TY - JOUR
T1 - Histopathology and ARID1A Expression in Endometriosis- Associated Ovarian Carcinoma (EAOC) Carcinogenesis Model with Endometrial Autoimplantation and DMBA Induction
AU - Wuyung, Puspita Eka
AU - Rahadiati, Familia Bella
AU - Tjahjadi, Hartono
AU - Salinah, Salinah
AU - Kusmardi, Kusmardi
AU - Kodariah, Ria
AU - Wiweko, Budi
N1 - Copyright:
This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine
PY - 2021/2/1
Y1 - 2021/2/1
N2 - BACKGROUND: Ovarian carcinoma is one of the most deadly malignancies in the gynecologic field. The cause is not yet known, and the clinical symptoms are not specific. Endometrioid carcinoma and ovarian clear cell carcinoma can originate from endometriosis and are known as endometriosis-related ovarian carcinoma (EAOC). Development of EAOC experimental animal models is needed for basic research and clinical preparation of human tissue tests. This study aimed to determine the role of the ARID1A gene mutation in the carcinogenetic process of EAOC in experimental animal models induced with DMBA. METHODS: In this study, the EAOC experimental model was developed using the autoimplantation technique and DMBA induction. This study involved placebo surgery mice (sham), endometrial autoimplantation, and a combination of endometrial autoimplantation and DMBA induction, which were sacrificed at weeks 5, 10, and 20, respectively. Histopathological assessment and immunohistochemical ARID1A staining with an assessment of positive percentages were carried out on 200 cells. RESULTS: This study produced 1 (20%) atypical endometriosis and 1 (20%) clear cell carcinoma at implantation and after 10 weeks of DMBA induction, and 100% endometrioid carcinoma in the DMBA-induced group. ARID1A staining did not show any significant difference (p = 0.313) in all groups. CONCLUSION: The combination of endometrial autoimplantation techniques and DMBA induction in the ovary produced atypical endometriosis, clear cell carcinoma, and endometrioid carcinoma, where time is an important factor. There was no significant difference in ARID1A expression between the treatment and control groups.
AB - BACKGROUND: Ovarian carcinoma is one of the most deadly malignancies in the gynecologic field. The cause is not yet known, and the clinical symptoms are not specific. Endometrioid carcinoma and ovarian clear cell carcinoma can originate from endometriosis and are known as endometriosis-related ovarian carcinoma (EAOC). Development of EAOC experimental animal models is needed for basic research and clinical preparation of human tissue tests. This study aimed to determine the role of the ARID1A gene mutation in the carcinogenetic process of EAOC in experimental animal models induced with DMBA. METHODS: In this study, the EAOC experimental model was developed using the autoimplantation technique and DMBA induction. This study involved placebo surgery mice (sham), endometrial autoimplantation, and a combination of endometrial autoimplantation and DMBA induction, which were sacrificed at weeks 5, 10, and 20, respectively. Histopathological assessment and immunohistochemical ARID1A staining with an assessment of positive percentages were carried out on 200 cells. RESULTS: This study produced 1 (20%) atypical endometriosis and 1 (20%) clear cell carcinoma at implantation and after 10 weeks of DMBA induction, and 100% endometrioid carcinoma in the DMBA-induced group. ARID1A staining did not show any significant difference (p = 0.313) in all groups. CONCLUSION: The combination of endometrial autoimplantation techniques and DMBA induction in the ovary produced atypical endometriosis, clear cell carcinoma, and endometrioid carcinoma, where time is an important factor. There was no significant difference in ARID1A expression between the treatment and control groups.
KW - ARID1A
KW - DMBA
KW - EAOC
KW - Endometriosis
KW - experimental animal model
UR - http://www.scopus.com/inward/record.url?scp=85102225233&partnerID=8YFLogxK
U2 - 10.31557/APJCP.2021.22.2.553
DO - 10.31557/APJCP.2021.22.2.553
M3 - Article
C2 - 33639673
AN - SCOPUS:85102225233
SN - 1513-7368
VL - 22
SP - 553
EP - 558
JO - Asian Pacific journal of cancer prevention : APJCP
JF - Asian Pacific journal of cancer prevention : APJCP
IS - 2
ER -