# Why do we get melanoma later in life? **URL:** \ **Category:** Factual Questions\ **Created:** [December 12, 2012, 9:09am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815 "2012-12-12T09:09:11Z")\ **Posts on this page:** 20\ **Page:** 1
**Author:** ![firepanda](https://avatars.discourse-cdn.com/v4/letter/f/ed655f/32.png) [@firepanda](https://boards.straightdope.com/u/firepanda)\ **Post date:** [December 12, 2012, 9:09am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/1 "2012-12-12T09:09:11Z")
All right, first post, so please be nice. 🙂 UVB and UVA are both carcinogenic, although they do work differently. If you are exposed to large amounts of these during adolescence, you have an increased chance of getting cancer. However, the vast majority of people get cancer around 60. My question is, what’s up with the delay? Why do you get exposed to a mutagen and, 40 years later, get the tumours going? Does the cancer, lurk in your bloodstream, waiting for the right time? ---
**Author:** ![naita](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/naita/32/5862_2.png) [@naita](https://boards.straightdope.com/u/naita)\ **Post date:** [December 12, 2012, 9:50am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/2 "2012-12-12T09:50:35Z")
> [@firepanda](#): > > All right, first post, so please be nice. 🙂 > > UVB and UVA are both carcinogenic, although they do work differently. If you are exposed to large amounts of these during adolescence, you have an increased chance of getting cancer. However, the vast majority of people get cancer around 60. > > My question is, what’s up with the delay? Why do you get exposed to a mutagen and, 40 years later, get the tumours going? Does the cancer, lurk in your bloodstream, waiting for the right time? Only for some weird definition of “vast majority”: > **[Melanoma skin cancer incidence statistics](https://www.cancerresearchuk.org/health-professional/cancer-statistics/statistics-by-cancer-type/melanoma-skin-cancer/incidence)** > > The latest melanoma skin cancer incidence statistics for the UK for Health Professionals. See data for sex, age, trends over time and more. Actual data shows skin cancer rates rise steadily with age. ---
**Author:** ![KarlGauss](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/karlgauss/32/3713_2.png) [@KarlGauss](https://boards.straightdope.com/u/KarlGauss)\ **Post date:** [December 12, 2012, 10:22am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/3 "2012-12-12T10:22:16Z")
[For many cancers, there is a presumed sequence of development whereby more and more genetic mutations accumulate over time](http://en.wikipedia.org/wiki/Carcinogenesis#Multiple_mutations). Simply put, the more time that’s passed, the more mutations will accumulate. Eventually, it’s believed that a critical threshold of mutations is passed and the cancer ‘begins’. As to why there are ‘more and more’ mutations as time goes on, in part it’s simply statistics - the older you are, the more cell divisions there’ve been, and hence the more chances there have been for mutations to occur. Likewise, the older you are, the more (cumulative) exposure there’s been to natural causes of mutations such as radiation from sunlight and cosmic rays, from the earth’s interior, naturally occurring carcinogens, etc. ---
**Author:** ![Smeghead](https://avatars.discourse-cdn.com/v4/letter/s/f1d935/32.png) [@Smeghead](https://boards.straightdope.com/u/Smeghead)\ **Post date:** [December 12, 2012, 12:33pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/4 "2012-12-12T12:33:58Z")
> [@KarlGauss](#): > > [For many cancers, there is a presumed sequence of development whereby more and more genetic mutations accumulate over time](http://en.wikipedia.org/wiki/Carcinogenesis#Multiple_mutations). Simply put, the more time that’s passed, the more mutations will accumulate. Eventually, it’s believed that a critical threshold of mutations is passed and the cancer ‘begins’. Further, there is presumably a gap between when the cancer “begins” and when the doctor sits you down and says “I have some bad news…” ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [December 12, 2012, 1:05pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/5 "2012-12-12T13:05:06Z")
While the answers given make sense, in particular the accumulation of damage over the years, I wonder if the op might also end up having a different answer. Both aging and cancer are related to cellular senescence. It may be that understanding the mechanisms involved in normal aging will provide better understanding of cancer and that there is overlap between the processes - not restricted to the accumulation of mutations and damage over the years. That said I do not believe that understanding yet exists. ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [December 12, 2012, 1:40pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/6 "2012-12-12T13:40:34Z")
Quickly searching some one area I can find of overlap is focused on the mitochondria. [One, in relation to aging (“Aging: The Biology of Senescence”)](http://www.ncbi.nlm.nih.gov/books/NBK10041/): > [@](#): > > The mutation rate in mitochondria is 10–20 times faster than the nuclear DNA mutation rate (Johnson et al. 1999). It is thought that mutations in mitochondria could (1) lead to defects in energy production, (2) lead to the production of ROS by faulty electron transport, and/or (3) induce apoptosis. Age-dependent declines in mitochondrial function are seen in many animals, including humans (Boffoli et al. 1994). A recent report (Michikawa et al. 1999) shows that there are “hot spots” for age-related mutations in the mitochondrial genome, and that mitochondria with these mutations have a higher replication frequency than wild-type mitochondria. Thus, the mutants are able to outcompete the wild-type mitochondria and eventually dominate the cell and its progeny. Moreover, the mutations may not only allow more ROS to be made, but may make the mitochondrial DNA more susceptible to ROS-mediated damage. [Two](http://www.nature.com/onc/journal/v25/n34/abs/1209607a.html), in relation to cancer (“Mitochondrial mutations in cancer”): > [@](#): > > The metabolism of solid tumors is associated with high lactate production while growing in oxygen (aerobic glycolysis) suggesting that tumors may have defects in mitochondrial function. The mitochondria produce cellular energy by oxidative phosphorylation (OXPHOS), generate reactive oxygen species (ROS) as a by-product, and regulate apoptosis via the mitochondrial permeability transition pore (mtPTP). … Therefore, mtDNA mutations in tumors may fall into two main classes: (1) severe mutations that inhibit OXPHOS, increase ROS production and promote tumor cell proliferation and (2) milder mutations that may permit tumors to adapt to new environments. The former may be lost during subsequent tumor oxygenation while the latter may become fixed. Hence, mitochondrial dysfunction does appear to be a factor in cancer etiology So it may be that both normal aging and an increasing predisposition to cancer with age are the result of common processes. ---
**Author:** ![Smeghead](https://avatars.discourse-cdn.com/v4/letter/s/f1d935/32.png) [@Smeghead](https://boards.straightdope.com/u/Smeghead)\ **Post date:** [December 12, 2012, 3:14pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/7 "2012-12-12T15:14:13Z")
It is certainly clear that oxidative damage accumulates as we age. That’s been known for years. Whether it’s due to leaky mitochondria, or decreased activity of ROS scavenging enzymes, or some other mechanism isn’t entirely clear. But these molecules can and do damage DNA, amongst other molecules, and that damage builds up as we get olde. ---
**Author:** ![Michael63129](https://avatars.discourse-cdn.com/v4/letter/m/3da27b/32.png) [@Michael63129](https://boards.straightdope.com/u/Michael63129)\ **Post date:** [December 12, 2012, 6:58pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/8 "2012-12-12T18:58:36Z")
One thing I have wondered is why animals like mice and rats are so cancer-prone when they don’t live that long; there simply isn’t much time for mutations to accumulate. Even when you consider their rate of aging, they surely have fewer cell divisions than a human over their lifetime. ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [December 13, 2012, 2:50am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/9 "2012-12-13T02:50:55Z")
That is a very interesting point **Michael63129**. In fact mice and humans [both](http://users.physics.harvard.edu/~wilson/publications/ppaper805.pdf) get cancer at the same fraction of their maximal lifespan: > [@](#): > > The data from the ED01 study show unequivocally that > cancer age-specific incidence in mice, assumed to be well > correlated with age-specific cancer mortality and morbidity, turns over after about 800 days for all tumour sites and > doses discussed except for the highest doses. Because of the > reliance on mortality and morbidity data, the data are > limited to those sites where the cancer is fatal and near > fatal. The age (about 800 days) of maximum incidence is > about 80% of the maximum age. This may be compared to > the age at peak incidence of people of about 85 years, > which is also about 80% of maximum lifetime. So cancer and aging do not accumulate linearly with time, but do co-vary. It therefore follows that if both are a result of accumulated insults/damage (oxidative or otherwise) then they both depend at least as much on DNA repair/protection mechanisms that vary greatly between species of different lifespans. Or the insult/damage model is not the whole story and alternatively there are mechanisms that have been evolutionarily _selected_ to occur that cause an individual past reproductive age (and past additional benefit greater than cost to subsequent gene copies being passed on) that limit lifespan, cause aging, and increase cancer risk. ---
**Author:** ![Lasciel](https://avatars.discourse-cdn.com/v4/letter/l/e79b87/32.png) [@Lasciel](https://boards.straightdope.com/u/Lasciel)\ **Post date:** [December 13, 2012, 3:01am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/10 "2012-12-13T03:01:47Z")
> [@DSeid](#): > > That is a very interesting point **Michael63129**. In fact mice and humans [both](http://users.physics.harvard.edu/~wilson/publications/ppaper805.pdf) get cancer at the same fraction of their maximal lifespan: > So cancer and aging do not accumulate linearly with time, but do co-vary. It therefore follows that if both are a result of accumulated insults/damage (oxidative or otherwise) then they both depend at least as much on DNA repair/protection mechanisms that vary greatly between species of different lifespans. Or the insult/damage model is not the whole story and alternatively there are mechanisms that have been evolutionarily _selected_ to occur that cause an individual past reproductive age (and past additional benefit greater than cost to subsequent gene copies being passed on) that limit lifespan, cause aging, and increase cancer risk. That’s really interesting. There have been experiments with mice I believe where they were put on starvation diets to prolong their lives (I’d rather die young, thanks) - do you know whether they tested those mice for incidents of cancer, and whether the timing of those matched the baseline mouse lifespan, or the longer skinnymouse lifespan? ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [December 13, 2012, 3:29am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/11 "2012-12-13T03:29:31Z")
I did not know but a quick search shows [this](http://www.sciencedirect.com/science/article/pii/S0047637405001478): > [@](#): > > The present study aimed to evaluate, on a particular strain of mice, the efficacy of alternate-day fasting on the mitochondrial production of free radical species and on the incidence of a specific cancer (lymphoma) in aged mice. Alternate fasting, that was initiated in middle age mice through a 4 month period, reduced significantly the incidence of lymphoma (0% versus 33% for controls). No remarkable difference was observed in the overall food consumption between alternate-fed (AF) and ad libitum (AL) mice, suggesting that the efficacy of alternate fasting did not really depend on calorie restriction. and [this](http://cancerres.aacrjournals.org/content/59/7/1642.short) > [@](#): > > caloric restriction (CR), which is known to oppose cancer development and increase maximum life span in rodents … CR from middle age increased longevity, the age at which tumor-bearing mice died, and the percentage of mice dying with cancers, suggesting that CR may retard promotion and/or progression of existing lymphoid cancers. … (Please note the same did not hold true in the recent primate models. But that is another subject.) ---
**Author:** ![firepanda](https://avatars.discourse-cdn.com/v4/letter/f/ed655f/32.png) [@firepanda](https://boards.straightdope.com/u/firepanda)\ **Post date:** [December 13, 2012, 10:34am UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/12 "2012-12-13T10:34:12Z")
Erghk. Thanks guys. Biology is so complicated… 😕 ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [December 13, 2012, 12:45pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/13 "2012-12-13T12:45:58Z")
Sorry if my response at least was less than clear. Your specific example though illustrates why there has to more to it than exclusively the accumulation of damage over time - melanoma has a peak of new cases in the 60s (as you stated and as illustrated in the link provided by **naita** - but the risk for melanoma is mainly determined by exposure early in life. The oft quoted stat is that one blistering sunburn in childhood doubles melanoma risk compared to five blistering sunburns during adulthood to double the risk. The damage is mostly done early but does not come out until later. I am _guessing_ that we have pretty good detection and control systems that keep those potentially cancerous cells in check, and that eliminate any of those cells that begin to get out of control, but that begin to lose efficacy as we age … i.e. not as much that there is so much more cancer cell producing damage occurring as that our ability to monitor/contain the results of that damage deteriorates with age - resulting both in the aging process itself and in increased cancer risk. And that loss of monitoring/containment ability is to some large degree intrinsic to any particular species. ---
**Author:** ![Michael63129](https://avatars.discourse-cdn.com/v4/letter/m/3da27b/32.png) [@Michael63129](https://boards.straightdope.com/u/Michael63129)\ **Post date:** [December 13, 2012, 7:45pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/14 "2012-12-13T19:45:50Z")
> [@DSeid](#): > > I did not know but a quick search shows [this](http://www.sciencedirect.com/science/article/pii/S0047637405001478): > and [this](http://cancerres.aacrjournals.org/content/59/7/1642.short)(Please note the same did not hold true in the recent primate models. But that is another subject.) On the other hand, a smaller body size within a species, [including humans](http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071721/) (why do women live longer and have lower rates of CHD? Mostly because they are smaller than men, according to this paper, which also suggests that caloric restriction increases lifespan due to a smaller body size), is highly correlated to a reduced risk of chronic diseases, including cancer, possibly because a smaller body requires less upkeep (cell divisions, repair). ---
**Author:** ![Ann\_Hedonia](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/ann_hedonia/32/319_2.png) [@Ann\_Hedonia](https://boards.straightdope.com/u/Ann_Hedonia)\ **Post date:** [December 13, 2012, 9:14pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/15 "2012-12-13T21:14:43Z")
Sunburn is an interesting subject. I picked up the tidbit below form Sam Kean’s book The Violinist’s Thumb UV radiation damages the double helix shaped DNA strands in a very specific manner. Wherever there are two thymine bases side by side, UV radiation fuses them together at an angle. This kinks up the DNA strand causing redness and burning. If the strand gets really kinked it will break at points. The DNA is good at self-repair if the break is on one side of the double helix strand. When both sides of the strand break the repair is less precise, especially if there are a lot of repairs from a severe sunburn. In these instances base pairs can be replaced incorrectly or deleted ( shortening the strand), causing mutations. These mutations are not always cancerous but they do accumulate over time. This is also interesting in terms of excessive sun exposure causing early aging at the cellular level. Telomeres are the non-coding repetitve strands that mark the end of each chromosone. Research into aging has shown that the telomeres shorten with age – ( this is a BIG problem with cloning, animals cloned from adult cells have shorter telomeres which decreases life-span ) The repetitive sequence that makes up the telomeres includes 2 adjacent Thymine pairs … the human telomere sequence is TTAGGG. Damage to the T bases in telomeres can result in them being shortened during repair, causing the cell to age faster ---
**Author:** ![Lasciel](https://avatars.discourse-cdn.com/v4/letter/l/e79b87/32.png) [@Lasciel](https://boards.straightdope.com/u/Lasciel)\ **Post date:** [December 13, 2012, 9:28pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/16 "2012-12-13T21:28:44Z")
> [@DSeid](#): > > I did not know but a quick search shows [this](http://www.sciencedirect.com/science/article/pii/S0047637405001478): > and [this](http://cancerres.aacrjournals.org/content/59/7/1642.short)(Please note the same did not hold true in the recent primate models. But that is another subject.) Thank you very much, that was quite interesting! ---
**Author:** ![Hermitian](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/hermitian/32/470_2.png) [@Hermitian](https://boards.straightdope.com/u/Hermitian)\ **Post date:** [December 13, 2012, 9:53pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/17 "2012-12-13T21:53:47Z")
> [@naita](#): > > Only for some weird definition of “vast majority”: > > [Melanoma skin cancer incidence statistics | Cancer Research UK](http://www.cancerresearchuk.org/cancer-info/cancerstats/types/skin/incidence/uk-skin-cancer-incidence-statistics#age) > > Actual data shows skin cancer rates rise steadily with age. Those statistics were from the UK. It is widely known that the UK hasn’t seen a sunny day since 1973. ---
**Author:** ![naita](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/naita/32/5862_2.png) [@naita](https://boards.straightdope.com/u/naita)\ **Post date:** [December 14, 2012, 1:49pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/18 "2012-12-14T13:49:17Z")
> [@Hermitian](#): > > Those statistics were from the UK. It is widely known that the UK hasn’t seen a sunny day since 1973. According to my sources you can get a tan from standing in the English rain. If it can give you a tan it ought to have similar cancer-causing effects as sunlight. 😃 ---
**Author:** ![DSeid](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/dseid/32/20194_2.png) [@DSeid](https://boards.straightdope.com/u/DSeid)\ **Post date:** [December 14, 2012, 2:22pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/19 "2012-12-14T14:22:00Z")
The possibilities that the emergence of cancer with aging is a) to some degree a consequence of the same normal programming, possibly evolutionarily selected for programming, that causes normal aging and b) a consequence to a great degree of diminished function (with age) in how systems identify and eliminate misbehaving always extant precancerous cells, keeping their numbers in check and eliminating the most dangerous ones before they turn into full blown cancer cells and spread, more so perhaps than even how many of those precancerous cells there are suggests to me a somewhat different focus for future research than has, to my non-expert eye, than has been emphasized to date. I wonder what work has been done on those areas? ---
**Author:** ![Smeghead](https://avatars.discourse-cdn.com/v4/letter/s/f1d935/32.png) [@Smeghead](https://boards.straightdope.com/u/Smeghead)\ **Post date:** [December 14, 2012, 4:24pm UTC](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815/20 "2012-12-14T16:24:40Z")
I think aging and cancer is very much an active area of research. I helped out on a study many years ago looking at sort of the flip side, which was figuring out the cause of childhood cancers. Childhood cancers tend to be very different from adult cancers, and there’s not a whole lot of overlap between them. I tested some samples of heel-stick blood from newborns who later developed childhood lymphomas. It turned out that many of them had been born with one of the characteristic genetic defects associated with this type of lymphoma. This suggested that perhaps there’s a period during pregnancy and development where the infant genome is particularly susceptible to at least some types of chromosomal rearrangements. They can easily pick up one of the mutations required for cancer, making it more likely that they’ll develop it down the line. Anyway, the point is that researchers have been paying attention to the age factor for a good long time. [Next page](https://boards.straightdope.com/t/why-do-we-get-melanoma-later-in-life/643815.md?page=2)