HIV Drug Shows Efficacy In Treating Mouse Models Of HER2+ Breast Cancer
 

The HIV protease inhibitor, Nelfinavir, can be used to treat HER2-positive breast cancer in the same capacity and dosage regimen that it is used to treat HIV, according to a study published October 5 in the Journal of the National Cancer Institute. Breast cancer is one of the most common causes of cancer deaths in the U.S. with approximately 39,520 women succumbing to the disease in 2011...

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Re: HIV Drug Shows Efficacy In Treating Mouse Models Of HER2+ Breast Cancer
 

This is exciting? nother option to trial and already known drug.

Re: HIV Drug Shows Efficacy In Treating Mouse Models Of HER2+ Breast Cancer
 

Sounds like a personalized medicine for me! Just posted this abstract on the same link that was re-posted in the Her2 Forum:

Sure is a good news for us Her2 gals. Did some digging and found the below 2010 abstract:

Breast Cancer Res. 2010;12(4):R45. Epub 2010 Jul 1.
Tamoxifen enhances the cytotoxic effects of nelfinavir in breast cancer cells.

Brüning A, Friese K, Burges A, Mylonas I.
Source

Department of Obstetrics and Gynaecology, Campus Innenstadt, Ludwig-Maximilians-University Munich, 11 Maistrasse, Munich 80337, Germany. ansgar.bruening@med.uni-muenchen.de

Abstract

INTRODUCTION:

The HIV protease inhibitor nelfinavir is currently under investigation as a new anti-cancer drug. Several studies have shown that nelfinavir induces cell cycle arrest, endoplasmic reticulum stress, autophagy, and apoptosis in cancer cells. In the present article, the effect of nelfinavir on human breast cancer cells is examined and potential combination treatments are investigated.
METHODS:

The effects of nelfinavir and tamoxifen on the human breast cancer cell lines MCF7, T47 D, MDA-MB-453, and MDA-MB-435 were tested by analysing their influence on cell viability (via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay), apoptosis (annexin binding, poly(ADP-ribose) polymerase cleavage), autophagy (autophagy marker light chain 3B expression), endoplasmic reticulum stress (binding protein and activating transcription factor 3 expression), and the occurrence of oxidative stress (intracellular glutathione level).
RESULTS:

Nelfinavir induced apoptosis in all four breast cancer cell lines tested, although the extent of autophagy and endoplasmic reticulum stress varied among the cell lines. The concentration of nelfinavir needed for an efficient induction of apoptosis in breast cancer cells could be reduced from 15 μg/ml to 6 μg/ml when combined with tamoxifen. At a concentration of 6 μg/ml, tamoxifen substantially enhanced the endoplasmic reticulum stress reaction in those cell lines that responded to nelfinavir with binding protein (BiP) upregulation (MCF7, T47D), and enhanced autophagy in cell lines that responded to nelfinavir treatment with autophagy marker light chain 3B upregulation (MDA-MB-453). Although tamoxifen has been described to be able to induce oxidative stress at concentrations similar to those applied in this study (6 μg/ml), we observed that nelfinavir but not tamoxifen reduced the intracellular glutathione level of breast cancer cells within hours of application by up to 32%, suggesting the induction of oxidative stress was an early event and an additional cause of the apoptosis induced by nelfinavir.
CONCLUSIONS:

The results demonstrate that nelfinavir may be an effective drug against breast cancer and could be combined with tamoxifen to enhance its efficacy against breast cancer cells. Moreover, the cytotoxic effect of a tamoxifen and nelfinavir combination was independent of the oestrogen receptor status of the analysed breast cancer cells, suggesting a potential benefit of a combination of these two drugs even in patients with no hormone-responsive tumours. We therefore recommend that clinical studies on nelfinavir with breast cancer patients should include this drug combination to analyse the therapeutic efficacy as well as the safety and tolerability of this potential treatment option.