Ovarian and endometrial endometrioid adenocarcinomas have distinct profiles of microsatellite instability, PTEN expression, and ARID1A expression
Hsien-Neng Huang
Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Pathology, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu, Taiwan
H.-N.H. and M.-C.L. contributed equally to this work.Search for more papers by this authorMing-Chieh Lin
Department of Pathology, National Taiwan University Hospital, Tapei, Taiwan
H.-N.H. and M.-C.L. contributed equally to this work.Search for more papers by this authorLi-Hui Tseng
Department of Medical Genetics, National Taiwan University Hospital, Tapei, Taiwan
Search for more papers by this authorYing-Cheng Chiang
Department of Obstetrics and Gynaecology, National Taiwan University Hospital, Tapei, Taiwan
Search for more papers by this authorLiang-In Lin
Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Tapei, Taiwan
Search for more papers by this authorYu-Feng Lin
Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Tapei, Taiwan
Search for more papers by this authorHsin-Ying Huang
Department of Mathematics Education, National Taichung University of Education, Taichung, Taiwan
Search for more papers by this authorCorresponding Author
Kuan-Ting Kuo
Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Pathology, National Taiwan University Hospital, Tapei, Taiwan
Address for correspondence: K-T Kuo, 3rd floor, No. 7, Chung Shan South Road, Taipei, Taiwan 10001. e-mail: [email protected]Search for more papers by this authorHsien-Neng Huang
Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Pathology, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu, Taiwan
H.-N.H. and M.-C.L. contributed equally to this work.Search for more papers by this authorMing-Chieh Lin
Department of Pathology, National Taiwan University Hospital, Tapei, Taiwan
H.-N.H. and M.-C.L. contributed equally to this work.Search for more papers by this authorLi-Hui Tseng
Department of Medical Genetics, National Taiwan University Hospital, Tapei, Taiwan
Search for more papers by this authorYing-Cheng Chiang
Department of Obstetrics and Gynaecology, National Taiwan University Hospital, Tapei, Taiwan
Search for more papers by this authorLiang-In Lin
Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Tapei, Taiwan
Search for more papers by this authorYu-Feng Lin
Department of Clinical Laboratory Sciences and Medical Biotechnology, College of Medicine, National Taiwan University, Tapei, Taiwan
Search for more papers by this authorHsin-Ying Huang
Department of Mathematics Education, National Taichung University of Education, Taichung, Taiwan
Search for more papers by this authorCorresponding Author
Kuan-Ting Kuo
Graduate Institute of Pathology, College of Medicine, National Taiwan University, Taipei, Taiwan
Department of Pathology, National Taiwan University Hospital, Tapei, Taiwan
Address for correspondence: K-T Kuo, 3rd floor, No. 7, Chung Shan South Road, Taipei, Taiwan 10001. e-mail: [email protected]Search for more papers by this authorAbstract
Aims
To understand the role of and differences in molecular alterations between endometrial and ovarian endometrioid adenocarcinomas.
Methods and results
We investigated the microsatellite status of 26 ovarian endometrioid adenocarcinomas (OVEMs), 42 endometrial endometrioid adenocarcinomas (EMCAs), and 19 concurrent (endometrial and ovarian) endometrioid adenocarcinomas. We evaluated the expression of the mismatch repair proteins, PTEN and ARID1A, and mutations of PTEN, KRAS, CTNNB1, and PIK3CA. High levels of microsatellite instability (MSI-H) were present in one of 26 OVEMs, 12 of 42 EMCAs, and four of 19 concurrent endometrioid adenocarcinomas. Only four of 19 concurrent endometrioid adenocarcinomas showed identical molecular alterations in their endometrial and ovarian components. Loss of ARID1A or loss of PTEN expression, and MSI-H, were more common in EMCAs than OVEMs (P = 0.044, P = 0.004, and P = 0.012, respectively). MSI-H in endometrial endometrioid adenocarcinomas was also related to loss of ARID1A expression (P < 0.001). In the cohort of MSI-H endometrioid adenocarcinomas involving the endometrium (n = 16), MSH6-deficient cases showed higher frequencies of CTNNB1 and PIK3CA mutations (P = 0.008 and P = 0.036, respectively), but lower frequencies of KRAS mutation (P = 0.011), than PMS2-deficient cases.
Conclusions
The different frequencies of molecular genetic alterations between endometrial endometrioid adenocarcinomas and ovarian endometrioid adenocarcinomas imply that distinct processes may be involved in their tumorigenesis or tumour progression.
Supporting Information
Filename | Description |
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his12543-sup-0001-TableS1.docWord document, 137 KB | Table S1. Clinical data and molecular findings for EMCAs and OVEMs in this study. |
his12543-sup-0002-TableS2.docWord document, 43.5 KB | Table S2. Comparison of molecular alterations in different histological grades of pure endometrial and ovarian endometrioid adenocarcinomas. |
Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
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