Abstract

Like cancer cells during tumor development, placental cells need to invade their host’s tissues, escape its immune system and access its blood supply system in order to establish pregnancy.

Thus, studying the molecular circuits involved in the development of the placenta might provide insights into cancer. Moreover, such studies can lead to the development of innovative therapeutic approaches and lab tests in oncology as well as in gynecology and obstetrics. For example, research programs on angiogenic growth factors (vascular endothelial growth factors, placental growth factor, etc.) have led to the development of anti-angiogenic anti-cancer therapies and screening tests for preeclampsia.

Numerous epigenetic studies have led to the identification of diverse mechanisms involved in the regulation of the molecular circuits of cancer cells during their transformation. Among other epigenetic characteristics, the DNA methylation of these cells displays characteristic alterations: their DNA is globally hypomethylated and locally hypermethylated.

We hypothesized that DNA methylation of the placenta during its development might undergo modifications similar to those observed in tumors during their development. Conducting the first direct and genome-wide comparison of DNA methylation during placentogenesis and cancerogenesis, we identified in the placenta patterns of regulation previously described in solid tumors.These patterns of regulation may be reprogramming marks allowing tumors to use molecular circuits of the placenta in order to develop, spread and resist anti-cancer drugs.

This work, largely based on advanced bioinformatic methods, may allow the development of innovative approaches to the management of drug resistance in oncology.

Author
Akpéli Nordor
Author
Akpéli Nordor
Category
Oncology
Publication type
Abstract
Year
2016
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