variation of the mutation between ER+ and ER- in Her2+

fullofbeans · 02-21-2012, 04:17 PM

Significant mutation variation between the 2 groups:

http://www.biomedcentral.com/1471-2407/10/539/table/T1

JennyB · 02-21-2012, 11:54 PM

Full of beans,

I'm sorry but I do not understand that one bit - what does it mean??

Jenny

Hopeful · 02-22-2012, 07:39 AM

Here is a link to the paper from which the table in the above link was taken: http://www.biomedcentral.com/1471-2407/10/539

The researchers were trying to determine what the differences were between hormone positive Her2+ bc and hormone negative Her2+ bc. It appears there are a wealth of differences at the genetic level.

This is the take away for me:

"Upregulated ESR1, GATA3, ERBB4, TFF1 and TFF3 gene expression was associated with ER+ ERBB2-amplified tumors. These genes are typically associated with the luminal subtype, suggesting that the ER+ ERBB2-amplified tumors could be a branch of the luminal tumors and could share the same progenitor."

Luminal tumors (ER+ Her2-) are normally lower grade, slower growing tumors with a good prognosis that respond to endocrine therapy. Maybe the low response to endocrine therapy sets the Her2+'s apart?

Hopeful

KristinSchwick · 02-22-2012, 10:36 AM

My take away from this..... ER+, Her-2+ cancers are a genetically distinct subset from ER-, Her-2+ cancers. What does this mean to us patients; ER+ cancers will behave differently than ER- cancers AND they won't necessarily respond to the same cocktail of chemo. So take that as either positive or negative.

Hopeful · 02-22-2012, 10:45 AM

I think it also means that a "one size fits all" approach to Her2+ bc treatment is not the way to go.

Hopeful

fullofbeans · 03-05-2012, 07:59 AM

Sorry for the delay in replying yes indeed I agree with all the former comments. the hormonal status indicates a difference in the co-mutation (beside Her2+) of the two groups.

Indeed Hopeful is right that this variation should indicates that different approaches apply when the aim of the treatment is to block over express receptors. It seems that generally for ER neg one the embryo-genesis process is swith on via the Wnt pathway. Off course, things are still not clear cut just like they have now discovered that the her2+ can be p95Her2 (not responding to herceptin) but responding to TK..