metformin (common anti diabetes drug)inhibits breast cancer cell growth, colony form-
 

ation, and induces cell cycle arrest (so they can't multiply)

I have previously posted that metformin decreases her2 protein levels by 85%(put metformin and Lani into the Search on the yellow line above if you want to find that thread)

All work done in cancer cell lines, not in intact people so far:

Cell Cycle. 2009 Mar 26;8(6). [Epub ahead of print]Links

Metformin inhibits breast cancer cell growth, colony formation and induces cell cycle arrest in vitro.

Alimova IN, Liu B, Fan Z, Edgerton SM, Dillon T, Lind SE, Thor AD.
Department of Pathology, University of Colorado Denver School of Medicine, Aurora, Colorado USA; Department of Carcinogenesis and Oncogerontology, Prof. N.N. Petrov Research Institute of Oncology, St. Petersburg, Russia.
The anti-diabetic drug metformin reduces human cancer incidence and improves the survival of cancer patients, including those with breast cancer. We studied the activity of metformin against diverse molecular subtypes of breast cancer cell lines in vitro. Metformin showed biological activity against all estrogen receptor (ER) positive and negative, erbB2 normal and abnormal breast cancer cell lines tested. It inhibited cellular proliferation, reduced colony formation and caused partial cell cycle arrest at the G(1) checkpoint. Metformin did not induce apoptosis (as measured by DNA fragmentation and PARP cleavage) in luminal A, B or erbB2 subtype breast cancer cell lines. At the molecular level, metformin treatment was associated with a reduction of cyclin D1 and E2F1 expression with no changes in p27(kip1) or p21(waf1). It inhibited mitogen activated protein kinase (MAPK) and Akt activity, as well as the mammalian target of rapamycin (mTOR) in both ER positive and negative, erbB2-overexpressing and erbB2-normal expressing breast cancer cells. In erbB2-overexpressing breast cancer cell lines, metformin reduced erbB2 expression at higher concentrations, and at lower concentrations within the therapeutic range, it inhibited erbB2 tyrosine kinase activity evidenced by a reduction of phosphorylated erbB2 (P-erbB2) at both auto- and Src- phosphorylation sites. These data suggest that metformin may have potential therapeutic utility against ER positive and negative, erbB2-overexpressing and erbB2-normal expressing breast cancer cells.
PMID: 19221498

Lani,

Do you think they will do more studies with this drug? Very interesting article.

Amelia

Lani, Very Intriguing article. How does eone go about knowing if they are erb2. I have looked over all of my path reports and none of them show that. I am surrently taking a drug called Naltrexone (low dose) that also causes cancer cell aptosis. It is given to people who are coming off of opiate drugs, as well as, many other things. I am going to research your drug further. Thank you so much for posting it. I always love to hear what you have found. Love, Vickie

reply
 

yes, the article suggested a trial

erbb2 is the same as her2

Since metformin is a drug used to treat a disease (diabetes) and is by prescription only (which means it has side effects and shouldn't be used by those without that disease unless for another disease for which it is effective and for which it gives more benefit than the risk of adverse side effects) this is something to go over with your doctor.

If you are very overweight and have been borderline diabetic and your doctor read this and discussed the possible side effects with you... it is still not clear that what happens in a petri dish happens in people. Sometimes the effect of a drug is nonexistant or THE OPPOSITE in whole humans and sometimes the effect is opposite depending what dose is taken (how do we know the correct dose for the effect and if that dose is safe?)

Trial may take a while as no new blockbuster drug still under patient is involved.

As always..thanks for the info.

connections
 

Thanks for all the interesting discussions, Lani. This one is really intriguing.