Since
our proposal of a dualistic model of epithelial ovarian carcinogenesis
more than a decade ago, a large number of molecular and histopathologic
studies were published that have provided important insights into the
origin and molecular pathogenesis of this disease. This has required
that the original model be revised and expanded to incorporate these
findings. The new model divides type I tumors into three groups:
i) endometriosis-related tumors that include endometrioid, clear cell,
and seromucinous carcinomas; ii) low-grade serous carcinomas; and iii)
mucinous carcinomas and malignant Brenner tumors. As in the previous
model, type II tumors are composed, for the most part, of high-grade
serous carcinomas that can be further subdivided into morphologic and
molecular subtypes. Type I tumors develop from benign extraovarian
lesions that implant on the ovary and which can subsequently undergo
malignant transformation, whereas many type II carcinomas develop from
intraepithelial carcinomas in the fallopian tube and, as a result,
disseminate as carcinomas that involve the ovary and extraovarian sites,
which probably accounts for their clinically aggressive behavior. The
new molecular genetic data, especially those derived from
next-generation sequencing, further underline the heterogeneity of
ovarian cancer and identify actionable mutations. The dualistic model
highlights these differences between type I and type II tumors which, it
can be argued, describe entirely different groups of diseases.
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