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12-18-2005, 11:32 AM

I too am diverting from other things I should be doing.

I have not done any specific reading on this subject but have seen numerous references to insulin derivatives featuring in Breast Cancer.

I attach the result of a search on the NCBI site which returned 1736 items to the term "breast cancer insulin".

http://www.ncbi.nlm.nih.gov/entrez/q...+breast+cancer

Here is one of the trials from the above that might suggest at my simplistic level of undestanding that insulin is along with many other factors at the heart of the issue.

The more one has time to read the more evident how complex, interlinking and interdependent it all is.

From recollection many health and nutrition writers suggest minimizing refined foods including sugar, as empty nutrition. Good nutrition is arguably a good base point to start from.

Thought provoking.

RB

http://www.ncbi.nlm.nih.gov/entrez/q...831&query_hl=5

1: J Mol Endocrinol. 2005 Dec;35(3):433-47. Related Articles, Links
Click here to read
Role of estrogen receptor (ER) {alpha} in insulin-like growth factor (IGF)-I-induced responses in MCF-7 breast cancer cells.

Zhang S, Li X, Burghardt R, Smith R 3rd, Safe SH.

Department of Veterinary Physiology and Pharmacology.

Insulin-like growth factor-I (IGF-I) is a mitogenic polypeptide that induces proliferation of MCF-7 breast cancer cells, and cotreatment with the phosphoinositide 3-kinase (PI3-K) inhibitor LY294002 and the antiestrogen ICI 182780 inhibits IGF-I-induced growth. The role of estrogen receptor alpha (ERalpha) in mediating responses induced by IGF-I was investigated in cells transfected with small inhibitory RNA for ERalpha (iERalpha). The results showed that IGF-I-dependent phosphorylation of Akt and mitogen-activated protein kinase, induction of G(1)-S-phase progression and enhanced expression of cyclin D1 and cyclin E were dependent on ERalpha. Moreover, these same IGF-I-induced responses were also inhibited by the antiestrogen ICI 182780 and this was in contrast to a previous report suggesting that ICI 182780 did not affect IGF-I-dependent activation of PI3-K or induction of cyclin D1 expression. ICI 182780 exhibits antimitogenic activity and iERalpha inhibits G(1)-S-phase progression and proliferation of MCF-7 cells treated with IGF-I, suggesting that the effects of the antiestrogen are primarily related to downregulation of ERalpha.

PMID: 16326831 [PubMed - in process]

12-18-2005, 11:32 AM	#3
Unregistered Guest Posts: n/a	I too am diverting from other things I should be doing. I have not done any specific reading on this subject but have seen numerous references to insulin derivatives featuring in Breast Cancer. I attach the result of a search on the NCBI site which returned 1736 items to the term "breast cancer insulin". http://www.ncbi.nlm.nih.gov/entrez/q...+breast+cancer Here is one of the trials from the above that might suggest at my simplistic level of undestanding that insulin is along with many other factors at the heart of the issue. The more one has time to read the more evident how complex, interlinking and interdependent it all is. From recollection many health and nutrition writers suggest minimizing refined foods including sugar, as empty nutrition. Good nutrition is arguably a good base point to start from. Thought provoking. RB http://www.ncbi.nlm.nih.gov/entrez/q...831&query_hl=5 1: J Mol Endocrinol. 2005 Dec;35(3):433-47. Related Articles, Links Click here to read Role of estrogen receptor (ER) {alpha} in insulin-like growth factor (IGF)-I-induced responses in MCF-7 breast cancer cells. Zhang S, Li X, Burghardt R, Smith R 3rd, Safe SH. Department of Veterinary Physiology and Pharmacology. Insulin-like growth factor-I (IGF-I) is a mitogenic polypeptide that induces proliferation of MCF-7 breast cancer cells, and cotreatment with the phosphoinositide 3-kinase (PI3-K) inhibitor LY294002 and the antiestrogen ICI 182780 inhibits IGF-I-induced growth. The role of estrogen receptor alpha (ERalpha) in mediating responses induced by IGF-I was investigated in cells transfected with small inhibitory RNA for ERalpha (iERalpha). The results showed that IGF-I-dependent phosphorylation of Akt and mitogen-activated protein kinase, induction of G(1)-S-phase progression and enhanced expression of cyclin D1 and cyclin E were dependent on ERalpha. Moreover, these same IGF-I-induced responses were also inhibited by the antiestrogen ICI 182780 and this was in contrast to a previous report suggesting that ICI 182780 did not affect IGF-I-dependent activation of PI3-K or induction of cyclin D1 expression. ICI 182780 exhibits antimitogenic activity and iERalpha inhibits G(1)-S-phase progression and proliferation of MCF-7 cells treated with IGF-I, suggesting that the effects of the antiestrogen are primarily related to downregulation of ERalpha. PMID: 16326831 [PubMed - in process]