Prolactin is a tumor promoter in rat liver

Arthur R. Buckley; Charles W. Putnam; Diane H. Russell

doi:10.1016/0024-3205(85)90616-2

Prolactin is a tumor promoter in rat liver

Arthur R. Buckley, Charles W. Putnam, Diane H. Russell

Surgery

Research output: Contribution to journal › Article › peer-review

61 Scopus citations

Abstract

Since prolactin, like the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate, induces ornithine decarboxylase and plasminogen activator activities, biochemical markers of a trophic response, this hormone might likewise promote neoplasia. To test this theory, rats were initiated with a hepatocarcinogen followed by six weeks of ovine prolactin. This regimen caused hepatomegaly and the development of enzyme-altered foci. Promotion with prolactin for 23 weeks further increased the numbers of enzyme-altered foci. We suggest that prolactin is an endogenous tumor promoter for chemically initiated cells.

Original language	English (US)
Pages (from-to)	2569-2575
Number of pages	7
Journal	Life Sciences
Volume	37
Issue number	26
DOIs	https://doi.org/10.1016/0024-3205(85)90616-2
State	Published - Dec 30 1985

ASJC Scopus subject areas

General Pharmacology, Toxicology and Pharmaceutics
General Biochemistry, Genetics and Molecular Biology

Access to Document

10.1016/0024-3205(85)90616-2

Cite this

@article{7b5d0176dc3d46f79b68f10c43671a2c,

title = "Prolactin is a tumor promoter in rat liver",

abstract = "Since prolactin, like the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate, induces ornithine decarboxylase and plasminogen activator activities, biochemical markers of a trophic response, this hormone might likewise promote neoplasia. To test this theory, rats were initiated with a hepatocarcinogen followed by six weeks of ovine prolactin. This regimen caused hepatomegaly and the development of enzyme-altered foci. Promotion with prolactin for 23 weeks further increased the numbers of enzyme-altered foci. We suggest that prolactin is an endogenous tumor promoter for chemically initiated cells.",

author = "Buckley, {Arthur R.} and Putnam, {Charles W.} and Russell, {Diane H.}",

note = "Funding Information: A portion of this study was presented at the UCLA Symposium on the Biochemical and Molecular Epidemiology of Cancer, Steamboat Springs, Colorado, April 7-14, 1985. This work was supported by a grant from VA Central Office to CWP and by USPHS ES-03587 to DHR.",

year = "1985",

month = dec,

day = "30",

doi = "10.1016/0024-3205(85)90616-2",

language = "English (US)",

volume = "37",

pages = "2569--2575",

journal = "Life Sciences",

issn = "0024-3205",

publisher = "Elsevier Inc.",

number = "26",

}

TY - JOUR

T1 - Prolactin is a tumor promoter in rat liver

AU - Buckley, Arthur R.

AU - Putnam, Charles W.

AU - Russell, Diane H.

N1 - Funding Information: A portion of this study was presented at the UCLA Symposium on the Biochemical and Molecular Epidemiology of Cancer, Steamboat Springs, Colorado, April 7-14, 1985. This work was supported by a grant from VA Central Office to CWP and by USPHS ES-03587 to DHR.

PY - 1985/12/30

Y1 - 1985/12/30

N2 - Since prolactin, like the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate, induces ornithine decarboxylase and plasminogen activator activities, biochemical markers of a trophic response, this hormone might likewise promote neoplasia. To test this theory, rats were initiated with a hepatocarcinogen followed by six weeks of ovine prolactin. This regimen caused hepatomegaly and the development of enzyme-altered foci. Promotion with prolactin for 23 weeks further increased the numbers of enzyme-altered foci. We suggest that prolactin is an endogenous tumor promoter for chemically initiated cells.

AB - Since prolactin, like the tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate, induces ornithine decarboxylase and plasminogen activator activities, biochemical markers of a trophic response, this hormone might likewise promote neoplasia. To test this theory, rats were initiated with a hepatocarcinogen followed by six weeks of ovine prolactin. This regimen caused hepatomegaly and the development of enzyme-altered foci. Promotion with prolactin for 23 weeks further increased the numbers of enzyme-altered foci. We suggest that prolactin is an endogenous tumor promoter for chemically initiated cells.

UR - http://www.scopus.com/inward/record.url?scp=0022353327&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022353327&partnerID=8YFLogxK

U2 - 10.1016/0024-3205(85)90616-2

DO - 10.1016/0024-3205(85)90616-2

M3 - Article

C2 - 2867449

AN - SCOPUS:0022353327

SN - 0024-3205

VL - 37

SP - 2569

EP - 2575

JO - Life Sciences

JF - Life Sciences

IS - 26

ER -

Prolactin is a tumor promoter in rat liver

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this