Acta Scientific Cancer Biology

Mini ReviewVolume 2 Issue 1

Inadequate Pancreatic GABA Controls that Explain Cancer Metabolism

Maurice Israel*

CNRS, Director (Retired), Institut Alfred Fessard, Bures sur Yvette, France

*Corresponding Author: Maurice Israel, CNRS, Director (Retired), Institut Alfred Fessard, Bures sur Yvette, France.

Received: January 21, 2017; Published: January 29, 2018

Citation: Maurice Israel. “Inadequate Pancreatic GABA Controls that Explain Cancer Metabolism”. Acta Scientific Cancer Biology 2.1 (2018).


  In cancer, mitotic tumor cells display an active anabolic metabolism associated to a geometric increase of their number, while differentiated cells of the body, liver, adipocytes and other tissues, provide the necessary nutrients for building up the tumor, as if differentiated cells responded preferentially to catabolic signals for feeding the tumor. In fact it is slightly more complicated, since tumor cells gain such a metabolic advantage over other cells, by rewiring their metabolic pathways into a new hybrid mode, resulting from their dual sensitivity to both anabolic and catabolic signals, while differentiated cells resistant to anabolic hormones respond preferentially to catabolic ones. Stem cells committed to repair a tissue, display this dual sensitivity and become the dominant population, forming a tumor in the tissue they should have repaired.

  The phosphorylation of key enzymes controlling anabolic or catabolic actions is indeed compatible with this view, but where is the starter for such a process? We came to the conclusion that an alteration of GABA controls in the endocrine pancreas, would explain the metabolic rewiring observed in cancer, with the hope that an early correction with adequate compounds will prevent or heal the disease.

Keywords: Cancer Metabolism; GABA; Glucagon; Insulin; PKC; Stem Cells

Copyright: © 2018 Maurice Israel. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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