Abstract: High
grade serous ovarian cancer (HGSC), the most lethal and frequent type
of epithelial ovarian cancer (EOC), has poor long term prognosis due to a
combination of factors: late detection, great metastatic potential and
the capacity to develop resistance to available therapeutic drugs.
Furthermore, there has been considerable controversy concerning the
etiology of this malignancy. New studies, both clinical and molecular,
strongly suggest that HGSC originates not from the surface of the ovary,
but from the epithelial layer of the neighboring fallopian tube
fimbriae. In this paper we summarize data supporting the central role of
fallopian tube epithelium in the development of HGSC. Specifically, we
address cellular pathways and regulatory mechanisms which are modulated
in the process of transformation, but also genetic changes which
accumulate during disease progression. Similarities between fallopian
tube mucosa and the malignant tissue of HGSC warrant a closer analysis
of homeostatic mechanisms in healthy epithelium in order to elucidate
key steps in disease development. Finally, we highlight the importance
of the cancer stem cell (CSC) identification and understanding of its
niche regulation for improvement of therapeutic strategies.
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