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Medical Forum / Diseases and Disorders / Breast Cancer / October 2003question for the pros
I was reading the other day that breast cancer was a systemic disease, not a localized one. That it does not begin in the breast and spread but is systemic. Is this true? I will see if I can find the link. TIA > I was reading the other day that breast cancer was a systemic disease, > not a localized one. That it does not begin in the breast and spread > but is systemic. Is this true? I will see if I can find the link. > TIA I don't think so, I think someone has misunderstood. The phrase "systemic disease" is used in respect of metastatic disease where there are secondary cancers elsewhere in the body. Once a cancer has reached this stage and secondaries have been detected in other organs then it is considered systemic because it is assumed to have also spread around the body, even though it has not yet produced any other detectable tumours. Breast cancers begin in the breast and spread. If this were not true then removing part or all of the affected breast would not cure 95% of patients with small cancers detected early, as it does appear to. Of course one might argue that the -causes- of breast cancer are not uniquely in the breast, or even in the individual, but are related to social factors, pollution, lifestyle, race, diet, whatever your flavour of the month. But that is getting philosophical and I don't think is what you meant. I think there is no question that the point at which a bunch of conditions come together to form what is recognisably a breast cancer, is an event which occurs in the breast. Tim Jackson (amateur, not pro) > > I was reading the other day that breast cancer was a systemic disease, > > not a localized one. That it does not begin in the breast and spread [quoted text clipped - 8 lines] > it is considered systemic because it is assumed to have also spread around > the body, even though it has not yet produced any other detectable tumours. This philosophy has been around for years. I think it originated in the observation that in many types of tumor one is able to 'harvest' tumor cells from the blood, even in early tumor stages. Its unclear why so few of these cells go on to become metastases. An anecdote in connection with tumor harvesting: A colleague of mine had a liver tumor removed 1.5 years ago, its histology was a mystery to the pathologists, despite specimens being sent all over the world for help with the diagnosis. Because no-one knew what to do he (a radiologist BTW) had tumor cells harvested from his blood and assayed in Germany. They were able to provide a list of chemos which would work (at least in vitro) against the tumor. We all thought it was a bit 'alternative' to go this route, (because of the reputations of institutes that offer such services) but why not if it helped... He backed off getting the 'strong' chemo schedule in the end because of the reservations he had about the tumor's malignancy. This week he started chemo for stage IV pancreatic Ca, after removal of 3 more liver mets and a primary tumor in the tail of the pancreas. So maybe there's something to the idea of cancer in general being a systemic disease, although in this case with first manifestation in stage IV its not surprising that it was already systemic..  Signaturemadiba Madiba wrote << This philosophy has been around for years. I think it originated in the observation that in many types of tumor one is able to 'harvest' tumor cells from the blood, even in early tumor stages. Its unclear why so few of these cells go on to become metastases. An anecdote in connection with tumor harvesting: >> I have a question about mets. When someone is first dx'd they are often given chemo to take care of any possible cancer cells that are scattered throughout the body. Let's say, for whatever reason, the chemo did not take care of all the cells. This person is shown to have mets, which are 'small' some time later. Why would the cancer, for the most part, be considered not curable at that point. If that is the case, wasn't it uncuurable form the start? > Madiba wrote << This philosophy has been around for years. I think it > originated in the [quoted text clipped - 9 lines] > later. Why would the cancer, for the most part, be considered not curable at > that point. If that is the case, wasn't it uncuurable form the start? When adjuvant chemotherapy is given after surgical removal of a primary cancer it is hoped that and (micro)metastases are small enough that the chemo will destroy them, lets say for the sake of argument 1000 cell clusters or around three years' growth. Chemotherapy won't kill detectable tumours, which are around a billion cells or ten year's growth, it will only shrink them. Think of it like peeling a potato, the chemo can only penetrate so far into the tumour, in the example I suggested, only the outermost 5 or 6 cells get killed. That's why you need surgery as well. (however as tumours tend to be leggy things, it can reduce the volume they occupy quite a lot, hence neo-adjuvant chemotherapy (before surgery) for large tumours). So there is a big gap between the size of tumours that chemo can destroy and the size that is detectable. There are unknown quantities of how long the tumour has been metastatic, and how fast the metastases are growing. If these turn out to be low then the cancer is cured. If they turn out to be high, then it isn't. When the secondaries finally grow to detectable size, the primary has been generating them for about thirty division times, and there are bound to be lots of free cells circulating in the blood and micrometastases all over the body. There seems to be some sort of mutual suppression effect (perhaps a competition for scarce resources), which means that only a few grow to large size. But if you remove the large ones, more quickly pop up to take their place. This is why is it considered incurable. Although it doesn't look much different from a primary, what is going on in the body is quite different. Now, if we knew how the large tumours suppress the small ones.... Tim Jackson Tim wrote << When adjuvant chemotherapy is given after surgical removal of a primary cancer it is hoped that and (micro)metastases are small enough that the chemo will destroy them, >> Right, but what if, for some reason, that the chemo that is given doesn't do that and these cells continue to grow. Could not a different chemo be given at some point that might kill all the remaining cells? Or another scenario, what if the chemo started killing the cells but was terminated before all could be given. Would it not have been possible to have given a higher dose or more chemo then and/or in the future? If not, why? > Tim wrote << When adjuvant chemotherapy is given after surgical removal of a > primary [quoted text clipped - 8 lines] > terminated before all could be given. Would it not have been possible to have > given a higher dose or more chemo then and/or in the future? If not, why? Detection is the problem. If you knew that there were still micrometastases around then you could give stronger treatment in those cases. But if you start giving stronger treatment to everyone, just in case, then you kill too many people. Tim Tim wrote << If you knew that there were still micrometastases around then you could give stronger treatment in those cases. But if you start giving stronger treatment to everyone, just in case, then you kill too many people. Yes, but there are newer treatments that are safer or other meds that can be given along with them to make them safer. There are also different combos of meds that are relatively safe or safer that could be used. Tim wrote << When the secondaries finally grow to detectable size, the primary has been generating them for about thirty division times, and there are bound to be lots of free cells circulating in the blood and micrometastases all over the body.>> Just a thought, could it also be possible that the secondaries are also generating them so that the amount becomes exponential? Also, take a situation like mine. I had an invasive core biopsy done in 5 areas of the tumor on my upper chest (almost above breast on chest wall). After the biopsy several bruises formed which did not heal. I am assuming that new blood vessels were forming in an attempt to heal that area. I then had surgery 23 days after the biopsy. My understanding is that the rate of growth for normal cancer cells is every 23 days. I can only imagine the rate of growth for aggressive cells. What may have happened to my body, cancer-wise, between the biopsy and the actual surgery? <<There seems to be some sort of mutual suppression effect (perhaps a competition for scarce resources), which means that only a few grow to large size. But if you remove the large ones, more quickly pop up to take their place. >> Couldn't removing the main tumor result in that happening as well? If that is the case, then why bother removing the tumor? Also, what takes place in someone when a lumpectomy is done and clear margins are not obtained? How does that affect that cancer and future proliferation? <<This is why is it considered incurable. Although it doesn't look much different from a primary, what is going on in the body is quite different. Now, if we knew how the large tumours suppress the small ones....>> I had heard that theory and one dr. suggested that may be a reason for not doing a bilateral... > Tim wrote << When the secondaries finally grow to detectable size, the primary > has been [quoted text clipped - 4 lines] > Just a thought, could it also be possible that the secondaries are also > generating them so that the amount becomes exponential? Big secondaries surely are. The little ones are suppressed so they aren't growing so they aren't spreading. The amount is already growing geomtrically until it gets resource-limited, which it mostly is by the time it gets symptomatic. The seeding mechanisms get less relevant once you've got lots of seeds. > Also, take a situation like mine. I had an invasive core biopsy done in 5 > areas of the tumor on my upper chest (almost above breast on chest wall). [quoted text clipped - 4 lines] > growth for aggressive cells. What may have happened to my body, cancer-wise, > between the biopsy and the actual surgery? This point has been raised here several times. One might expect that biopsies would enhance the spread of cancer, but retrospective statistics fails to detect such an effect. One reason is that metastasis isn't simply a matter of breaking through a lypmh/vein wall, there has to be a change in the tumour to make is less cohesive. Normal tissues after all don't go sheeding cells into the bloodstream . It seeems that if you biopsy a non-metastatic tumour it doesn't make it metastatic. There are researchers currently examining the genes involved in the changes in cohesion, and the significant genetic differences between metastatic primary tumours and their metastases. This is a poorly understood area so far. > <<There seems to be some sort of mutual suppression effect (perhaps a > competition for scarce resources), which means that only a few grow to large [quoted text clipped - 3 lines] > Couldn't removing the main tumor result in that happening as well? If that is > the case, then why bother removing the tumor? Well yes, it does, but only at stage IV. Usually we remove tumours in the hope that they have not yet become metastatic. In cancers where metastasis is already proven, then resectng the primary tumour would usually only be done for palliative reasons. The preferred treatment would be chemotherapy alone. > Also, what takes place in > someone when a lumpectomy is done and clear margins are not obtained? How does > that affect that cancer and future proliferation? If clear margins are not obtained then further surgery is done, usually within a division time, until it is clear, so there is no history of this situation. As far as surgery spreading the cancer is concerned, the same answer applies as for biopsy. > <<This is why is it considered incurable. Although it doesn't look > much different from a primary, what is going on in the body is quite [quoted text clipped - 3 lines] > I had heard that theory and one dr. suggested that may be a reason for not > doing a bilateral... Maybe. Tim wrote << Big secondaries surely are. The little ones are suppressed so they aren't growing so they aren't spreading. The amount is already growing geomtrically until it gets resource-limited, which it mostly is by the time it gets symptomatic. The seeding mechanisms get less relevant once you've got lots of seeds. Do we know for sure that this is the case or just another plausible theory? << . It seeems that if you biopsy a non-metastatic tumour it doesn't make it metastatic. >> True, but if you biopsy a malignant area in an invasive manner and then don't treat it for a period of time that is greater than the established time of routine doubling or growth, it suggests that the procedure had the propensity to help the tumorous areas that were disturbed establish new blood supplies and further proliferate. Then, who knows what else might happen to a cancer that is found to be aggressive or have a faster rate of doubling or growth? As far as making that fact known, that could have dire implications and consequences, especially in areas where there is not the staff to treat in a more timely manner. It is quite easy to gloss over the results or possibilities and use the stats in their favor, and also emphasize the unknown factors which exist to some extent in every scenario. Common sense and knowledge of basic science, however, suggests otherwise... > Tim wrote << Big secondaries surely are. The little ones are suppressed so > they aren't [quoted text clipped - 5 lines] > > Do we know for sure that this is the case or just another plausible theory? I think it is fairly well established that the growth rate slows as the cancer gets more advanced, for one reason or another. For example big tumours go nectrotic in the centre for lack of blood supply. It's known that resecting secondaries rarely gives much benefit. I don't think all the mechanisms are well understood. > << . It seeems that if you biopsy a > non-metastatic tumour it doesn't make it metastatic. >> [quoted text clipped - 11 lines] > some extent in every scenario. Common sense and knowledge of basic science, > however, suggests otherwise... It doesn't quite add up. Of course we don't want delays, all delays increase risk, and there is no clinical reason for delay at this stage except to allow for treatment decisions and for the patient to come to terms with the dx. But whatever proliferation you generate in this process will not have time to grow into chemo-resistant clusters, which must take years unless the cancer is extremely fast growing, so as long as you get chemo within the next couple of years it should clean up. The critical time for metastasis was years before surgery. Tim Tim wrote << I think it is fairly well established that the growth rate slows as the cancer gets more advanced, for one reason or another. For example big tumours go nectrotic in the centre for lack of blood supply. >> I thought it was the other way around--that growth rate was more rapid as cancer advanced? <<It's known that resecting secondaries rarely gives much benefit. I don't think all the mechanisms are well understood.>> I gather that much--re the last sentence. However, latest research suggests that if there are only one or two mets, then resection appears to increase long-term survival -- i.e. for lung and liver mets, at least. |
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