Abstract:
:Ovarian cancer (OVAC) remains the most lethal gynecological malignancy; it is ranked fifth among the most common types of cancer that affect women worldwide. Several aspects of the disease, including molecular pathogenesis, epidemiology, histological subtypes, poor prognosis at early stages due to the absence of specific signs and symptoms, and curative treatments in the advanced stages are all responsible for the poor survival rate, which is evaluated to be at 5 years once the cancer is diagnosed and treatment begins. A better understanding of the pathogenesis of ovarian cancer is therefore crucial, even though unexplored pathways, in order to improve the prognosis of patients with OVAC and to develop novel therapeutic approaches. Accordingly, the tumor microenvironment, defined as the combination of proteins produced by all tumor cells and by non-cancerous cells or the stroma, and composed of several cells, including those from the immune, inflammatory and adipose systems, as well as the mesenchymal stem, endothelial and fibroblasts cells, has recently attracted attention. Of particular interest are fibroblasts, which can be activated into cancer-associated fibroblast (CAFs) to become a potent supporter of carcinogenesis, promoting the initiation of epithelial tumor formation, tumor growth, angiogenesis and metastasis, as well as therapeutic resistance and immunosuppression. Thus, the targeting of CAFs for early diagnosis and effective therapy warrants our attention. In this review, we discuss the mechanisms through which CAFs may affect the structure, composition and microenvironment of the ovarian tumor. We also aim to highlight important aspects of OVAC pathobiology involving CAFs, in an attempt to provide insight into novel diagnostic windows and provide new therapeutic perspectives.
journal_name
Oncol Lettjournal_title
Oncology lettersauthors
Sun W,Fu Sdoi
10.3892/ol.2019.10587subject
Has Abstractpub_date
2019-09-01 00:00:00pages
2173-2178issue
3eissn
1792-1074issn
1792-1082pii
OL-0-0-10587journal_volume
18pub_type
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