ovarian Neoplasms/genetics ; Poly(ADP-ribose) Polymerase Inhibitors ; Synthetic Lethal Mutations ; Transcription Factors/genetics ; Transcription Factors/metabolism
Chemical Substances	ARID1A protein, human ; Chromatin ; DNA-Binding Proteins ; Histones ; Nuclear Proteins ; Poly(ADP-ribose) Polymerase Inhibitors ; Transcription Factors
Language	English
Publishing date	2022-09-19
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-022-00856-5
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Zs.A 4037: Show issues

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Article ; Online: Case Report: Tubal Atypical Placental Site Nodule.

Yen, Ting-Tai / Anderson, Jean / Shih, Ie-Ming

International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists

2021 Volume 41, Issue 5, Page(s) 530–534

Abstract: Placental site nodule (PSN) is a benign proliferation of chorionic-type intermediate trophoblastic cells that forms a tumor-like lesion. Most PSNs are intrauterine, but a few have been reported outside the uterus, including in fallopian tubes. PSN is ... ...

Abstract	Placental site nodule (PSN) is a benign proliferation of chorionic-type intermediate trophoblastic cells that forms a tumor-like lesion. Most PSNs are intrauterine, but a few have been reported outside the uterus, including in fallopian tubes. PSN is related to epithelioid trophoblastic tumor (ETT) in that both are composed of chorionic-type intermediate trophoblastic cells, while ETT is hypercellular and contains trophoblastic cells with increased nuclear atypia and a higher Ki-67 proliferation index as compared with PSN. Occasionally, an intermediate stage between a PSN and an ETT is observed, and such a lesion is often recognized as an atypical PSN (aPSN) characterized by trophoblastic cells exhibiting morphologic features in transition from a conventional PSN to an ETT. aPSN has been thought to exhibit benign behavior; however, it has also been reported that up to 15% of aPSN lesions either coexist with, or subsequently develop into, ETT. To the best of our knowledge, there has been no case report of an aPSN in an extrauterine site. Here, we reported a highly unusual case of tubal aPSN, which illustrates several key features associated with PSN and its possible pathogenesis.
MeSH term(s)	Fallopian Tubes/pathology ; Female ; Gestational Trophoblastic Disease/pathology ; Humans ; Placenta/pathology ; Pregnancy ; Trophoblastic Neoplasms/pathology ; Trophoblasts/pathology ; Uterine Neoplasms/pathology
Language	English
Publishing date	2021-09-27
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	604859-6
ISSN	1538-7151 ; 0277-1691
ISSN (online)	1538-7151
ISSN	0277-1691
DOI	10.1097/PGP.0000000000000825
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Article ; Online: Oncogenic BRAF and KRAS mutations in endosalpingiosis.

Chui, Michael Herman / Shih, Ie-Ming

The Journal of pathology

2019 Volume 250, Issue 2, Page(s) 148–158

Abstract: Endosalpingiosis, a microscopic lesion composed of ectopic Fallopian tube epithelium, frequently involves the peritoneum and lymph nodes in patients with ovarian serous borderline tumour or low-grade serous carcinoma, but its pathogenic significance ... ...

Abstract	Endosalpingiosis, a microscopic lesion composed of ectopic Fallopian tube epithelium, frequently involves the peritoneum and lymph nodes in patients with ovarian serous borderline tumour or low-grade serous carcinoma, but its pathogenic significance remains unclear. Using laser-capture microdissection and droplet digital PCR, we investigated whether endosalpingiosis harbours the driver mutations in BRAF and KRAS that characterise ovarian low-grade serous neoplasms. Somatic mutations were detected in 14 (33%) of 43 endosalpingiotic lesions analysed. Of 21 women with endosalpingiosis associated with a synchronous or metachronous ovarian low-grade serous tumour, mutations were identified in endosalpingiotic lesions from 11 (52%) women, with most cases (10/11, 91%) demonstrating identical mutations in both tumour and endosalpingiosis. In contrast, of 13 cases of endosalpingiosis not associated with an ovarian tumour, only one harboured a KRAS mutation. The proliferative activity as assessed by Ki-67 immunohistochemistry was lower in endosalpingiosis than in low-grade serous tumours, and endosalpingiosis with either a BRAF or KRAS mutation had a significantly lower Ki-67 index than those without. Ectopic expression of KRAS
MeSH term(s)	Cell Proliferation/genetics ; Cell Transformation, Neoplastic ; Cells, Cultured ; Choristoma/genetics ; Choristoma/pathology ; Cystadenocarcinoma, Serous/genetics ; Epithelial Cells/pathology ; Fallopian Tubes ; Female ; Humans ; Laser Capture Microdissection/methods ; Lymphatic Diseases/genetics ; Lymphatic Diseases/pathology ; Mutation ; Ovarian Neoplasms/genetics ; Peritoneal Diseases/genetics ; Peritoneal Diseases/pathology ; Precancerous Conditions/genetics ; Precancerous Conditions/pathology ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins p21(ras)/genetics
Chemical Substances	Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2019-11-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.5353
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