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« Back to Contents OVARIAN CANCER

LiFE re

Literature for ENYGO

Pathology/pathogenesis of malignant ovarian tumours

Editor Dogan Vatansever King et al. reviewed animal models on endometriosis. The evidence
shows that endometriosis is a precursor of clear cell and endometri-
Descriptive summary oid ovarian cancer. They describe various models that can be used
to study the malignant transformation of endometriosis to epithelial
Original Research ovarian cancer.

Hong et al. demonstrated that transfer of L1-CAM-specific CE7R+T Morin et al. also reviewed the animal models of epithelial ovarian
cells may offer a novel immunotherapy strategy for advanced ovari- cancer (EOC). The mouse models generated were based on the belief
an cancer. Recent clinical trials demonstrated that chimeric antigen that the ovarian surface epithelium was the cell origin of disease
receptor (CAR)-redirected T cells have a therapeutic role in haemato- and may need to be re-evaluated as more recent evidence suggest
logical cancers, and there are emerging studies for a similar effect in that, rather, the fallopian tube epithelium may be the origin of EOC.
solid cancers. They showed that L1-CAM, an adhesion molecule, is They examined the mouse models of both and summarise the data
highly overexpressed in ovarian cancer cell lines and primary ovarian that led to this paradigm shift.
cancer tissue specimens. They genetically modified human memo-
ry-derived T cells to express an anti-L1-CAM CAR (CE7R) and found
that CE7R+T cells are able to target primary ovarian cancer cells.

Du et al. reported the synergistic effect of c-Met and PARP inhibi-
tors. Please see the report from S. Giovannoni on “Hereditary ovari-
an cancer (BRCA1/2 mutation, genetic counselling, management).”

Strickland et al. reported significantly higher predicted neo-antigens
in BRCA1/2-mutated tumours compared to tumours without muta-
tion. Hypermutated lesions such as melanomas and lung carcinomas
harbour more tumour-specific neo-antigens that cause recruitment
of increased number of tumour-infiltrating lymphocytes (TILs) coun-
terbalanced by overexpression of immune checkpoints such as PD-1
or PD-L1. In this study, BRCA1/2-mutated high-grade serous ovarian
cancers (HGSOCs) exhibited a higher mutational load and increased
number of TILs and PD-1/PD-L1 expression. HR proficient HGSOCs
with low number of TILs have a poor prognosis and BRCA1/2-mutated
tumours with high number of TILs have a good prognosis. The results
also suggest that BRCA1/2-mutated HGSOCs may be more sensitive to
PD1/PD-L1 inhibitors compared to HR-proficient HGSOCs.

Reviews

Perets and Drapkin reported evidence of the tubal origin of ovarian
cancer in this review article. They also summarised different exper-
imental model systems (ex vivo, cell line, genetically engineered
mouse models, and patient-derived tumour xenograft models).

Bregar et al. presented preclinical data that support the role of phos-
phatidyl-inositol-3-kinase (PI3K) pathway in ovarian, endometrial, and
cervical cancers. Despite the differences among these cancer types,
they share activation of the PI3K pathway as a common signature.
They reported that up to 70 % of ovarian cancers show alterations in
the PI3K pathway and summarised the preclinical and clinical data.

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International Journal of Gynecological Cancer, Volume 26, Supplement #1 Page 12