Figure 2.

The revised dualistic model in the pathogenesis of ovarian epithelial cancer. Type I carcinomas comprise low-grade serous, clear cell, endometrioid, and mucinous carcinomas. Seromucinous carcinomas and malignant Brenner tumors are rare and not shown. Type II carcinomas are largely composed of high-grade serous carcinomas. Carcinosarcoma and undifferentiated carcinoma are relatively uncommon and not illustrated. The areas in individual histotypes reflect their relative prevalence. The inner circle indicates the likely cell of origin of the different type I and type II neoplasms. The origin of mucinous carcinomas is not well established and is discussed in the text. The molecular pathway alterations that characterize each tumor subtype are summarized in the square boxes. Some of the pathway abnormalities are shared by some tumor types and they are shown in two-color fill in boxes. ARID1A, AT-rich interaction domain 1A; BRAF, B-Raf proto-oncogene, serine/threonine kinase; CCNE1, cyclin E1; ERRB2, estrogen-related receptor β2; HR DDR, homologous recombination-mediated DNA damage repair; KRAS, Kirsten rat sarcoma viral oncogene homolog; MEK, mitogen-activated protein (MAP) extracellular signal-related kinase (ERK) kinase; MMR, DNA mismatch repair; NF1, nuclear factor 1; PI3K, phosphatidylinositol 3-kinase; PTEN, phosphatase and tensin homolog; Rb, retinoblastoma protein.