Adjvnt Therapy: Destroys or delays growth of stray BC cells?
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And yes Susan, I definately agree that my Mammogram found the start of a very small tumor, and without finding it that fast, it could have been a lot worse. It WAS invasive, even though it was as big as my small fingernail......but growing fast. But clear margins, & no nodes involved, THEN radiation with the Mammo-Site device...so I'd like to think I am "done!"....
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Susan, sadly, the studies are showing that mammograms have no statistically significant effect on mortality (if a mammo saved you or me, that does not change this fact, since I am talking about large groups and not individuals). Cancers are being caught earlier but some would have died by themselves if left untreated. The conundrum is that we don't know which ones. It's so frustrating, because the evidence is so often epidemiological but hard to explain at the petri dish level, if you will.
The "early detection saves lives" mantra is fading and has been fading for the past two years or so. Even the idea of a "breast self exam" has been replaced by the rather cryptic "breast self awareness."
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Susan... Recall what my doctor told me, "With breast cancer, you never know."
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Here is a meta-analysis of relevant, randomized controlled trials of various chemotherapy and hormonal therapies with 15-years of follow-up. You can see how at the various time points, there are fewer recurrences and deaths among those who got treatment (it varies a lot, of course, for age, stage, receptors, etc.)
"Effects of chemotherapy and hormonal therapy for early breast cancer on recurrence and 15-year survival: an overview of the randomized trials."
http://www.ctc.usyd.edu.au/cochrane/publications/EBCTCGpaper.pdf
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My MIL had cancer in her 40s. The cancer came back in her bones 25 YEARS later. She had a mastectomy when the cancer was discovered, but no other procedures as this was many years ago. When her cancer returned she had chemo, and survived 5 years.
I had a mastectomy 28 years ago. No other treatment was given. I then got a NEW cancer in the other breast, not a recurrence.
So I guess I could still get a recurrence from the first cancer and also the new one.
You just never know---my surgeon says we all have embryonic cancer cells and if we knew what triggered them we would have a cure. But we don't. He also said cancer cannot ever be said to be cured; it is in remission.
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Here's another population-based look at breast cancer death rates from 1996 to 2006. You can see that they have declined for all age groups. I think it's most interesting to look at the info for the women under 40, since this is a group that does not get mammograms (therefore, their cancers are more likely to be detected in lump form, and are NOT super-early stage.) And yet, death rates have also dropped dramatically for this age group (by 30 percent) even though incidence has held steady or even increased.
http://www.prb.org/Articles/2009/breastcancer.aspx
The only explanation that I can think of that would explain this data is that treatments are working and "curing" more women than in the past. (By "cure" I mean making sure that breast cancer cells do not threaten the woman for the rest of her life.)
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Morning gals...Athena, that sounds about right, that Mammograms do not make any difference on the mortality, but I'm thinking that since they DO show (sometimes) small tumors that have just started, that if I had not found that tumor with a Mammogram, and it was allowed to grow & infect my lymph nodes, my mortality would have been affected.....
And thanks Beeb for posting those links.... I couldn't ever find too many articles about Breast Cancer in women as old as me, ha! My own opinion is.... That if I DO get cancer again, that it is a new one. That since my lymph nodes were clear, and I had clear margins, that if I DO get it again, it sprang up on it's own....like a wart! Not to make light of it, but does anyone absolutely KNOW that your second time is related to the first?
I'm just lucky that at my age, I can pick and choose what treatment I want and need...Your young age makes a big difference....I mean I think....
Man, I don't know....but it's nice to kick all this around in my brain & try & understand.... 0 -
© 2011 by American Society of Clinical Oncology
Breast Cancer Adjuvant Therapy: Time to Consider Its Time-Dependent Effects AuthorsIsmail JatoiUniversity of Texas Health Science Center, San Antonio, TXWilliam F. AndersonNational Cancer Institute, Bethesda, MDJong-Hyeon Jeong and Carol K. RedmondUniversity of Pittsburgh, Pittsburgh, PABreast cancer is a chronic and heterogeneous disease that may recur many years after initial diagnosis and treatment.1 This has important implications for the practicing oncologist. For instance, an early effect of adjuvant treatment may diminish over time after cessation of therapy, or, alternatively, there may exist a lag time before some treatment effects become pronounced. Indeed, the risk of breast cancer recurrence and death (hazard rate) varies over time (ie, is nonproportional) according to prognostic and predictive factors (Figs 1 and 2; Table 1).6,13 The hazard curve for breast cancer death peaks between 2 and 3 years after initial diagnosis and then declines sharply, suggesting that the biologic mechanisms responsible for early and late cancer-specific events are fundamentally different. Thus the early and late effects of adjuvant therapy may vary accordingly.
View larger version:In this windowIn a new windowPowerPoint Slide for TeachingFig 1.Annual hazard rates for breast cancer death and ER-negative to ER-positive hazard ratios (Table 1) using the National Cancer Institute's Surveillance, Epidemiology, and End Results 13 Registries Databases (1992 to 2007) for invasive female breast cancer.2 Annual hazard rates for breast cancer death overall (all cases combined, n = 401,693), estrogen receptor (ER) -negative (n = 74,567), and ER-positive (n = 257,426) breast cancers. The annual hazard rate for cancer-specific death describes the instantaneous rate of dying from cancer in a specified time interval after initial cancer diagnosis. Hazard rate curves were modeled using cubic splines with join-points selected by Akaike's information criteria3,4; 95% CIs were applied with bootstrap resampling techniques.5 Under the null hypothesis of no interaction over time, annual hazard rates for ER-positive and ER-negative breast cancers would be proportional (or similar) with follow-up after initial breast cancer diagnosis. The overall rate of breast cancer death for all cases peaks near 3% per year between the second and third years after initial breast cancer diagnosis and then declines to 1% to 2% per year by the sixth through eighth years. The annual hazard rates for women with ER-negative and ER-positive tumors demonstrate peaks of approximately 6.5% and 2% near the first through third years after initial breast cancer diagnosis, respectively (> three-fold difference). An ER-negative to ER-positive hazard rate cross-over occurs between the seventh and eighth years after breast cancer diagnosis, and then women with ER-negative tumors had a somewhat paradoxically lower rate of breast cancer death than those with ER-positive breast cancers. 
View larger version:In this windowIn a new windowPowerPoint Slide for TeachingFig 2.Percent relapse-free survival (A, C, E) and annual hazard rates for breast cancer relapse (B, D, F) using data that was provided in supplemental Table 1 of Fan et al.6 Relapse-free survival in panels A, C, and E was obtained with the Kaplan-Meier product-limit estimator.7 Percent annual hazard rates for breast cancer relapse in panels B, D, and F were modeled as described in Figure 1.3,4 Plots for relapse-free survival and annual hazard rates for breast cancer relapse are shown for the intrinsic molecular subtypes (A, 
,8 MammaPrint prognostic molecular signatures (C, D),9-11 and Oncotype DX prognostic scores (E, F).12 All plots demonstrate nonproportional relapse-free survival and nonproportional annual hazard rates for breast cancer recurrence. (A, Unsupervised hierarchal molecular clustering demonstrates two main breast cancer classes according to estrogen receptor (ER) expression and/or epithelial cell of origin (luminal or basal). There are two ER-negative (HER2 and basal-like) and two ER-positive (ie, luminal A and molecular signatures.8 Relapse-free survival is most favorable for luminal A and least favorable for non-luminal A tumors (luminal B, HER2 positive, and basal-like breast cancers). (C, D) MammaPrint is a dichotomous 70-gene prognostic signature.9-11 Relapse-free survival is most favorable for a good and least favorable for a poor molecular signature. (E, F) Oncotype DX is a 21-gene prognostic score.12 Relapse-free survival is most favorable for low and least favorable for intermediate and high molecular score. View this table:In this windowIn a new windowTable 1.ER-Negative to ER-Positive HRs Over TimeFor example, Figure 1 shows the annual hazard rates for breast cancer deaths (percent per year) after initial diagnosis among women in the National Cancer Institute's Surveillance, Epidemiology, and End Results 13 Registries database.2 The average annual rate of breast cancer deaths is nonproportional overall and by estrogen receptor (ER) expression.14 Thus the annual hazard rate for all cases peaks near 3% per year between the second and third years after diagnosis and then declines to 1% to 2% per year by the sixth through eighth years. The hazard rates for ER-negative and ER-positive tumors peak at approximately 6.5% and 2% per year, respectively, between the first and third years (ie, > three-fold difference). Notably, ER-negative to ER-positive hazard rates cross between the seventh and eighth years, after which women with ER-negative tumors have a lower rate of breast cancer death than those with ER-positive tumors. Table 1 further shows the fold difference for ER-negative compared with ER-positive tumors over time. ER-negative to ER-positive hazard ratios (HR) were more than 1.0 before the eighth year, after which HRs were less than 1.0. Similar nonproportional hazard rates are evident for large versus small tumors, positive versus negative lymph nodes, high versus low tumor grade,13 the intrinsic molecular breast cancer subtypes,6,8 and the molecular prognostic signatures Oncotype DX12 and Mammaprint9-11 (Fig 2). Thus hazard rates for relapse among high-risk tumors (eg, nonluminal A, Mammaprint poor signature, and Oncotype high-risk score) show a sharp peak soon after initial diagnosis, similar to ER-negative cancers (Fig 1). Conversely, hazard rates for low-risk tumors (eg, luminal A, Mammaprint good signature, and Oncotype low- and intermediate-risk score) lack a sharp peak, similar to ER-positive tumors. These hazard curves suggest that the biologic mechanisms responsible for early and late breast cancer events differ and may therefore respond differently to the same treatment. Although randomized clinical trials compare the outcomes of two treatment groups (and therefore two distinct hazard functions) over time,15 trial results are often summarized as a single value of the hazard ratio based on the Cox proportional hazards regression model.16 The underlying assumption is that the effect of an experimental treatment in comparison with that of a standard treatment is proportional over time. If an experimental treatment reduces the risk of recurrence by 25% at 3 years, then it is assumed to have the same proportional benefit throughout all other time points as well. Thus a 25% proportional benefit implies that the risk of recurrence is reduced from, say, 8% to 6% at year 3, 6% to 4.5% at year 4, 2% to 1.5% at year 6, and so on. Although the absolute benefit varies, the relative benefit (the hazard ratio) remains constant over time. In essence, the Cox model allows for estimation of a treatment effect without regard to any potential time-dependent fluctuations. Yet there is now compelling evidence that commonly used adjuvant therapy regimens exert their effect primarily on the early hazard peak of recurrences and deaths (reducing the risk of events during the first 4 years after initial diagnosis). Jeong et al17 demonstrated nonproportional disease-free survival among patients treated with adjuvant tamoxifen versus placebo, with treatment affecting primarily the early hazard peak. Similarly, data from the National Tumor Institute of Milan revealed that nearly all the beneficial effect of adjuvant chemotherapy with cyclophosphamide, methotrexate, and fluorouracil occurred during the initial 4 years after diagnosis.18 Additionally, analysis of the Cancer and Leukemia Group B and US Breast Cancer Intergroup data revealed that high-dose versus low-dose adjuvant cyclophosphamide, doxorubicin, and fluorouracil reduced the risk of an event (recurrence or death) by 55% in the first year and 30% in the second year, with no advantage after 3 years.19 Alternatively, there are now data suggesting that the benefit of adjuvant immunotherapy could occur later, if at all.20-22 Thus a breast cancer adjuvant immunotherapy trial may have a very different hazard ratio over time than the previous trials of adjuvant chemotherapy and endocrine therapy. Further evidence of the nonproportional treatment effects for adjuvant therapy comes from the Early Breast Cancer Trialists Cooperative Group worldwide overviews.23Table 2 (adapted from Fig 4 in the Early Breast Cancer Trialists Cooperative Group overview23) shows the average annual recurrence hazard ratio by follow-up intervals for women allocated to adjuvant polychemotherapy versus none. Although hazard ratios are lower (better) for women younger than 50 years than 50+ years for all time periods, the greatest impact of treatment occurs during the first 2 years among both younger and older women (P for time trend < .001). Treatment significantly reduces overall breast cancer mortality through 15 years of observation. However, the average overall effect on mortality ratios is less than that for recurrence, particularly among women in the older age group, and there is no statistically significant trend over time (P for time trend > .1). View this table:In this windowIn a new windowTable 2.Worldwide Overview Hazard Ratios for Breast Cancer Recurrence and Mortality for Selected Age Groups and Time Intervals After Diagnosis The popular simple log-rank test, which is identical to the score test from the Cox model when there is a single binary covariate, is optimal only when the proportional hazards assumption holds. If the log-rank test is used inappropriately for nonproportional hazards data, some loss of efficiency of the test is inevitable.24 In this case, an optimal weight function needs to be included in the log-rank test statistic, such as the Harrington-Fleming test.25Statistical methods for dealing with nonproportional hazards using extensions of the Cox model or other parametric survival models have been available since the 1970s, although they are rarely used in the design or primary analysis of breast cancer trials.26 Several methods exist, including stratification of covariates with nonproportional effects, stratification of the time scale, incorporating time-varying covariates for treatment, or the fitting of parametric models.27,28 Also, the concept of frailty might be appropriate to address the issue of nonproportionality.24 In the frailty model, optimal weight functions for the log-rank test can be obtained from the distribution of an omitted covariate in the Cox model that induces the nonproportionality.24 In addition, there is a substantial risk of dying from non-breast cancer causes as the length of follow-up increases, and this should be considered in the development of survival models.29,30 To distinguish breast cancer-specific mortality from other causes of death, the concept of competing risks or a cure rate model could be used to estimate the proportion correctly. The alternative methods in the preceding paragraph can also be problematic. For example, there can be lack of flexibility in using parametric methods, even though they can provide more accurate results as long as the assumed model fits the data well. Models with time-dependent covariates may suffer from unclear interpretation of the results, biases, and/or overfitting of the data set.31 Competing risk data are common, but the statistical methods for analysis should be chosen with caution. For example, if one is interested in inferring the proportion of breast cancer deaths, then the method should be based on the cumulative incidence function rather than the Kaplan-Meier survival curve.7,29 Also, designing a study with breast cancer mortality as the primary end point would entail larger sample sizes to meet the proposed true error probabilities for a competing risk model. To fully elucidate the long-term effects of novel therapies, long-term follow-up of patients enrolled in breast cancer clinical trials might be necessary. Indeed, if early- and long-term treatment effects are nonproportional, then the early stoppage of clinical trials might obscure important late effects. Alternatively, some adjuvant treatments may only have early benefits, and longer follow-up may dilute those effects. Thus, when developing time lines for the primary analysis of particular trials, it is essential to consider scientific, statistical, and ethical issues, as well as practical concerns such as increases in cost. Elucidation of the time-dependent effects of adjuvant therapy will become increasingly important in the years ahead as the number of long-term breast cancer survivors continues to increase. Given that the Cox proportional hazards methods generally ignore the potential time-dependent effects of adjuvant therapy, alternative models that incorporate concepts of breast cancer heterogeneity and competing risks of mortality should now be considered in the design, reporting, and interpretation of clinical trials. 0 -
Basically, what the authors are saying in the recent ASCO journal article that I just posted is that most of the data that is collected regarding treatment protocols is lacking. Their last sentence highlights the need when analyzing data to spell out the "time-dependent effects of adjuvant therapy" (which they know exists based on the different types of breast cancers) and create a model of analysis that includes "concepts of breast cancer heterogeneity and competing risks of mortality" when they report, design and interpret trials.
This article speaks to the question that we are all trying to answer. And to answer THIS question, the authors are saying that there is a better way to find out.....
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what???
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Chevyboy...I had to read the article a few times to understand it.
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Just KIDDING! I tried to understand this, and do believe that EACH of us are different, and given the same DX and adjuvant treatment, each of us will re-act differently.... I mean only a very small percentage of older women taking Tamoxifen have lost their hearing... while a a much larger percentage of women, probably because they were younger, have done fine with it.....
Honestly I believe that our chances are so much greater now, of surviving breast cancer than they ever were. The initial surgery, and follow-up treatments have come so far, since my Mom had a radical mastectomy 15 years before she died of heart problems......
Thanks for posting this VReader.... I love reading articles like this, & trying to learn something new!
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I've read similar before, that B/C is a heterogeneous disease and that "Breast Cancer" is just a big umbrella label to cover it all. At this point, with B/C's behaving so differently and having different characteristics, how can you have a "one size fits all" cure? You can't. Over time, as much more research is done, the treatment of women in the sub-groups may be much different.
So, back to SG's OP, even if an individuals fate is not 100% predetermined at the time of surgery, the individual is on one of the diverging paths and to make any prediction on what the future holds for an individual, a lot more information needs to be discovered.
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VR: The last sentence of the article you post really needs to be hammered home.
The fact that death prevalence rates for a disease may have fallen says nothing about whether treatment for the disease is working. This is because a mere death prevalence rate depends on too many factors outside the disease such as: other diseases that spread, wars, pollution, etc... I used this example in another thread - it's extreme but good because it is clear: in Poland, 1 in 5 people died during World War II, obviously due to the fighting/pogrons, etc... So imagine how the death prevalence rate of cancer must have declined! A miracle cure? Only if you consider being bombed or gassed or shot as treatment. Unfortunately, many like to say that the death prevalence rates from cancer are likely a result of treatment. But that is speculation, at best, because too many other factors are interfering for anything specific to be said about BC.
The way to measure how well people do with a specific disease is to isolate the figures and set aside other circumstances that could interfere with the "purity" of your data. Since we can die of so many things, death prevalence rates won't tell us anything specific about how deadly a single disease is for the population. Rather, you have to ask the question: "if 100 people get disease X today, what proportion, if any, will die of it?" How about 20 years ago? 50 years ago? Let's compare.
But even that answer can be skewed if the population, during those time frames, has aged overall. So you have to control for age variables.
Once you have age- and population-adjusted figures for today, 1950 and 1980 (I am choosing those dates at random) you can properly answer the question - has mortality from disease x improved significantly since the advent of y or z therapies?
For many cancers, including breast, the answer is hardly to my satisfaction. Here is a favorite of mine. Unfortunately, this type of data is rarely mined - you have to be a statistician to do it:
http://www.nytimes.com/2009/04/24/health/research/24cancerside.html?ref=policy
Big note/caveat: Any analysis of death/treatment is by necessity several years old. We cannot know how recently dx'd people will do, just as it is too early to tell how well the Oncotype test predicts recurrence or how well Herceptin works. So these figures, for those of us treated in the last few years, have to be taken carefully. And, as VR's article suggests, data from clinical trials should also be read cautiously.
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Chevy, articles on BC.org mention tamoxifen being used before surgery to help shrink tumors so that a woman could have a lumpectomy instead of a masectomy. That is the tumor shrinking that I was referring to. Sorry I'm not good at figuring out how to put links in my messages.
I never heard about tamoxifen being hard on the hair follicles just like chemo. Initially, my hair seemed to be thinning a little on tamoxifen, but could have been due to normal aging/going through menopause. However, the past year, it seems to have thickened up a bit more and the hairdresser still says I have plenty of it all over.
If it was causing me any unacceptable side effects, like uterine issues or like your hearing loss, I would stop it in a heartbeat. I actually have already taken a break from it earlier on for about a month due to libido/sexual issues and intolerable hot flashes, which all did improve somewhat from the break. I refuse to start taking meds to combat the side effects of other meds or to start removing body parts just to stay on a medication that may be minimally benefitting me.
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Athena , you say:
Rather, you have to ask the question: "if 100 people get disease X today, what proportion, if any, will die of it?" How about 20 years ago? 50 years ago? Let's compare.
By that standard, we have made amazing strides in breast cancer! Because the actual numbers of breast cancer cases have risen dramatically over time, while the actual numbers of deaths from breast cancer have fallen. So more people are getting the disease, but fewer people are dying from it. How to explain?
There are two thoughts:
1) Mammogram technology has enabled us to detect very early (and easily treatable) breast cancers, and perhaps even cancers that would never have been a threat to a woman's life. So we count those as diagnoses when they might have been the kinds of cancers that would never have grown fast or metastasized.
2) The treatments for breast cancer are "curing" some women. (And I always use the word "cure" to say that they are doing something to the cancer cells -- killing them, making them dormant, knocking the tumors back to a level that they don't come back to threaten the women before she dies of something else.)
That's why I suggested looking at the data for young women. You can isolate out the mammogram effect and see the treatment effect. Young women don't get mammograms, so their cancers are still not caught early -- yet, they get aggressive treatment and their death rates from cancer have dropped.
P.S. Also to address the idea of competing causes of death -- we haven't had a WWIII, or major epidemic, and medicine is doing better in terms of treating other potential causes of death like heart disease, AIDS, etc. Lifespan is increasing, so I don't think that plays strongly into the data. Rather, I would argue that cancer is increasing in its prevalence because we *don't* have those competing causes of death. People are avoiding the early killers of the past (like childbirth, infectious disease) and living long enough to get cancers, which generally increase as we age.
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Okay, so in other words, what VR said is so true...."You just never know."........... If just 2 of us had the same surgery, the same size, same 0/3 nodes involved, same type of radiation and adjuvant treatment....that doesn't mean that we would stay the same, or have the same prognosis. .....
So we can't judge what happens by stats, or by what happened to our friends.... We are just plain different, we can only do the best we know how.... and accept any treatment available...and hope for the best....
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VR,
Interesting article: the info that jumps out at me:
Treatment significantly reduces overall breast cancer mortality through 15 years of observation.
And...
In addition, there is a substantial risk of dying from non-breast cancer causes as the length of follow-up increases,
Well, isn't that the whole point? I mean, no one is going to avoid death entirely. It will be the final outcome for us all. But our goal after a breast cancer diagnosis is to keep the disease from killing us. If something else kills us eventually, we've achieved that goal.
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I'm just repeating what the statisticians say - I'm no expert so I could never give an opinion on the best way to measure any rate of anything. If you get breast cancer today ("today" being 4 or 5 years ago) your chances of surviving it are not much better than they were in 1950.
But you bring up an interesting point re: early detection with mammograms, because that is not such a good thing in its totality (even if it may be a lifesaver for some individuals). We do get lots of DCIS that "skew" the data compared to way back when, when feeling a lump was still the principal mode of discovery. Researchers say that some DCIS would have disappeared anyway and that early detection may lead to earlier distress - but of course a person would be crazy not to get the DCIS out, since it could lead to a kill eventually. And for those tumours that were going to grow and invade, the mortality benefit from it being caught early is unclear.
I think that treatments for breast cancer are curing some women and I use that word in the usual sense. In some cases, it happens. To be honest, for early stage, I trust plain old surgery the most. Some treatments are killing women. Others are doing nothing one way or the other, and others still are delaying the inevitable.
On this board we have seen all cases happen. We just don't know which for sure. Fingers crossed.
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Athena, you say:
If you get breast cancer today ("today" being 4 or 5 years ago) your chances of surviving it are not much better than they were in 1950.
What makes you think that?
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Again, it's not my thought - I am not the expert here. I would re-reference this, and related articles:
http://www.nytimes.com/2009/04/24/health/research/24cancerside.html?ref=policy
Beebe, just to touch on this, you say:
Also to address the idea of competing causes of death -- we haven't had a WWIII, or major epidemic, and medicine is doing better in terms of treating other potential causes of death like heart disease, AIDS, etc. Lifespan is increasing, so I don't think that plays strongly into the data.
The experts say it does. Rather, I would argue that cancer is increasing in its prevalence because we *don't* have those competing causes of death.
The point is to isolate data and isolate causes of death - that is why cancer death prevalence rates in the whole population cannot be used to measure cancer treatment progress. This is so regardless of whether lifespan is increasing and we are curing illnesses. It is a methodological issue.
BTW, some types of cancer death have declined dramatically, like pediatric cancers, whereas others, like lung cancer, have increased in both incidence and, therefore, death. Important to cancer rate studies in the United States is that blacks were not tracked in the distant past (before the 60s) and now they are. This may cause a revelation about cancers one way or the other and just adds extra equations that make statisticians' work harder.
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Athena,
That New York Times article is old, and it uses even older data (death rates from 1990-1994.) And yet if you look at the interactive chart for breast cancer, it shows a downturn in the death rate that began at about that time.
In the 70s and 80s, it was pushing 30 per 100,000 women (age and population adjusted)
In 2000 it was 27.1 per 100,000 women (age and population adjusted)
It's currently 24 per 100,000 women (age and population adjusted)
(Note that the US population is about 312 million people, so a drop of 6 per 100,000 means about 10,000 fewer women PER YEAR, will die of breast cancer, than would have in the past.) And, breast cancer incidence has risen over time.)
So contrary to what you wrote above...
If you get breast cancer today ("today" being 4 or 5 years ago) your chances of surviving it are not much better than they were in 1950.
... quite the opposite is true. You have a *much* better chance of surviving it today.
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And let me just post two data points.
In 1996, 184,300 women were diagnosed with breast cancer; 44,300 died of it.
In 2010, 209,840 women were diagnosed with it, and 39,840 died of it.
So you can see your chances of surviving breast cancer today are much better today than they were even in the mid-90s.
It's hard to find data going back to the 1950s, and frankly, I don't see how it would be very useful anyway, since as you rightly point out, data collection was different back then, and the useful treatments for BC didn't come about until the 90s. (Tamoxifen became the standard of care in the mid-90s, and the chemo regimens have developed over the past decade, with dose-dense ACT and Herceptin arriving in about 2005.)
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Be careful of mixing percentages and raw numbers. My chances cannot be measured against the backdrop of a raw figure. And 30 to 25 percent is not good, IMO. Especially considering how much the current therapies are touted, the fact that there is a so-called War on Cancer, that so much money is spent and the ACS itself is the world's biggest non profit. My view is that the data are very disappointing, and I am not alone. The Times article is from 2009 - not very old. But as I said before, mortality data will always be "old." Recurrence data is very old, for example. In fact the Adjuvant! data and cancer math data go back as far as 30 years. They have to.
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I was just looking for a research article I recall seeing here not too long ago that talked about a 15% improvement in bc outcomes across the board in recent years. Haven't found it yet, but just came across this, which I think is another interesting point in this entire discussion, and one reason why, after my own experience, I continually preach to newly dx'd women about getting an opinion from a breast surgeon, preferably at an NCI-designated cancer center:
http://www.medicinenet.com/script/main/art.asp?articlekey=124458
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I didn't use percentages at all. I used rates and raw numbers. The data for breast cancer in the Times article stops at 1994. That's really old and there is much more recent data available (2003-2007 is the most recent data set). I provided some of it above.
No woman's individual outcome can be predicted based on statistics, of course. But we can look at the big picture, and if 10,000 fewer women per year are dying of breast cancer, that's really excellent for those 10,000 women and their families and they are all really thrilled about it.
That women still die of breast cancer, that anyone dies of any cancer, is more than disappointing to me. It's devastating. Still, that doesn't mean we can't be glad about the progress that *has* been made and the lives that *have* been saved.
And we don't need to spout falsehoods to raise outrage. It only kills credibility. The provable facts are bad enough -- nearly 40,000 women die of breast cancer every year in the U.S. Treatment doesn't work for everyone and better ones are needed. But they do work for many, thank goodness.
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Beeb75... Regarding the statement that treatment significantly reduces mortality through 15 years of observation....That statement comes directly from the study that you posted yesterday...The Early Breast Cancer Trialists Cooperative Group. However, if you look carefully at the NEXT SENTENCE from this ASCO study, there is a HUGE HOWEVER which is critical of the study. "However, the average overall effect on mortality ratios is less than that for recurrence, particularly among women in the older age group and this is no statisticaly significant trend over time. These authors are taking issue with how the data is collected and examined and they say that future studies need to discern the nonproportional treatment effects.
The authors maintain that if early and long term effects are non proportional "..early stoppage of clinical trials might obscure important late effects. Alternatively, some adjuvant treatments may only have early benefits and longer follow-up may dilute those effects."
And regarding more people being diagnosed with breast cancer and fewer deaths, that is also a conundrum that has been discussed many times before. It is obvious with more screening we are diagnosing more breast cancer. But are the mortality rates truly going down because of that screening, or are more indolent breast cancers being diagnosed that wouldn't lead to death in the first place being found? The same debate is raging with prostate cancer..... While both of might be taking Tamoxifen to reduce our chances of recurrence by almost 50%, the absolute benefit for one person may be much greater than for the next person.
"With breast cancer, you never know," as my doctor says. BUT, perhaps if we used this formula that the authors present, MAYBE we might get a more definitive answer.
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Regarding The New York Times article that 1Athena! links, Gina Kolota did a wonderful job on her series regarding the War on Cancer. I think everyone should read the series of articles, TWICE.
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Cancer has a way of mutating. I have a feeling if there are "strays" maybe the are still "young & stupid" so chemo, als and or tamox will starve them or stop them from multiplying and setting up camp in organs. Maybe it just gets the "floaters" where as once you are metastatic or mets you have "cling-ons" and they are tougher to eradicate.
Finally some cells may be in your system but dormant. I'm not sure if chemo, Als, Tamox etc have any effect on dormant cells but I would think not. The cell must be dividing and "eating" for them to have an effect. Years later something wakes them up and we get mets.
spendygirl We don't keep doing chemo because it is not good for our bodies. We will end up with other health issue, possible even to get a different cancer. This is why they don't treat mets as aggressively. If they did the body would wear out a lot faster. Also cancer is very adaptive. With mets the cancer seems to learn and mutate. A drug might be effective for a while but eventually fails but in some cases does go into remission.
SusanGarden My understanding is chemos slow/stop growth.Kinda F@*&s it up. Seems the Als/Tamox remove/block the fuel so they starve it.
I don't think it's just a delay. I t hink it has to do with dormant cells. It seems more women in early stage seem to live long lives than get recurrence. We just see a lot of the recurrence and stage IVs on this forum.BTW I'm currently reading "The Emperor of all Maladies : The History of Cancer" I'm reading it slowly though.
dlb823 you are correct. Bone marrow transplant is not effective for breast cancer. They don't do it anymore. I read that in the book about the making of Herceptin.
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OK I've just read all of page 1. Still need to read page 2 & 3 so I hope I don't repeat anything that has already been said.
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Lago....According to Dr. Michael Gnant and the Austrian Study and Zometa:
Although exactly how Zometa reduces the risk of recurrence isn't known, lead researcher Dr. Michael Gnant, a professor of surgery at the Medical University of Vienna, said he thinks "it prohibits dormant tumor cells in the bone marrow from 'waking up.'"
"Zometa actually hardens the bone and makes it more difficult for the cancer to actually implant," Brawley added.
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