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Kaye · 08-01-2006, 08:00 AM

I would be very interested in knowing how the PR receptor figured into all this. I read Dr. Lee's book (can't recall the name) a few years ago. He felt that the PR receptor played just as much of a role, if not a greater one than the ER receptor. However, my PR receptor status was not tested or not listed -- although am not sure why. When I asked I was given the explanation--there was no need since there was no treatment directed towards it--either way. In retrospect, I am wondering if they did know and whatever it was indicated that Tamoxifen would be less effective but they wanted to go ahead and offer me Tamoxifen, which they did.
However, by the time I was ready to start hormonal treatment, I/we (husband and I) had read enough that made me a bit uneasy about Tamoxifen. It was my husband, who has his PhD in biological chemistry and previously did cancer research, who suggested to my onc that perhaps the failure rate of Herceptin (which was around 30%) was being seen in those who were also Her2+ My onc thought that was an interesting possibility which later, according to research findings, turned out to be the case.
Because of that possibility (before it was known), I refused Tamoxifen. It turned out that that was the only way I could get an aromatase inhibitor. I was then offered Arimidex. I asked for Femara but my luck didn't go that far--would only approve Arimidex. That was 5+ years ago.
As far as being 'rare' -- it wasn't only being Her2+ and ER+ that was rare for me. I also had a rare presentation of IBC (in nipple only) and main type (or at least what was found in area biopsied) turned out to be not only lobular (which 12 to15% have) but a rare variant of that--pleomorphic invasive lobular which, if I recall correctly, only 5% have (although instead of 5% that may have been 1 to 2% asa well). Whatever--most of what I had going on was rare--which, I guess, was a good thing because on that basis (or at least that was what he wrote as a rationale) allowed me to get Herceptin out-of-protocol.
I was stage II at the time--however, even that is somewhat debatable--may have been stage IV from the start--depending on who (oncologist or cancer facility) evaluates. (Path report from biopsy said stage II. After mastectomy they wrote stage IIb. However, in addition to having advanced bc that path report stated I had a separate tumor in nipple w/dermal lymphatics which he said meant I had IBC. I then asked, that if I had IBC isn't that more advanced than stage II? He then changed my charts to read stage III. Another 2nd opinion dr told me that what they listed as staging was not what was important--it was the treatment that was important. In retrospect--made us wonder, if perhaps, I was stage IV from the start, not only because of ALL (in addition I also had high grade dcis with extensive comedo necrosis and the nipple also had 'Pagetian' spreadO,I had going on, but because tumor markers were elevated as well. The early scans found many enlarged retroperitoneal/aortocaval nodes (largest being 2.5 cm, lengthwise--never biopsied) and a lesion in the liver (never biopsied). There were also remaining axillary lymph enlarged nodes matted together, according to scan report. (Path report stated only 12 were removed; 9 of those were positive).
So, reading 'between the lines' it sure seemed like I had more than stage II or III...I guess at this point that isn't as relevant since I am still around to write about it...

08-01-2006, 08:00 AM	#42
Kaye Senior Member Join Date: May 2006 Posts: 52	I would be very interested in knowing how the PR receptor figured into all this. I read Dr. Lee's book (can't recall the name) a few years ago. He felt that the PR receptor played just as much of a role, if not a greater one than the ER receptor. However, my PR receptor status was not tested or not listed -- although am not sure why. When I asked I was given the explanation--there was no need since there was no treatment directed towards it--either way. In retrospect, I am wondering if they did know and whatever it was indicated that Tamoxifen would be less effective but they wanted to go ahead and offer me Tamoxifen, which they did. However, by the time I was ready to start hormonal treatment, I/we (husband and I) had read enough that made me a bit uneasy about Tamoxifen. It was my husband, who has his PhD in biological chemistry and previously did cancer research, who suggested to my onc that perhaps the failure rate of Herceptin (which was around 30%) was being seen in those who were also Her2+ My onc thought that was an interesting possibility which later, according to research findings, turned out to be the case. Because of that possibility (before it was known), I refused Tamoxifen. It turned out that that was the only way I could get an aromatase inhibitor. I was then offered Arimidex. I asked for Femara but my luck didn't go that far--would only approve Arimidex. That was 5+ years ago. As far as being 'rare' -- it wasn't only being Her2+ and ER+ that was rare for me. I also had a rare presentation of IBC (in nipple only) and main type (or at least what was found in area biopsied) turned out to be not only lobular (which 12 to15% have) but a rare variant of that--pleomorphic invasive lobular which, if I recall correctly, only 5% have (although instead of 5% that may have been 1 to 2% asa well). Whatever--most of what I had going on was rare--which, I guess, was a good thing because on that basis (or at least that was what he wrote as a rationale) allowed me to get Herceptin out-of-protocol. I was stage II at the time--however, even that is somewhat debatable--may have been stage IV from the start--depending on who (oncologist or cancer facility) evaluates. (Path report from biopsy said stage II. After mastectomy they wrote stage IIb. However, in addition to having advanced bc that path report stated I had a separate tumor in nipple w/dermal lymphatics which he said meant I had IBC. I then asked, that if I had IBC isn't that more advanced than stage II? He then changed my charts to read stage III. Another 2nd opinion dr told me that what they listed as staging was not what was important--it was the treatment that was important. In retrospect--made us wonder, if perhaps, I was stage IV from the start, not only because of ALL (in addition I also had high grade dcis with extensive comedo necrosis and the nipple also had 'Pagetian' spreadO,I had going on, but because tumor markers were elevated as well. The early scans found many enlarged retroperitoneal/aortocaval nodes (largest being 2.5 cm, lengthwise--never biopsied) and a lesion in the liver (never biopsied). There were also remaining axillary lymph enlarged nodes matted together, according to scan report. (Path report stated only 12 were removed; 9 of those were positive). So, reading 'between the lines' it sure seemed like I had more than stage II or III...I guess at this point that isn't as relevant since I am still around to write about it...