Effects of prolactin or growth hormone on growth of carcinogen-induced mammary tumors of adreno-ovariectomized rats

1970 ◽  
Vol 6 (3) ◽  
pp. 488-495 ◽  
Author(s):  
Hiroshi Nagasawa ◽  
Reiko Yanai
Keyword(s):  
Growth Hormone ◽  
Mammary Tumors ◽  
Ovariectomized Rats

scholarly journals Activation of the prolactin receptor but not the growth hormone receptor is important for induction of mammary tumors in transgenic mice.

1997 ◽  
Vol 100 (11) ◽  
pp. 2744-2751 ◽  
Author(s):  
H Wennbo ◽  
M Gebre-Medhin ◽  
A Gritli-Linde ◽  
C Ohlsson ◽  
O G Isaksson ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Transgenic Mice ◽  
Hormone Receptor ◽  
Growth Hormone Receptor ◽  
Prolactin Receptor ◽  
Mammary Tumors

scholarly journals Mammary Tumors Growing in the Absence of Growth Hormone Are More Sensitive to Doxorubicin Than Wild-Type Tumors

Endocrinology ◽  
2021 ◽  
Vol 162 (4) ◽  
Author(s):  
Daniel D Lantvit ◽  
Christopher J Unterberger ◽  
Michelle Lazar ◽  
Paige D Arneson ◽  
Colin A Longhurst ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Hormone ◽  
Endogenous Growth ◽  
Mammary Tumors ◽  
Wild Type ◽  
Sprague Dawley ◽  
Doxorubicin Treatment ◽  
Sprague Dawley Rats ◽  
Almost All ◽  
Treat Breast Cancer

Abstract Previously, we reported that N-methyl-N-nitrosourea (MNU)-induced mammary tumors could be established in mutant spontaneous dwarf rats (SDRs), which lack endogenous growth hormone (GH) by supplementing with exogenous GH, and almost all such tumors regressed upon GH withdrawal. When the highly inbred SDR line was outcrossed to wild-type (WT) Sprague-Dawley rats, MNU-induced mammary tumors could still be established in resulting outbred SDRs by supplementing with exogenous GH. However, unlike tumors in inbred SDRs, 65% of mammary tumors established in outbred SDRs continued growth after GH withdrawal. We further tested whether these tumors were more sensitive to doxorubicin than their WT counterparts. To accomplish this, MNU-induced mammary tumors were established in WT rats and in SDRs supplemented with exogenous GH. Once mammary tumors reached 1 cm3 in size, exogenous GH was withdrawn from SDRs, and the subset that harbored tumors that continued or resumed growth in the absence of GH were selected for doxorubicin treatment. Doxorubicin was then administered in 6 injections over 2 weeks at 2.5 mg/kg or 1.25 mg/kg for both the WT and SDR groups. The SDR mammary tumors that had been growing in the absence of GH regressed at both doxorubicin doses while WT tumors continued to grow robustly. The regression of SDR mammary tumors treated with 1.25 mg/kg doxorubicin was accompanied by reduced proliferation and dramatically higher apoptosis relative to the WT mammary tumors treated with 1.25 mg/kg doxorubicin. These data suggest that downregulating GH signaling may decrease the doxorubicin dose necessary to effectively treat breast cancer.

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