[Lani]

but I believe the answer is "they just don't know" Until fifteen months or so ago most articles stated that only 10% of her2neu+ breast cancers were ER+
Now most articles quote something around 45%.

In truth, until recently many countries and many hospitals within the US did not test her2 or did not test it well. I posted an article on how even ER and PR are not that well tested!

The good news is that in the HERA and No. American Herceptin adjuvant trials it appears on the initial reports that hormonally positive her2s (tested well because that was a requirement for an institution participating in the trial) did as well as hormonally negatives ie, their risk of recurrence in the period of the trial was halved by adding herceptin to chemo. I believe different antihormonal agents were used between US and Europe and even within Europe.

Noone knows the best antihormonal and whether they need to be given with herceptin to be effective or are effective after herceptin on their own.
(Sorry to throw this in, but they do not know yet)

The good news is we had some multiyear survivors with Stage IV on this site who were hormone positive (not the most scientific result, just anecdotal, but good to know)

As far as I know there are no breast cancers that always recur. Even triple negatives do not always. They are generally considered those with the worst prognosis. From what I read her2s were, before herceptin, the next worst, but they did not separate them by ER+ and ER-.

An abstract from a conference almost a year ago may hold the key to this, but as far as I can determine it was never published in full:

Oral Presentation

Molecular distinctions among ERBB2-overexpressing breast cancers
SS Jeffrey
Stanford University, Stanford, California, USA

from The Third International Symposium on the Molecular Biology of Breast Cancer
Molde, Norway. 22–26 June 2005

Breast Cancer Research 2005, 7(Suppl 2):S.22 doi:10.1186/bcr1065

Published

17 June 2005




HER2 or c-ERBB2/neu is a member of the epidermal growth factor receptor (EGFR) family and encodes a tyrosine kinase receptor. Overexpression of HER2 protein is generally attributable to gene amplification. HER2 is overexpressed in 20–30% of primary invasive breast carcinomas and in a greater proportion of in situ breast cancers. Invasive breast cancers that overexpress HER2 are generally higher stage, show lymph node positivity, and have higher S-phase. Moreover, they are often associated with poor prognosis, particularly in node-positive patients.

Microarray studies have subdivided breast cancers into several subtypes. HER2-overexpressing ER-negative tumors are generally classified within a single subtype denoted ERBB2-overexpressing. However, ER-positive HER2-overexpressing tumors are usually intermixed with other ER-positive tumors that do not show HER2 overexpression.

Our recent population-based study evaluating HER2 overexpression and hormone receptor status has unexpectedly found that the majority of HER2-overexpressing tumors are hormone receptor-positive and are more common than HER2-overexpressing ER-negative breast cancers. This implies that the ERBB2-overexpressing molecular subtype, which is associated with ER-negative status, only includes a minority of HER2-overexpressing tumors. We therefore studied gene expression patterns of HER2-overexpressing breast cancers and found several tumor subtypes with distinctive molecular signatures. These ERBB2-overexpressing subtypes spanned the range of hormone receptor status and highlighted different biological characteristics. Since the clinical course varies among patients with HER2-positive tumors, as does their response to targeted therapy, differences in global gene expression among HER2-overexpressing tumors could be important in distinguishing patients for the design and delivery of individualized targeted therapies.

Am sure many on this board would be interested in the full text of this!

Lani