growth rate of primary & recurrence diagnoses

Can somebody shed some light for me?

Suppose you got originally diagnosed with primary breast cancer of which it indicated fast growth (aggressive type), then later in your recurrence diagnosis (mets from same breast cancer, not secondary), your tumors came back in other organs at a different growth rate, either slower or faster?

Would that be possible? I have always thought that once you were first diagnosed, your recurrences would have the same type of tumors (regardless the numbers of recurrneces), meaning always the same growth rate each time. Huh? <scratching on my head in puzzlement>

Thanks

I've heard where your primary was er/pr - and the secondary came back positive. So I guess it can change

Kathie

When its mets from the primary it would remain the same. Such as breast cancer mets to liver is still breast cancer and treated as such it is not liver cancer. That is why it is always tested to see if it is still brrast cancer or a new primary then being secondary. I hope this is clear. I have had people tell me they have bone cancer and after talking to them they will tell me they started out with breast cancer and it went to the bone. They think now they have bone cancer when it is still breast cancer spread to the bone. The treatment will be for breast cancer and not bone cancer, the same when it spreads to liver or lung. I am sure others will post on this. The ER/PR remains the same as the primary but can change with a new primary then being secondary. Hugs, Sandy

Thats the way I heard it, Breast Cancer and then metesasises to another site but still BC. Now having said that when I had the biopsy done on lymph glands on other side of neck, pathology came back as similar cells not same so go figure. first cancer was agressive but the lump in my neck was there for 12 months before diagnoses and only enlarged quickly when biopsied, cells disturbed I put it down to and the neck is still thick and lumpy but I am NED and that treatment started in February last year so it has been there now for 2 years even longer because that was when I could actually feel a lump and started campaigning to get rid of it, so not the same cells is good so perhaps the cells have altered from the Herceptin treatments? anything is possible this disease does not discriminate maybe just changes sides which is a good thing, after all everyone is supposed to have ccancer cells in there body and just needs something to mutate it and maybe Herceptin can change it back.

Loev & Hugs Lyn.

Interesting question about growth rate. I've never seen any studies on it. As for the ER/PR, that CAN change on a metastasis. My primary bc was er/pr pos, but it was er/pr neg on my liver met.

Love and light,

Lisa

Lisa this is interesting to know ER/PR can change with mets! I was told at SABCS that Her2 status can change with mets. Need to be tested with new mets. It doesn't happen often but can. There is always something new to learn with this disease. Suppose that is one small reason why a cure has not been found? This disease is smarter then the people treating it! Just a thought that ran past me this morning. I know that isn't the only reason. Hugs, Sandy

Sandy,

VERY interesting...I'd be willing to bet that few if any of us have been re-tested for HER2 with recurrences.

Love and light,


Lisa

Quite a few doctors are not aware that ERPR and HER2 can change...

Chemotherapy or even hormonal therapy could be a cause for the changes. There isn't broad understanding of what really does what, which is why I am somewhat hesitant to even start on a SERM or an aromatase inhibitor.

I am NED now, after chemotherapy. So theoretically if I use a SERM like tamoxifen, and it changes some of the characteristics that are favorable (like being ER+PR+), and I have recurrence/METS, it could mean I would be in a worse position with a recurrence than I was without using the SERM (or the aromatase inhibitor, or the Herceptin).

There is so much that they don't know. And in my opinion it is because women have not collectively found a way to build a common database that follows them from diagnosis to whatever they die from (including secondary causes that originated with cancer). If we all were part of that database on a consistent basis that showed what medications or alternatives we use or what treatments we got and didn't get, we would know a lot more...

Isn't that what makes cancer so sneaky?? It is forever changing: if it was predictable then we would have a cure by now. When Linda got AC & T as her original chemo for the breast tumor (HER2+) to down-size it, it shrank like crazy but her liver mets kept growing, albeit slowly. It wasn't until she got chemo + herceptin that the liver mets responded. Does that lead us to conclude that the secondary tumor was more HER2+ than the primary? Life is never simple.
Al