(2012) Endometrioid adenocarcinoma of the ovary arising in atypical endometriosis

 Brief Communication/open access

Discussion
Malignant transformation of endometriosis is
rare but occurs in 0.7%, according to the data
of Nishida et al [2]. They found 1 case of ovarian
malignancy of the 147 cases of ovarian
endometriosis. On the other hand, Stern et al
[8] showed that the incidence of endometriosis
was 5% of ovarian malignancies associated
with ovarian endometriosis. The most common
malignancies arising in endometriosis of the
ovary is endometrioid adenocarcinoma and
clear cell adenocarcinoma. According to
Yoshikawa et al [3], malignancies in endometriosis
are clear cell (39.2%), endometrioid
(21.2%), serous (3.3%), and mucinous type
(3.0%).
In endometrioid adenocarcinoma, the
frequency of endometriosis is reported to be
3/22, 14% [4], 11/42, 26% [5], 9/23 39% [6],
and 3/7, 43% [7]. In the present study, the incidence
was 6/15 (40%).
The ovarian endometriosis is classified into
typical and atypical endometriosis based on
the cellular atypia. The atypical endometriosis
has a close association with ovarian epithelial
malignancies [9]. Ogawa et al [7] reported that
endometriosis associated with ovarian malignancies
was typical endometriosis in 35 cases
and atypical endometriosis in 29 cases. In the
present 6 cases, all the 6 cases were of atypical
endometriosis, suggesting that atypical
endometriosis is closely associated with the
development of endometrioid adenocarcinoma.
In the present study, gradual merges
between atypical endometriosis and carcinoma
cells were recognized, suggesting that the atypical
endometriosis develop into endometrioid
carcinoma after initiation and promotion. The
author speculates that an endometrial cyst
develops in the ovary. Its epithelium undergoes
initiation, thus giving rise to atypical endometriosis
consisting of dysplastic or intraepithelial
neoplastic epithelium. The atypical epithelium
ultimately leads to endometrioid adenocarcinoma
showing an unilocular cyst or multilocular
cyst with foci of atypical endometriosis.
The pathogenesis of endometriosis-associated
ovarian malignancies is unknown. Recent studies
have suggested the role of PTEN and hepatocyte
nuclear factor-1β [10, 11]. P53, bcl-2,
cyclin D-1, c-erbB2, and chromosomal genetic
alterations may play a role in the development
of ovarial carcinomas from endometriosis [12].
In summary, the present findings suggest that
atypical endometriosis transforms into endometrioid
carcinoma.