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Alcohol, Retinoic Acid, and Cancer

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Alcohol and Cancer

Abstract

The first observation potentially linking alcohol consumption and vitamin A deficiency was published over 70 years ago (Patek and Haig 1939). Since then, numerous studies have provided solid evidence that alcohol indeed interferes with vitamin A and its analogs, collectively termed retinoids, both in experimental models and in humans. In addition, many experimental and epidemiological studies demonstrated that such interferences might result in impaired tissue regeneration and cancer development. Furthermore, since vitamin A deficiency (or excess) increases the risk for a number of human cancers, and since alcohol impairs the body’s retinoid homeostasis, interactions between vitamin A and alcohol may represent central mechanisms by which alcohol induces multiorgan pathology and carcinogenesis.

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Abbreviations

ADH:

Alcohol dehydrogenase

ALD:

Alcoholic liver disease

AP-1:

Activating protein 1

APC:

Adenomatous polyposis coli

APL:

Promyelocytic leukemia

ATRA:

All-trans-RA

COX-2:

Cyclooxygenase-2

CRABP:

Cellular retinoic acid-binding protein

CRBP:

Cellular retinol-binding protein

ECS:

Embryonic stem cells

FABP:

Fatty acid binding protein

FFA:

Free fatty acid

HAT:

Histone acetylase

HDAC:

Histone deacetylase

HSC:

Hepatic stellate cells

LRAT:

Lecithin retinol acyltransferase

PPAR:

Peroxisome proliferator-activated receptor

RA:

Retinoic acid

RALDH:

Retinaldehyde dehydrogenase

RAR:

Retinoic acid receptors

RARE:

Retinoic acid response element

RBP4:

Retinol binding protein 4

RE:

Retinyl ester

REH:

Retinylester hydrolase

ROH:

Retinol

RXR:

Retinoid X receptors

SC:

Stem cells

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Radaeva, S. (2011). Alcohol, Retinoic Acid, and Cancer. In: Zakhari, S., Vasiliou, V., Guo, Q. (eds) Alcohol and Cancer. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-0040-0_7

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