Question about EGFR

[michele u]

I'm getting my tumor checked for PTEN and they are going to check EGFR also. Does anyone know alot about this biomarker? I think I want the PTEN to positive right? What about the EGFR? do i want that or not want that? Sometimes i get confused. The way i understand it is that if i do have EGFR then Lapatinib might work for me if my cancer comes back? Maybe someone can shed light on this

[Gina]

is not a good thing...smile..., just so you know.., I have it and I, too, would LOVE to learn more about it.

Please let us know your serum her-2 marker as soon as you find out. Also, if you go back and read the pathology report of your original tumor closely, it may already say whether or not the tumor was positive for EGFR. Just a thought.

I don't know when you are getting these markers done, but for interesting comparisons, you might also try to see where your CA 27/29 is at about the same time.

Thanks for finding all of this stuff out for us. It is really helpful. Many of us in the Chat room tonight were very grateful for the contact information.

Take care,
Gina

[al from Canada]

Michelle,

Checkout the final link I sent lani on PI3K inhibitors, your answer may lie there. It is a webcast from SABCS

http://209.196.53.174/2004/player/ms3_02.html

Al

[al from Canada]

http://clincancerres.aacrjournals.or.../full/10/2/428

A

[michele u]

Al,

thanks, i went through both of these studies. It looks like the PTEN is pretty straight forward. You want that to be positive, then the Herceptin has a better c hance of working. The EGFR i not as straiaght forward. The don't know really what to do with that one. There are alot of EGFR inhibitors, so if you have mets then these might work for you. But the studies are not conclusive. So i guess i want that one to be negative?

[al from Canada]

Hi Michelle,
I happen to disagree, The most untreatable of all the breast cancers is the triple negative group. Recent data (which I posted earlier) suggests that being HER2 +++ is a better prognostic indicator (because of herceptin), than the more common ER+ cancers.

If you are EGFR+ and HER2+ your treatment options have improved. You now have a choice of lapatinib or herceptin + iressa or herceprtin + tarceva or lapatinib + herceptin or herceptin + many others in clinical trials.

My understanding of one piece of this complicated puzzel is; if you are hER2+ and respond to herceptin, eventually the cancer will find a way to by-pass the her2 mechanism through another pathway. If we know one of those pathways is EGFR, we can block it. We also know that the result of blocking 2 pathways is bettr than blocking either one or the other separately. Another example of this is herceptin + arimidex or herceptin + faslodex. Another pathway that we can block is VEGF through avastin.

The whole theory behind targetted therapies is testing for active pathways and developing drugs that block those pathways.

I hope this helps,
Al

[Julie2]

Isn't EGFR nothing but her1?

Julie

[al from Canada]

Julie,
yes it is

Al

[Joe]

EGFR constitutes the entire HER Family. For more info go to:


http://www.egfr-info.com/

Regards
Joe

[al from Canada]

for the most part when studies refer to EGFR they refer to HER1; specifically to Michelle's case, she has already been tested for HER2 so when her oncs test for EGFR, I assume they are testing for HER1.

Any clarification from Michelle?

Regards,
Al

[al from Canada]

More info on this Michelle. This is the drug Linda will ad to her regime in 2 weeks for the reasons stated in the article........Al

Induction of remission in a patient with metastatic breast cancer refractory to trastuzumab and chemotherapy following treatment with gefitinib ('Iressa', ZD1839).
Anti-Cancer Drugs. 15(3):235-238, March 2004.
Schneeweiss, Andreas a; Kolay, Sema a; Aulmann, Sebastian b; von Minckwitz, Gunter c; Torode, Julie d; Koehler, Maria e; Bastert, Gunther a


Abstract:
Despite new therapies and several treatment options, metastatic breast cancer (MBC) remains incurable. One reason for the low median survival rate may be intense cross-talk between growth factor receptors such as the epidermal growth factor receptor (EGFR/HER1) and the HER2 growth factor receptor. This report describes the case history of a patient with MBC whose disease had progressed despite surgery, radiotherapy and four different chemotherapy regimens, including trastuzumab (a monoclonal antibody that specifically blocks HER2) combined with docetaxel. However, treatment with 500 mg/day gefitinib ('Iressa', ZD1839), an EGFR tyrosine kinase inhibitor, and trastuzumab (2 mg/kg/week) caused a rapid and sustained regression of breast cancer metastases in skin and lymph nodes. Thus, for patients with MBC whose tumors co-express EGFR and HER2, gefitinib in combination with trastuzumab may prevent receptor cross-talk, improving the outcome of MBC.

(C) 2004 Lippincott Williams & Wilkins, Inc.