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Postgrad Med. 2019 Sep 5:1-10. doi: 10.1080/00325481.2019.1657358. [Epub ahead of print]

Intersections and Clinical Translations of Diabetes Mellitus with Cancer Promotion, Progression and Prognosis.

Author information

1
Main Line Health System , Wynnewood , PA , USA.
2
University of Pennsylvania , Philadelphia , PA , USA.
3
Center for Spatial and Functional Genomics, Divisions of Human Genetics and Endocrinology, The Children's Hospital of Philadelphia , Philadelphia , PA , USA.
4
Montclair State University , Upper Montclair , NJ , USA.
5
Social Alchemy Ltd. Building Research Competency in the Developing World , Edgewater , NJ , USA.

Abstract

The association between cancer and dysglycemia has been well documented. It is underappreciated, however, that sustained dysglycemia could potentially be a catalyst toward a pro-cancer physiologic milieu and/or increase the burden of cancer. Hyperglycemia, hyperinsulinemia and energy metabolism at large impact a cascade of growth pathways, epi/genetic modifications, and mitochondrial changes that could feasibly link to tumor processes. Oxidative stress is a recurring motif in cell dysfunction: in diabetes, oxidative stress and reactive oxygen species (ROS) feature prominently in the damage and demise of pancreatic beta cells, as well as cell damage contributing to diabetes-related complications. Oxidative stress may be one intersection at which metabolic and oncogenic processes cross paths with deleterious results in the development of precancer, cancer, and cancer progression. This would augur for tight glucose control. Regrettably, some medical societies have recently relaxed hemoglobin A1c targets. A framework for the hyperglycemic state is presented that helps account and translate the full scope of effects of dysglycemia to ultimately improve clinical best practices.

KEYWORDS:

Type 2 diabetes; beta-cell–centric model; cancer; common origins of diabetes and its complications construct; egregious eleven; hyperglycemia

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