Catching Mets Early? Docs say it doesnt matter?
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"But would you rather live 5 years knowing you have mets or 1 year?"
That would be a really tough question for me. One of the issues is once you have mets they really can't say how long you have for sure. I think I would want to know if it would make my quality of life better.
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That's a great point about changing the outlooks of your family members and friends, barsco. I hadn't really thought of that part.
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"That's a great point about changing the outlooks of your family members and friends"
I think that's one of the things I'm afraid of. My sister and I still have spoken since 1 week after my BMX when I kicked her out. She was behaving badly (verbally abusive). She was supposed to be there to help/support me. I think she's still waiting for an apology. If I have 1 year or 40 I would hope people would be nice to me either way.
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My family and friends think Stage IV is a walk in the park. I don't really want to disabuse them. I want them to believe that for as long as I can give them that impression. Ironically, for myself I want to have full knowledge. I believe we can influence the epigenetics of our cancers to some degree.
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barsco: I agree with you on the illusion of having lived longer.
Also, I think family and friends would perhaps think of a mets diagnosis differently. Whether they should or not.
Personally, I figure I am already living on borrowed time. I try to remind myself of that when little stuff is irritating me, but I forget a lot, too.
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I'd rather get diagnosed earlier while the mets is still in the bone so it's easier to treat. Then, if it progresses to organs, I'd have to kick in the big guns, but at least I'd have had those years on just an AI or something for my bones.
IF I get mets to an organ, I don't think I want to know. I've read WAY too much over the years on this forum and don't have a particularly warm and fuzzy feeling about liver or brain mets. Lungs mets seem to be reasonably treatable, and that surprises me.
You can't assume that you would survive the same number of years (2017 for example as above) whether caught early or late. Caught late, the progression alone would wipe out a number of those years....
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lago ~ yes... I agreem the outlook of others could change for the good as well as the bad. That's too bad about your sister. Were you two very close before this happened?
I had a friend who was diagnosed with lung cancer at an early age (early 40's and never smoked by the way). I always admired the way he lived after his diagnosis. He had hope and was trying all treatments...but at the same time accepted his likely prognosis. He took trips with his family. He got together with old air force buddies he hadn't seen in years. He died within 4 years and at his funeral..so many people spoke and laughed about the great times they had with him throughtout his life..and especially in those last four years. He made a lot of awesome memories with his family and friends during that time.
How many of us put off that vacation..until we can afford it/retire.... or don't get together with friends enough..because we are so busy?
Heidihill ~ I could imagine people think it's a walk in the park if you don't "look" sick. I don't think anyone can truly understand until they are in those shoes. I read your bio...I liked your mention of hearing that exercise is more important than diet.
Because I'm finding it easier to exercise than put down the wine and chocolates right now!0 -
We were close enough. I only heard from my BIL once too during chemo. I do chat with my niece and nephew through facebook or skype at times though.
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lago - sorry that your sister has behaved badly and is not there to support you. Maybe one day she will be a good part of your life again.
When I mentioned that my families outlook changed, it isn't that they are treating me better, (my family has always been very close), it is that they are treating life differently - taking more opportunities that may have been overlooked before. They too are enjoying life more.
barbe58 - Although it is most common, mets don't always go to the bone first. My liver mets were discovered by routine testing about a week after my mx. I had/have no symptoms to suggest mets and to this point have not had any bone or other mets detected. I have been able to forgo the big guns for now. I am being treated with tamoxifen & zoladex. Thankfully my QOL has been great so far.
I know that even though mets to an organ is not great news (as with any mets), I am glad that they were discovered early enough so that I don't have to treat it aggressively right now.
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Another point to consider is that "biology is destiny." When I was at the MBCN conference in Indy one of the docs was talking about one of his patients who is doing very well, for many years, on anti-hormonal treatments only. Hers is more of the lazy, "indolent" disease, even though it is technically metastatic and will probably, eventually, be her cause of death.
Others have much more aggressive disease, and catching it early, either initally or at metastatic recurrence, is much harder because of how quickly it spreads. So there really isn't a single good answer for everyone, just guidelines based on past research and gut feeling by the MOs.
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Holy crap! Pip- the idea of scans waking up mets is soooo creepy!
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Love to all of you but, man this is a depressing thread......................
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Speaking of "biology is destiny" and to make faithfulheart a little more hopeful.....As we move towards a more individualized genomic approach to treating breast cancer, there will be more targeted therapies. Furthermore, based on an individual's genetic makeup, they will also know which therapies DON'T work and you will be spared having to take unnecessary treatment. Likewise, since you won't be wasting time on a therapy that doesn't work, hopefully, you will be given SOONER a potion that will blast your cancer cells to smithereens!
Here's what Eric Topol, MD said to ASCO recently. He's written this extraordinary book about the technological revolution of medicine that is underway:
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A Visionary Call for the ‘Creative Destruction' of MedicineA Conversation with Eric Topol, MDRonald PianaMarch 1, 2012, Volume 3, Issue 4According to nationally regarded cardiologist and geneticist Eric Topol, MD, Chief Academic Officer of Scripps Health, the next frontier of the digital revolution can create exponentially better health care. Dr. Topol, who is also Director of the Scripps Translational Science Institute and Professor of Genomics, The Scripps Research Institute, recently shared his thoughts with The ASCO Post on an unprecedented transformation in medicine, as described in his recently
published book, The Creative Destruction of Medicine: How the Digital Revolution Will Create Better Health Care (see book review). Here he discusses issues of value and cost in health care, the problems inherent in mass screening efforts, "individualized" vs "personalized" medicine, and how future innovations may be introduced to our health-care system.Radical Innovation
Congratulations on your new book. It's quite a provocative title; what was the inspiration?
The title simply captures the extraordinary opportunity we have to vastly improve the way we think about and practice medicine. The term "creative destruction" denotes a transformation that accompanies radical innovation. But this transformation is not likely to emanate from the medical community, the traditional way innovation jumps forward. In the current era of social networking, the transformation will likely come from a convergence of technology and consumerism, especially in the cancer space, which offers the most near-term opportunity for positive change.
As one example, when we have a tumor biopsy or tissue sample, it solely gets put in formalin, then fixed in paraffin, which is completely unacceptable. We need frozen tissue so we can rapidly conduct exome or whole-genome sequencing and use it to customize the right care for the individual's driver mutations of a particular cancer. We have this technology; however, we have a challenge getting surgeons, pathologists-basically the whole oncology community-to switch to frozen samples. Of course, this is just one of many "rules" that need to be broken in the oncology sector.
Value and Cost
The health-care debate seems to get mired in issues of value and cost. How can we make systemic improvements given our limited resources?
One of the steadfast rules is that when you introduce new technology into health care, it is invariably coupled with increased costs. But we have an opportunity to turn that model around by being able to track physiologic metrics, genomic sequences, and advanced imaging modalities. By making medicine more precise, these advances can markedly reduce costs while improving care. The convergence of digital technology and consumerism will provide real, actionable data attached to specific health needs, which will in turn drive costs down by eliminating the waste involved in population-based medicine.
Screening and Individualized Medicine
Many in the oncology community believe that if we could replicate the mass screening efforts that are routine in breast and prostate cancer for application in other cancers, it would have a large impact on cancer mortality. What are your thoughts on screening?
The problem is that we don't recognize the primacy and uniqueness of each individual. To date, the judgments we make and things we do in medicine-the old rules, whether it's screening or therapy-are related to large populations, not individuals. Previously, we didn't have the digital tools to do otherwise. But now we're at this exciting inflection point, where we are able to zoom in on individual patient characteristics.
I never use the popular term personalized medicine, which to me denotes a concierge-style model. Instead, individualized medicine can define a patient biologically, physiologically, and anatomically, aggregating into what I call homo digitus-in effect, digitizing a human being for all the essential characteristics that make that person tick.
That approach will lead to far better outcomes going forward. For instance, we won't have to have all women undergo routine mammograms after age 40 or 50, because a substantial proportion of women have no risk of developing breast cancer. We will ultimately identify that no-risk or extremely low-risk population, thus eliminating false-positives, biopsies, and the associated anxiety and attendant costs. In this case, mass screening disregards individual variability and promotes unnecessary medical procedures.
Further, once we have a diagnosis, with few exceptions we don't screen that person to see what drug will work; we give the same drug to all people with that diagnosis. In diabetes, everybody gets metformin even though metformin doesn't have any beneficial effect in 25% of those patients. However, in today's medical mindset, we don't take the patient off metformin; we simply add another drug, without screening to see if the drug is going to work. There are almost 400 million diabetics worldwide, so it's a huge issue of wasteful medical resources. Again, that's just one example of many.
Introducing Innovations
Considering that we have the tools to create "homo digitus" patients, how can we organize those tools to really make an impact on our vastly complicated system?
By self-organization-there are groups out there already taking the lead with online patient empowerment communities. The people in these communities trust their peers more than their doctors, for one reason, because their peers have like conditions that are discussed freely. We have already seen the profound impact of social networking in the health space, and it's just the tip of the iceberg. When people have their personal physiologic metrics and genomics on handheld devices, they'll band together, and you'll see a movement that will change medicine.Does a digital landscape fit into the strictures imposed by our limited financial resources?
Innovations moving forward cannot induce added cost pressures on the system. That would be untenable. We have a dual challenge with technologic innovation; it must improve health outcomes and significantly reduce expenditures. With creative destruction, you destroy very expensive methods with marginal benefit. In the United States, we spend $350 billion per year for prescription dugs, and we know at least one-third of that is total waste, offering no benefit or, even worse, inducing serious side effects.
Pharmacogenomics is a perfect way to destroy the old wasteful model of prescribing drugs. It's very inexpensive to run genotypes, once we have basically cracked the code-knowing the specific variant allele(s)-for each drug.
We have inexpensive ways to drill down to the things that produce good outcomes. For instance, I'm a cardiologist and I don't have to send a significant proportion of patients to a facility to have a formal echocardiogram, because I have a handheld high-resolution device that's just as good as the hospital laboratory. Why do we send people to facilities for sleep studies that reimburse at $3,000 per night when the same study could be done in the person's home for less than $100 and get the same data?
Closing Thoughts
Any last thoughts you would like to share?
I would like to see a transformation in which the medical community engages in the health-care revolution that will ultimately be consumer driven. We have a remarkable digital infrastructure including social networking that complements new opportunities to change the course of medicine, such as advances in genomics, biosensors, and imaging. There will be a superconvergence of human data capture that will give us the ability to digitally define the essential characteristics of each individual, not heterogeneous populations. I hope that my colleagues in medicine will acknowledge and embrace this unique opportunity to reboot medicine. ■
Disclosure: Dr. Topol reported no potential conflicts of interest.
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Great article!! Makes so much sense, but it seems it would be a long way off in acceptance. Really backs up what MJLtoday said, "biology is destiny". I guess that's what we've all been saying in a round-about way...cancer is a crapshoot. Using the tools from Dr. Topol, we'd have a better idea of who was going to roll the losing dice.
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Barbe....But getting the right targeted treatment at the right time might make all the difference in the world....
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Here's a comment from some one who was responding to a review of Dr. Topol's book that appeared in last week's Wall Street Journal... which I think is MOST important:
"I am glad this article includes a quote that the results of this study are in
fact old news. The message that should be taken from it is that cancer is not a
population-based disease, which means that our system of looking for median
outcomes in randomized clinical trials when trying to figure out how to treat
genetic diseases is utterly, completely, scientifically wrong. Also, old news.
So now, maybe in five or ten years, the NEJM will accept and publish an article
that calls for clinical testng approaches that actually fit what we know about
cancer - and if they get it right - the article will state that for most
cancers, randomized controlled trials are obsolete. Of course, those trials are
already known to be next to useless in cancer, but FDA and many in the clinical
research field still consider them to be the gold standard. An apt analogy. We
haven't been on the monetary gold standard for 70 years. We set it aside because
we had to. It wasn't working, and niether is the population-based approach for
cancer drugs mandated by the FDA's cancer drug office."0 -
But wouldn't blood testing (the genes) be fairly quick? Then the exact treatment would be known...
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I am very optimistic about gene therapy. Makes SO much sense!!
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According to Dr. Topol, the field of genomic technology is exploding and making it easier and faster to examine everyone's genes. The other side of the equation is once we have the unique make-up of everyone's genes, then we can begin targeting the therapies...like we are already doing with HER2 tumors (which he gives an example of in his book). But the HER2 example is only the beginning. As we find out more and more about everyones genes, the types of therapies appropriate for those tumors will hopefully grow easier to find. Remember, once we identified the HER2 component of the tumor...then it was off to the race to find a therapy.....
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Barbe...You always ask great questions and I also suspect that you are also a voracious reader!
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I read a book every 36 hours. I LOVE learning things in books, so tend to stick to authors that tell a story around something interesting. Like Dan Brown (is that his name?).
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I knew it! Us book lovers stick together!And yes, the author of the DaVinci Code is Dan Brown.....The only difference between us is that I generally stick to reading non-fiction......
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I read some non-fiction. LOVE reading about the body, especially the brain!! I don't read sci-fi at all, or romance, but don't mind a kiss or two.
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Speaking of a kiss or two...if you happen to read 50 Shades of Gray...you will give me details, won't you?
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I thought this was a fascinating article when I first read it. I'm a total math geek, I love reading about fractals and chaos theory and all that stuff. The fact that it is applicable to a cancer model makes total sense.
I think I will need to c&p the whole thing since you need a (free) medscape account to read it.
http://www.medscape.com/viewarticle/759877
One Biopsy Not Enough to Reveal Genetic Landscape of a Tumor
Zosia Chustecka
March 8, 2012 - A small study that shows a surprising complexity of genetic changes within a single tumor has far-reaching implications for the march toward personalized cancer therapy, according to researchers.
When the researchers examined 10 biopsies taken from a single kidney cancer, they found "an extraordinary amount of diversity" in the genetic changes that had taken place in different parts of the tumor. "There were more differences between biopsies from the same tumor at the genetic level than there were similarities," said senior author Charles Swanton, MD, PhD, from the Cancer Research UK, London Institute, and the University College London, United Kingdom.
The findings, published in the March 7 issue of the New England Journal of Medicine, were highlighted at a London press conference organized by Cancer Research UK, which funded the study.
The team also found differences in genetic changes between the primary tumor and metastases that developed both locally and at a distant site (in the chest wall). Similar findings have been documented by other research groups. Specifically, marked changes have been demonstrated between the primary tumor and metastases in breast cancer, which have led to calls for biopsies to be taken of the metastases.
What is surprising in this study is the extent of intratumoral heterogeneity, the researchers note.
The findings have far-reaching implications for the efforts currently being directed toward personalized cancer therapy, in which therapy is targeted at genetic changes identified in tumor tissue. An example of this is the SnaPshot broad genetic screen program being used in routine clinical practice at the Massachusetts General Hospital in Boston.
However, Dr. Swanton cautioned that "if you take only 1 biopsy, you could be misled clinically."
"The simple view of directing therapy on the basis of genetic tumor markers is probably too simple," agrees Dan Longo, MD, deputy editor of the New England Journal of Medicine, in an accompanying editorial.
"A whole new world has been anticipated in which patients will undergo a needle biopsy of a tumor in an outpatient clinic, and a little while later, an active treatment will be devised for each patient on the basis of the distinctive genetic characteristics of the tumor," Dr. Longo writes.
However, a serious flaw in this imagined future of oncology is the underestimation of tumor heterogeneity, he notes. "Not just heterogeneity between tumors, which is a central feature of the new image of personalized medicine, but heterogeneity within an individual tumor," he adds.
The study evolved out of research into kidney cancer and the E-PREDICT trial, which was aiming to find a biomarker that would predict response to everolimus (Afinitor, Novartis), explained coauthor James Larkin, MD, PhD, consultant medical oncologist at the Royal Marsden Hospital in Surrey, United Kingdom. In that trial, patients underwent a 6-week course of treatment with everolimus; after a week-long washout period, they underwent a nephrectomy. Several biopsies were taken from the primary tumor and from metastases both before and after treatment with everolimus.
The team analyzed the cancer genome in biopsy samples taken from 4 patients. For 2 patients, the analysis involved whole-exome multiregional spatial sequencing of DNA extracted from the biopsy samples; for the other 2 patients, a less expensive process was used, Dr. Swanton explained.
In total, 30 biopsies were taken from 4 primary tumors, and the genome analysis revealed that 26 of these 30 biopsies were different, he said.
In total, 118 different genetic mutations were identified. Some of these were "ubiquitous" mutations (n = 40), which were found in all of the biopsies from the primary tumor and from the metastases, but there were also some shared mutations (n = 53), which were found only in some primary tumors and/or only in some of the metastases. In addition, the researchers found some mutations that they described as "private mutations" (n = 25), which were found only in a single biopsy.
The researchers also noted that gene-expression signatures associated with a good prognosis and those associated with a bad prognosis were detected in different regions of the same tumor.
When the researchers modeled the genetic changes, they found an evolution pattern that resembles the trunk and branches of a tree. The tumor began with a number of genetic changes that developed early on in the "trunk"; over time, different groups of cells evolved different genetic changes and formed different "branches" of the cancer's evolutionary tree.
Another key finding was that different regions of the tumors had different faults in the same genes, corresponding to separate evolutionary changes (as occurs in convergent evolution).
At the press conference, Dr. Swanton likened this evolutionary tree pattern of genetic changes within the tumor to Darwin's descriptions of the evolution of species, and showed his team's diagrams alongside a diagram from Darwin's notes - both showed similar tree patterns with branches.
"For the first time, we've been able to use the pattern of genetic faults in a tumor to trace the origins of certain populations of cancer cells in much the same way that Darwin used his 'tree of life' theory to show how different species are related," Dr. Swanton explained.
This theory is in stark contrast to current cancer theories being taught in medical schools, Dr. Swanton said. A mainstay of the medical school curriculum is that cancer is a clonal disease that evolves in a linear fashion, with mutations arising in a sequential fashion. "This is what...is guiding our research, but this theory is driven by a single biopsy from a tumor," he said.
However, this revolutionary way of thinking about cancer is based on a very small sample size. "We only analyzed 4 patients," Dr. Swanton acknowledged. More work is needed, and is already underway as part of Cancer Research UK's Genomics Initiative.
Nevertheless, the theory could explain a number of clinical observations, Dr. Swanton said. Targeted agents that have already succeeded in the treatment of cancer could be acting on genetic mutations that occur early in the evolution - in the trunk of the tree, he explained. Examples of such agents are trastuzumab (Herceptin) for HER2-positive breast cancer and the EGFR inhibitors erlotinib (Tarceva) and gefitinib (Iressa) in the treatment of nonsmall-cell lung cancer.
Dr. Swanton is concerned that some of the newer drugs targeting new mutations will be acting only on the branches, so will not have a big impact on the cancer. "Just because a mutation is there doesn't mean that you are going to see a robust response when you target it," he told Medscape Medical News.
Also, different cancers could be imagined as having different tree shapes. Some would have a long trunk and short branches, like a palm tree; these could be dealt a deadly blow by a hit to the trunk, perhaps like vemurafenib (Zelboraf) acting on BRAF mutations in some cases of melanoma. "It may also explain why surgery to remove the primary kidney tumor can improve survival by decreasing the likelihood that resistant cells will...regrow the tumor after treatment," Dr. Swanton said.
Other cancers would have a very short trunk and many branches, perhaps like pancreatic cancer, which is notoriously difficult to treat and has not responded well to any targeted therapies.
"This research is going to change the way that we analyze cancers," predicted Peter Johnson, MD, chief clinician at Cancer Research UK, who also spoke at the press conference. "We are clearly only at the beginning of this process." The findings highlight the extreme complexity of cancer genetics, but they also point to a way forward despite this complexity, he said. "They suggest a way to improve the success rate of personalized medicine."
Dr. Swanton and several of his coauthors report receiving research grants from Novartis.
N Engl J Med. 2012;366:883-892,956-957. Abstract, Editorial
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MJLToday - Thanks for posting that. I remembered reading it somewhere, but couldn't remember where. It's fascinating how complex cancer is and rather depressing, too. Research has so far to go to make a dent in cancer deaths, but at least scientists are starting to get a glimmer of what it's going to take.
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Great article, that is why I hate just ONE tumour sample for biopsy!! I always wondered, what if they hit the part that didn't happen to have any active cancer cells in it?
! Also, smart to use kidney cancer as it is SO extremely slow growing. This will be interesting.....
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I stumble onto these threads that are in active topics and am not going to go back and read everything...obviously this one has stirred up a lot of interest since it was only started Mar 20 and it already 5 pages long. In my opinion, I do feel that the early detection of mets makes a difference....early would most likely mean not as advanced and maybe not as large and in the case of cancer less is better.
Mine had been going on for awhile before it was detected so it was not only in my bones, but also my lung and liver. That was in 1998 and I am still here so I feel very fortunate, but believe me I would have been much happier had it been found a year or so earlier when it was still only in my sternum. ( that was where I had been having pain and that went on for about two years before my former onco even did a bone scan)
So far as survival rates being better with early detection, I can't say. One would think if it was discovered early, the survival rate would be better, but mine was discovered late and I am still around. There are so many variables when it comes to cancer that it's difficult to classify a statement as true or false, black or white. One treatment works for one and not necessarily another with the exact same diagnosis.
I have never understood this term survivor anyway.....what's it mean?....to have survived cancer, to still be alive, what? I was in a breast cancer presentation they did several years ago where they asked for breast cancer survivors and I responded and said that I was still alive so if that qualified me as a survivor, I guessed I was and would be happy to be a part of their program and share my story. They accepted me so I guess being alive qualified me.
I think the earlier they discover the problem, the sooner they can start treating it so again in my opinion early detection is a good thing. Marybe
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From my limited experience and knowledge (so please correct me if I've got this wrong), it seems to me that survival has far more to do with an individual's luck in stumbling across their own, personal magic bullet. So someone with quite advanced mets (e.g. in multiple organs), who gets lucky with their first treatment could get to NED quickly and stay there for years. But someone diagnosed with less widespread mets initially who goes through numerous treatments without finding the one to really knock things back could progress and deteriorate more rapidly. Crap shoot... Which is why tailor-made treatments for individuals has to be the way forward.
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This reminds me of a story my onc just told me. A few years ago he "inherited" a patient from another state. He was shocked to see that she had been on Megace for 10 years, but when he looked over her file he learned that she had had mets throughout her body when she was first put on it and they had literally melted away. He gradually weaned her off the Megace and she is still NED to this day. Those are definitely the kind of mets I want! lol
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