Need help on quick question please!
 

Hello everyone,
I need to find info for a lady on the Komen site whose sister has just been dx with bone mets. Her initial tumour was her2+ but this one is triple negative. Does this definatly mean herceptin is no longer helpful for these mets and if so is there any other treatment anyone can suggest other than Zometa??
She's very scared right now so thank you anyone that can answer this for her.

her2+ breast cancer RARELY metastasizes as her2-
 

from what I have read, so retesting of both her primary and her met may be in order. Triple negative breast cancer is often EGFR (her1)+ (so Iressa or Tarceva may be of help) and recent evidence shows some are exquisitely sensitive to cisplatin (heard this at a bc conference at the end of June). It seems Tykerb has not been helpful for those with only EGFR+ but her2- breast cancer according to most papers.

Hope some of this helped!

Thank you Lani!
 

I'll pass on your thoughts to her as I know she'll be grateful for any idea's right now. I was surprised too at the change of her2 from + to - and really did'nt know what to suggest.
Thank you again from both of us:)

new agent (PPAR inhibitor, already in development for other diseases) for triple- bc
 

Research article
.
1, 1-Bis(3'-indolyl)-1-(p-biphenyl)methane inhibits basal-like breast cancer growth in athymic nude mice
Yunpeng Su , Kathryn Vanderlaag , Courtney Ireland , Janelle Ortiz , Henry Grage , Stephen Safe and Arthur Frankel

Breast Cancer Research 2007, 9:R56 doi:10.1186/bcr1761

Published 31 August 2007

Abstract (provisional)

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.


Introduction

1, 1-Bis (3'-indolyl)-1-(p-biphenyl) methane (CDIM9) has been identified as a new peroxisome proliferators-activated receptor gamma (PPARgamma) agonist that exhibits both receptor dependent and independent anti-tumor activities. CDIM9 has not been previously studied against basal-like breast cancer. Our goal of this study is to investigate the anti-basal-like breast tumor activity in vitro and in vivo of CDIM9.

Methods

The effects of CDIM9 on cell protein and DNA syntheses were determined in basal-like breast cancer MDA-MB231 and BT549 cells in vitro. Maximal tolerance dose (MTD) and dose-limited toxicity (DLT) were identified in BalB/c mice and the anti-tumor growth activities were assessed in MDA-MB231 basal-like breast tumor xenografts in athymic nude mice.

Results

CDIM9 showed selective cell cytotoxicity and anti-proliferation effects on basal-like breast cancer lines. In MDA-MB231 cell, CDIM9 induced caveolin-1 and p27 expression, which was significantly down regulated by co-treatment with the PPARgamma antagonist GW9662. Non-steroidal anti-inflammatory drug-activated gene (NAG-1) and activating transcription factor 3 (ATF3) were up regulated by CDIM9 through PPAR gamma-independent pathway. CDIM9 (i.p. 40 mg/kg daily for 35 days) inhibited the growth of s.c. MDA-MB231 tumor xenografts by 87%, and produced a corresponding decrease of proliferation index. Close to half of treated mice (46%) had complete durable remissions confirmed by histology. The growth of an established tumor was inhibited by CDIM9 treatment (i.p. 64 mg/kg daily for ten days) with a mean tumor growth inhibition of 67% compared to controls. CDIM9 induced increases in tumor caveolin-1 and p27 in vivo which may contribute to its anti-tumor activity in basal-like breast cancer.

Conclusions

CDIM9 showed potent anti-proliferative effects on basal-like breast cancer cell in tissue culture and dramatic growth inhibition in animal models at safe doses. These results warrant further development of this drug for therapy of basal-like breast cancer patients.