Definitive study shows no association between ARID1A mutation status and clinical outcome in endometriosis-related ovarian cancers‡

Khalique S, Saira Khalique, Nash S, Sarah H. Nash, Sarah Nash, Rachael Natrajan
The Journal of Pathology · 2022 · vol. 258(1) , pp. 1–3 · doi:10.1002/path.5973 · PMID:35647895 · PMC9540905 · W4281822350
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This study of 1,623 endometriosis-associated ovarian carcinomas found that ARID1A status has no independent prognostic value, but loss is associated with mismatch repair deficiency and increased CD8+ tumor infiltrating lymphocytes in endometrioid subtypes.

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This research evaluates the prognostic utility of ARID1A mutation status in patients with endometriosis-related ovarian cancers. The authors analyzed validated biomarker assays to determine whether ARID1A loss provides independent predictive value beyond established factors such as mismatch repair deficiency and CD8+ tumor-infiltrating lymphocyte infiltration. The study concludes that ARID1A loss is confounded by these other variables and does not offer any independent prognostic significance for clinical outcomes in this specific cancer subtype. Relevance to endometriosis: Centrally about endometriosis-associated ovarian carcinomas, specifically addressing the lack of prognostic value of ARID1A mutations in tumors arising from endometriosis.

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Abstract

The ARID1A tumour suppressor protein is a component of the SWI/SNF chromatin remodelling complex, which is mutated in approximately 20% of all human cancers. ARID1A mutational status is considered to hold prognostic significance in a range of solid malignancies, yet in endometriosis-related ovarian carcinomas there has been a lack of clarity of its prognostic role. Moreover, the relationship between ARID1A status and immune infiltrate is also poorly understood. In a recent issue of The Journal of Pathology, a large comprehensive study by Heinze, Nazeran et al addressed these areas by reviewing 1,623 endometriosis-associated ovarian carcinomas and correlating ARID1A status using standardised immunohistochemistry to infer mutation status, with comprehensive clinicopathological features, mismatch repair status and CD8+ tumour infiltrating lymphocytes. The study definitively showed that ARID1A status does not provide any independent prognostic value in endometriosis-associated ovarian carcinomas. ARID1A loss was, however, shown to be associated with mismatch repair deficiency and increased CD8+ tumour infiltrating lymphocytes in endometrioid ovarian carcinoma, which may be relevant for future studies. © 2022 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.
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This study was supported by The Institute of Cancer Research and Wellcome Trust. We acknowledge NHS funding to The Institute of Cancer Research/Royal Marsden Hospital Biomedical Research Centre.

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All authors were involved in writing and approving the final version of the manuscript.

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RN is an Associate Editor of The Journal of Pathology . No other conflicts of interest were declared. Invited commentary for K Heinze, TM Nazeran et al . Validated biomarker assays confirm that ARID1A loss is confounded with MMR deficiency, CD8 +  TIL infiltration, and provides no independent prognostic value in endometriosis‐associated ovarian carcinomas. J Pathol 2022; 256: 388–401.

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Condition tags

endometriosis

MeSH descriptors

Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid Carcinoma, Endometrioid

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