HER2 Support Group Forums - View Single Post - How best to treat hormone positive her2+ breast cancer seems to depend on PR status

Lani · 03-23-2006, 12:41 AM

There are.

For EGFR1 there are IRESSA and TARCEVA as well as Lapatinib (for EGFR1&2)--IRESSA's use has recently been curbed but Tarceva has approved uses I believe and Lapatinib will probably be submitted for FDA approval in the 4th quarter of 2006 or first quarter of 2007. They are
which are small molecule inhibitors of EGFR1. In addition there is ERBITUX ( a monoclonal antibody against EGFR1 which just got approved by the FDA this week for head and neck cancer) Not yet in/through clinical trials, but used in research are an irreversible EGFR inhibitor (EKB569) and pan-ERB inhibitors (canertinib which is irreversible and PKI166 which is reversible) and nother a monoclonal antibody against EGFR, Panitumumab.

Similarly, there are IGFR1 inhibitors used in research.(alpha IR3 is one I found in an article on the localization of IGF receptor in benign and malignant breast cancer cells).

I am uncertain what you mean by PgR--I have seen that used for progesterone receptor and have seen PDGFR as a receptor present on cells lining the new blood vessels formed in tumor directed angiogenesis.

I knew nothing about any of this until a few months ago.

All this information is available on the net.

I recommend an article by Carolyn Britten on Targeting ErbB receptor signaling: A pan-erbB approach to cancer. Mol Cancer Ther 2004:3 (10)
October 2004 as well as an article by Edith Perez previously cited by Robin P

It takes time for these agents to go through clinical trials and get FDA approval, luckily it seems less time for monoclonal antibodies as they are so targetted.

How many more?--It seems there are an infinite number of mutations possible to cause cancer and it often appears the number of pathways involved is TOO NUMEROUS TO COUNT

I think the biggest mistake is to simplify. There does not appear to be one cause of cancer, one way normal cells transform into cancer cells, one way cancer cells get resistant, or one way to fight cancer.

I am sure your frustration and exasperation are shared by all who post (and probably all who lurk) on this site.

Not everyone feels well enough to act on this frustration. But if they inspire others to turn their energies toward becoming activists/try to inspire a cancer researcher/ try to politicize their oncologist/write their congresspersons regarding FDA policies, etc. perhaps more of these targeted drugs will be more widely available sooner

03-23-2006, 12:41 AM	#3
Lani Senior Member Join Date: Mar 2006 Posts: 4,783	but there are! There are. For EGFR1 there are IRESSA and TARCEVA as well as Lapatinib (for EGFR1&2)--IRESSA's use has recently been curbed but Tarceva has approved uses I believe and Lapatinib will probably be submitted for FDA approval in the 4th quarter of 2006 or first quarter of 2007. They are which are small molecule inhibitors of EGFR1. In addition there is ERBITUX ( a monoclonal antibody against EGFR1 which just got approved by the FDA this week for head and neck cancer) Not yet in/through clinical trials, but used in research are an irreversible EGFR inhibitor (EKB569) and pan-ERB inhibitors (canertinib which is irreversible and PKI166 which is reversible) and nother a monoclonal antibody against EGFR, Panitumumab. Similarly, there are IGFR1 inhibitors used in research.(alpha IR3 is one I found in an article on the localization of IGF receptor in benign and malignant breast cancer cells). I am uncertain what you mean by PgR--I have seen that used for progesterone receptor and have seen PDGFR as a receptor present on cells lining the new blood vessels formed in tumor directed angiogenesis. I knew nothing about any of this until a few months ago. All this information is available on the net. I recommend an article by Carolyn Britten on Targeting ErbB receptor signaling: A pan-erbB approach to cancer. Mol Cancer Ther 2004:3 (10) October 2004 as well as an article by Edith Perez previously cited by Robin P It takes time for these agents to go through clinical trials and get FDA approval, luckily it seems less time for monoclonal antibodies as they are so targetted. How many more?--It seems there are an infinite number of mutations possible to cause cancer and it often appears the number of pathways involved is TOO NUMEROUS TO COUNT I think the biggest mistake is to simplify. There does not appear to be one cause of cancer, one way normal cells transform into cancer cells, one way cancer cells get resistant, or one way to fight cancer. I am sure your frustration and exasperation are shared by all who post (and probably all who lurk) on this site. Not everyone feels well enough to act on this frustration. But if they inspire others to turn their energies toward becoming activists/try to inspire a cancer researcher/ try to politicize their oncologist/write their congresspersons regarding FDA policies, etc. perhaps more of these targeted drugs will be more widely available sooner