Is Tamoxifen and AIs working?
Hi everyone,
I see my medical oncologist on 9-30-2015. My Oncotype test results should be in by that date as well.
I'm post-menopausal and 100% ER+/PR+.
I know he will prescribe either Tamoxifen or an aromatase inhibitor.
Aside from recurrence of cancer, is there a way to know if the Tamoxifen or AIs are working?
Is there a blood test such as estrogen levels that my oncologist will order to assess progress?
Thank you
Comments
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They wouldn't do an estradiol test for tamoxifen because it doesn't shut down estrogen production. It just prevents estrogen from binding to receptors.
I think the only usual test with an AI is to check to confirm you are menopausal before you start if there is any question about that. -
Hi Radgal:
You might be interested in this thread, started by someone else considering anti-endocrine therapy (start at top).
https://community.breastcancer.org/forum/78/topic/...
Note the discussion there of a baseline bone mineral density test (in the case of an AI). In some cases, consideration would be given to bone mineral density monitoring during treatment. In any event, if you have osteoporosis, low bone mineral density or risk factors for bone loss, you should inform your oncologist about it.
BarredOwl
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My onco told me there was no way to tell for me, I don't have any tumors to shrink.
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I think there is a test to see if you are metabolizing Tamoxifen.... CYPD26? I know that is not the correct name. I have osteoporosis and osteopenia, so Tam for me. I have read studies that suggest that Al's are a bit more effective for Post-meno women, in the prevention of a recurrence, than Tamoxifen. I don't think it's a significant amount.
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Hi keepthefaith:
Pretty close: CYP2D6
Per this relatively recent perspective (see link below), certain genetic changes in the CYP2D6 gene may cause a person to be a poor metabolizer of tamoxifen, which in turn, may decrease the effectiveness of tamoxifen. Regarding the estimated frequency of such genetic changes:
"Loss of functional genetic polymorphisms in CYP2D6 lead to the absence of functional CYP2D6 protein in approximately 5% to 10% of whites (people of European ancestry) and 1% to 2% of those of Asian and African ancestry. In the literature, these are commonly referred to as CYP2D6–poor metabolizers (PMs)."
The article discusses the history and some of the challenges of such testing, including the question of what is the appropriate sample source for ensuring that test results are a true reflection of germ-line genotype and what is going on in the liver (where CYP2D6 metabolism is occurring), and questions arising from this regarding the results of past studies that may have used other methods.
http://jnci.oxfordjournals.org/content/107/2/dju43...
It further notes:
"Genotyping this gene is difficult in normal settings, because it has a large number of single-nucleotide polymorphisms, gene deletions, duplications, and multiplications, along with adjacent pseudogenes, all of which make determination of the CYP2D6 genotype–determined phenotype the most complicated in pharmacogenetics."
The Goetz study referenced is behind a paywall, but there is a patient access option for those who wish to dive deeper.
[Edited to add:
The National Comprehensive Cancer Center guidelines (Version 3_2015) state (emphasis added by me):
"Given the limited and conflicting evidence at this time, the NCCN Breast Cancer Panel does not recommend CYP2D6 testing as a tool to determine the optimal adjuvant endocrine strategy. This recommendation is consistent with the ASCO Guidelines.]
BarredOwl
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