study: why we get cancer: Plain old bad luck per Johns Hopkins

I think this is too simplistic. I am sure everyone has random mutations but their immune systems eat up the faults. When immunity is low (from stress or environment) the mutations proliferate before they can be stopped. That is bad luck since no one can really deflect faulty immune systems most of the time but for scientists to call something like this bad luck is just weird. IMO

From the article posted by SpecialK, breast cancer was not included in this study.

Neither breast nor prostate cancers were included in the study because there are no satisfactory data on the stem cell division rates for these tissue types. The estimation for breast tissue is particularly complex because the rate of division is not linear with time (as it is for colon and other tissues).

As the study notes, the greater the number of cell divisions, the greater the possibility of a mutation. That is why, in general, Cancer is a disease associated with aging. I think the human inclination is to want to find a cause for the disease so that we can eliminate the cause and avoid Cancer altogether. Humans hate the notion that bad things happen randomly. For us breast cancer patients, this study, while not including our brand of cancer, does push researchers to find a cure rather than focusing on innumerable variables that likely have nothing to do with our disease. For instance instead of money going for studies to determine if things like PBA in plastic are related to cancer, maybe the money can go towards identifying and treating mutations that cause cancer.

I buy that it's mostly bad luck, some environmental and some stress, so the 2/3 ratio sounds about right. Aging however, no. Look at how many children are diagnosed with cancer...and I was 30 when diagnosed with breast cancer and know several more diagnosed even younger with all types of cancer. Not for a second do I buy that you can prevent it with a clean lifestyle. Don't we all know someone who lived to a ripe old age in spite of smoking like a chimney and a sustained diet of junk? Absolutely bad luck is part of it. Bevin, I agree too, that's why I enjoyed reading the article...very simplistic. Some things just don't need to be over- complicated. They are what they are.

Thanks. Good look behind all the hype.

To clarify. The "chemo working/not working" is my own personal definition. I'm sure oncs look at it differently. If you're disease free or stable for 3 or 6 months, big whoop. I'd be willing to bet that would probably happen without chemotherapy. I will always think cancer is a crap shoot.

http://www.euro.who.int/en/health-topics/noncommun...

Most types of cancer not due to bad luck
14-01-2015

The International Agency for Research on Cancer (IARC), WHO's specialized cancer agency, strongly disagrees with the conclusion of a scientific report on the causes of human cancer by Dr Cristian Tomasetti and Dr Bert Vogelstein, published in the journal "Science" on 2 January 2015 and widely reported in the mass media.

The study suggests that random mutations (or "bad luck") are the major contributors to cancer overall, often more important than either hereditary or external environmental factors.

"We already knew that, for an individual to develop a certain cancer, there is an element of chance, yet this has little to say about the level of cancer risk in a population," explains IARC Director Dr Christopher Wild. "Concluding that 'bad luck' is the major cause of cancer would be misleading and may detract from efforts to identify the causes of the disease and effectively prevent it."

According to current knowledge, nearly half of all cancer cases worldwide can be prevented.

http://www.iarc.fr/en/media-centre/pr/2015/pdfs/pr...

I have to say that I wonder about that percentage as well. Most of the people I know who have/had cancer lead/led pretty healthy lives. And even in the case of a few women I've known who died in their early 50s from lung cancer (smokers, yes) you do have to wonder why they contracted cancer at a relatively young age when so many others smoke for several more decades before cancer or emphysema or heart disease strikes.

I believe that breast cancer cannot be prevented, everyone wants to know why this happens but this disease existed long before plastics and other carcinogens.  I think there are some cases of cancer that do occur because of these things but I highly doubt that we could prevent almost 50% of the cancer cases.  I started to go down the road of diet being a major factor but I have found too many examples which were contradictory.  I am not saying that medical science should stop searching for answers, I just think that the answer is more in our genetics or in the fallibility of being a human (maybe this what they are trying to say is bad luck?) then it is in our environment and our food. 

http://www.womensforum.com/who-discovered-the-first-case-of-breast-cancer.html  (This short article talks a little about the history of breast cancer.  They do make the mistake of stating "Preventing Breast Cancer Through Awareness" , so far we can be aware but I don't think we can prevent.)

 

I was definitely going through a stressful 6 months prior to finding my lump, and I do tend to bottle things up. I have always felt this somehow contributed, but who knows

And yet more thoughts and analysis on the original article, this from a Harvard professor...

http://www.bostonglobe.com/opinion/2015/01/15/canc...

Here's another interesting article that makes me think that some cancers may be caused at least in part by exposure to substances no one has yet to fully investigate.

http://www.apha.org/policies-and-advocacy/public-h...

And yes, bevin, I think the statement about guilt is very true. Clearly some people don't want to acknowledge the possibility cancer can be prevented because they somehow experience that as judgment or blame or self-blaming. I don't see it that way, but who's to say anyone's way of dealing with this crappy dx is any better than anyone else's? We just all do the best we can at making sense of it.

This analysis by Jon Barron is one of the best yet. http://jonbarron.org/cancer-alternative-cancer-the...

Does Lifestyle Matter to Prevent Cancer or Is It Just All "Bad Luck"?

Published: February 12, 2016

The impressive progress in understanding cancer cell biology as well as access to human genome sequencing (now feasible on routine samples) has profoundly transformed oncology. Numerous novel therapies have emerged as a result, particularly small molecules often referred to as "biologicals" or "targeted therapies," which not only show activity in chemorefractory patients, but may also replace standard chemo in some situations in the future. Similarly, the ability to look at the broad genetic landscape of many types of cancer has shed light on the huge molecular diversity of the disease, both among patients and even within one individual (through baseline clonal heterogeneity and/or clonal evolution).

Every tumor harbors thousands of genetic (and epigenetic) alterations that are not present in the patient's germline DNA. The molecular complexity of cancer is daunting (over 3 million somatic mutations reported) making it difficult to "read the culprit." It is clear nowadays though that all mutations are not equal. Only a very small fraction of these alterations are in "driver genes," which when mutated lead to growth advantage over surrounding cells.

Meanwhile, numerous somatic mutations, which accumulate during the long process of tumorigenesis, appear "neutral" and are therefore referred to as "passenger" mutations. Comprehensive studies have shown that only about 200 genes (out of 20,000 in the human genome) can function as drivers when mutated. These driver genes are involved in 12 signaling pathways, which understandably regulate core cellular processes: cell fate and survival, proliferation and genome maintenance. A typical tumor contains 2 to 8 of these "driver genes," the rest being all passenger mutations.

The original theory over 30 years ago was that cancer was just the result of the random accumulation of successive mutations leading to cancer phenotype. We now have a better understanding of the sequence of events, particularly regarding the timing of these mutations, their impact, and some of the factors involved that might cause them.

Timing of Somatic Mutations

Tumors evolve with a multistep process—from benign to malignant lesions—which has been particularly well studied in colorectal cancers. The first, or, "gatekeeping," mutation provides a selective growth advantage to a normal epithelial cell, allowing it to outgrow its surrounding cells and become a microscopic clone.

The "founding" or "breakthrough" mutations in colon cancer most often affect the adenomatous polyposis coli (APC) pathway, particularly the APC gene and lead to the classical polyp or adenoma (seen in routine colonoscopies). The next step occurs when a second mutation in another gene—often KRAS—unleashes a second round of clonal expansion. This process of mutation/clonal expansion continues, with additional mutations in several other key genes, eventually generating a malignant tumor that becomes invasive and can metastasize to lymph nodes and distant organs, such as the liver, consistent with the picture of advanced stage colon cancer as we know in the clinic.

This process takes decades with each driver mutation providing only a small selective growth advantage; however, this slight increase, repeated once or twice per week, can result in a large mass, containing billions of cells. The multistep process is the same across all cancers, though the number of mutations varies with age and tissue type.

In organs with significant self-renewal compartment (to continuously replenish gastrointestinal lining, for example), the number of mutations observed is much higher compared with pancreatic or brain tumors. Also a colon cancer in a 90-year-old patient has twice as many mutations as a morphologically identical colorectal cancer in a 45-year-old patient (making them likely more resistant to treatment). In summary, the driver mutations process typically starts decades before the diagnosis with accumulation of a "sufficient" number of driver mutations and a highly variable (based on tissue and age) number of passenger mutations along the way.

Are the Mutations Just Random or Affected By Lifestyle?

Researchers at Johns Hopkins, in their effort to understand why some cancers are more likely to occur than others, concluded that in about two-thirds of cancer tissue types investigated, the development of cancer could be largely explained by the "bad luck" of random mutations that arise during DNA replication in normal nonmalignant stem cells of a given organ. According to this theory, cancer arises when stem cells go out of control and are not due to external factors. Needless to say, Tomasetti and Vogelstein's paper published last year in Science (2015;347[6217]:78-81), generated instant reaction and even some criticism due to the concern their theory might dismiss important cancer prevention efforts.

However, a new study just out in Nature (2016;529[7584]:43-47) might contradict the "bad luck" theory of cancer. Researchers at Stony Brook University in New York took another look at the data used by Tomasetti and Vogelstein. They noted that even taking into account the total number of stem cell divisions, some cancers were still more likely to occur than others. They found that for many cancers, including some of the most common ones, about 10% of the risk was traceable to random copying errors. More common cancers, they inferred, must have some additional external causes, such as the environment or lifestyle-related factors. Extensive epidemiological data support the role of the environment in cancer from carcinogens, to excess UV exposure or smoking. For example, lung cancers in smokers have 10 times as many somatic mutations as those from nonsmokers. Obesity and BMI definitely affect cancer incidence across many cancer subtypes, through complex mechanisms linked to chronic inflammation, cytokines, hormonal disturbances, and insulin resistance.

The benefit of physical exercise on the outcome of cancer patients has been shown in both solid tumors and blood cancers, including in some studies an improvement of overall survival. In our center, an exercise plan is now part of standard care recommendation. The mechanisms involved in the protective effects of exercise and nonsedentary lifestyles are definitely beyond this column but are well recognized by the medical community.

Though opposed, the two theories discussed above are actually complementary. There is no question that there is a minority of drivers in cancer, and those happen early on and over decades. The current ability to focus on such driver mutations and the pathways they control has rendered complex genome landscapes intelligible and exploitable. This provides an opportunity to develop relevant usable "profiles" for targeted therapy combinations (aiming at cancer vulnerabilities/ Achilles' heels) and true precision medicine. I also believe a promising future strategy in cancer will be through very early detection based on the presence of clones (liquid biopsies) with enough potential "drivers" to intervene either with small molecules or more likely immunotherapy to prevent progression to a true or clinically patent cancer. While chance has a role in determining who gets cancer and who does not, it's very clear that lifestyle and environmental factors together within the context of our genes can change the odds considerably.

Obesity Promotes Cancer

http://www.medicalnewstoday.com/releases/306549.php