Within the six modules, the activation of cellular processes and complexes, such as alternative mRNA splicing, translation initiation, nucleosome remodeling and deacetylase (NuRD) complex, SWItch/Sucrose Non-Fermentable (SWI/SNF) superfamily-type complex, chromatin remodeling pathway, and mRNA metabolic processes, were significant to SCLC.
This review discusses the recent progress in understanding SWI/SNF alterations in ovarian cancer and specifically focuses on: (i) <i>ARID1A</i> mutation in endometriosis-associated clear cell and endometrioid histologic subtypes of ovarian cancer; (ii) <i>SMARCA4</i> mutation in small cell carcinoma of the ovary, hypercalcemic type; and (iii) amplification/upregulation of <i>CARM1</i>, a regulator of BAF155, in high-grade serous ovarian cancer.
<b>Purpose:</b> Small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) is a rare, aggressive ovarian cancer in young women that is universally driven by loss of the SWI/SNF ATPase subunits SMARCA4 and SMARCA2.
Atypical teratoid/rhabdoid tumors (AT/RT) and renal/extrarenal malignant rhabdoid tumors of childhood, epithelioid sarcoma and small cell carcinoma of the ovary, hypercalcemic type (SCCOHT) represent the most commonly recognized SWI/SNF-driven neoplasms.
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.