HER2 Support Group Forums - View Single Post - HER2+, ER+, PR+ and are taking Tamoxifen.

astrid · 06-21-2006, 07:22 AM

I went to a lecture last night from a local oncologist who was asked to speak at our breast cancer support group on anti-estrogen therapy for Breast cancer. He asked if there were any questions, so of course I said “Yes, I am triple positive and have recently read that the combination of ER+ and HER2+ is creating Tamoxifen resistance in those patients. I have also heard that sometimes Tamoxifen actually acts like an activator instead of an antagonist. My ONC assures me these are only animal/lab studies and not done on humans. Is this correct?”

His lecture was fascinating. He covered everyone’s questions in his explanation on Tamoxifen and the newer Aromatase Inhibitors (AI). He compared the two and explained why AIs are not effective for pre menopausal women. As, I am pre menopausal there is no standard treatment other than Tamoxifen. The reason AIs will not work for pre menopausal women is that the ovaries and the pituitary gland have feed back to each other so when an AI tries to shut the estrogen down the pituitary gland says “Hey, I need more estrogen and the ovaries respond and create more. This does not happen when the ovaries are shut down either chemically or by menopause because there is no one home to answer the pituitary gland when it demands more so it basically shuts up” AIs are not strong enough to shut down all the estrogen that the ovaries produce. They work on the other systems that create estrogen such as your skin and adrenalglands.

He then went into what is becoming a newly discovered problem and that is the cross talk between the estrogen receptor and the HER2 receptor. He confirmed that these are only animal/lab studies and not done on humans; however what they have found is that when you add the biologic therapy of Herceptin that the Herceptin blocks the cross talk because it binds to the HER2 protein and blocks it from dividing and therefore makes the Tamoxifen effective again. So while on Herceptin, I will not have to worry about Tamoxifen activating residual cancer cells. He also said that the more ER+ you are the more effective Tamoxifen is. I am 16% ER+, so my chances of reoccurrence and DFS (Disease Free Survival) are improved by approximately 16%.

I start Tamoxifen today, and today I feel good about the drug.

06-21-2006, 07:22 AM	#8
astrid Senior Member Join Date: Jun 2006 Location: Central North Carolina, USA Posts: 112	Lecture last night I went to a lecture last night from a local oncologist who was asked to speak at our breast cancer support group on anti-estrogen therapy for Breast cancer. He asked if there were any questions, so of course I said “Yes, I am triple positive and have recently read that the combination of ER+ and HER2+ is creating Tamoxifen resistance in those patients. I have also heard that sometimes Tamoxifen actually acts like an activator instead of an antagonist. My ONC assures me these are only animal/lab studies and not done on humans. Is this correct?” His lecture was fascinating. He covered everyone’s questions in his explanation on Tamoxifen and the newer Aromatase Inhibitors (AI). He compared the two and explained why AIs are not effective for pre menopausal women. As, I am pre menopausal there is no standard treatment other than Tamoxifen. The reason AIs will not work for pre menopausal women is that the ovaries and the pituitary gland have feed back to each other so when an AI tries to shut the estrogen down the pituitary gland says “Hey, I need more estrogen and the ovaries respond and create more. This does not happen when the ovaries are shut down either chemically or by menopause because there is no one home to answer the pituitary gland when it demands more so it basically shuts up” AIs are not strong enough to shut down all the estrogen that the ovaries produce. They work on the other systems that create estrogen such as your skin and adrenalglands. He then went into what is becoming a newly discovered problem and that is the cross talk between the estrogen receptor and the HER2 receptor. He confirmed that these are only animal/lab studies and not done on humans; however what they have found is that when you add the biologic therapy of Herceptin that the Herceptin blocks the cross talk because it binds to the HER2 protein and blocks it from dividing and therefore makes the Tamoxifen effective again. So while on Herceptin, I will not have to worry about Tamoxifen activating residual cancer cells. He also said that the more ER+ you are the more effective Tamoxifen is. I am 16% ER+, so my chances of reoccurrence and DFS (Disease Free Survival) are improved by approximately 16%. I start Tamoxifen today, and today I feel good about the drug. __________________ DX 11/14/05, Stage 1C, Her2+ 3.4, ER+, PR+, K167 23%, Node Negative, MX0, Grade 3, 1.8CM, Lumpectomy 12/7/05; 6 rounds dense dose Taxol bi-weekly, 35 radiation, 1 year Herceptin, & Tamoxifen ongoing.