12 ms·

As we age, cancer rates go up as immune system winds down

313 points by okket 9y ago

throwaway521 9y ago
I-T-S A P-A-T-H-O-G-E-N Read Paul Ewald and Gregory Cochran
- reasonattlm 9y ago
  https://en.wikipedia.org/wiki/Immunosurveillance https://en.wikipedia.org/wiki/Immunosurveillance "Cancer immunosurveillance is a process by which an organism's immune system recognizes transformed cells in order to inhibit the growth of neoplastic tissue. It comprises the first phase of immunoediting and is also known as the elimination phase."
reasonattlm 9y ago
Paper: https://doi.org/10.1073/pnas.1714478115 https://doi.org/10.1073/pnas.1714478115 Which is a suggestive model, by the way, not direct evidence. The best direct evidence would be to restore the pace of immune cell creation - such as via regeneration of the thymus (via FOXN1, or BMP4, or tissue engineering), cell therapy to replace or increase the pool of hematopoietic stem cells, etc. - and then see what happens. This sort of thing is five years out; there are people working on it, though more of those and more funding would certainly be a good thing. It would certainly be possible to push forward a startup today based on thymic regeneration or hematopoietic stem cell transplantation; the science is more or less ready for it. -------- T cells develop from hematopoietic stem cells as part of the lymphoid lineage and have the ability to detect foreign antigens and neoantigens arising from cancer cells. In the thymus, lymphoid progenitors commit to a specific T cell receptor and undergo selection events that screen against self-reactivity. Cells that pass these selection gates then leave the thymus, clonally expanding to form the patrolling naive T cell pool. The vast majority of vertebrates experience thymic involution (or atrophy) in which thymic epithelial tissue is replaced with adipose tissue, resulting in decreasing T cell export from the thymus. In humans, this is thought to begin as early as 1 year of age. The rate of thymic T cell production is estimated to decline exponentially over time with a half-life of ∼15.7 years. Declining production of new naive T cells is thought to be a significant component of immunosenescence, the age-related decline in immune system function. With the recent successes of T cell-based immunotherapies, it is timely to assess how thymic involution may affect cancer and infectious disease incidence. It is clear from epidemiological data that incidence of infectious disease and cancer increases dramatically with age, and, specifically, that many cancer incidence curves follow an apparent power law. The simplest model to account for this assumes that cancer initiation is the result of a gradual accumulation of rare "driver" mutations in one single cell. Furthermore, the fitting of this power law model (PLM) can be used to estimate the number of such mutations. Exponential curves have also been used to fit cancer incidence data, resulting in worse fits than the PLM overall. Nevertheless, it is worth noting that exponential rates close to the declining curve for thymic T cell production can be seen to emerge from the incidence data, indicating the relevance of the thymic involution timescale. While the PLM fits well, it does not account for changes in the immune system with age. To better determine the processes underlying carcinogenesis, we asked whether an alternative model, based only on age-related changes in immune system function, might partly or entirely explain cancer incidence. Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data. Our hypothesis and results add to the understanding of infectious disease and cancer incidence, suggesting in the latter case that immunosenescence, rather than gradual accumulation of mutations, serves as the predominant reason for an increase in cancer incidence with age for many cancers. For future therapies, including preventative therapies, strengthening the functionality of the aging immune system appears to be more feasible than limiting genetic mutations, which raises hope for effective new treatments. -------
truculation 9y ago
If the immune system has finite resources, would reducing the lifetime drain on those resources by infectious diseases delay the age at which we can expect get cancer? For example, curing the common cold and/or developing a universal flu vaccine.
- vibrio 9y ago
  I'm not sure 'finite' is the right way to think about it. I'd be more inclined to think of infections acting to 'Exercise' the immune system, similar to how jogging keeps your heart healthy, rather than using up a limited number of immune cells.
- Retric 9y ago
  Reducing immune system load is fairly straightforward, low dose antibiotics is one approach that significantly reduces the effort put forth by the immune system. However, it does not seem to make a significant difference in lifespans.
- gojomo 9y ago
  Via mechanisms similar to either the hygiene hypothesis or hormesis, it's possible those might backfire. This is highly speculative, but: * the hygiene hypothesis suggests that allergies and auto-immune disorders can arise from having insufficient immune-system challenges, especially when young. Lacking the calibration from an 'expected' or 'optimal' level of dirt/allergens/infectious-diseases, the immune system starts doing unwanted self-destructive things. * hormesis is the observation that almost everything bad for you also turns out to be good in very-tiny exposures – radiation, poisons, cancer-causing chemicals, etc. It's as if tiny doses trigger beneficial self-repairs to occur even beyond the direct damage received, even as larger doses overwhelm that mechanism. Removing mild, survivable challenges from the environment could thus leave the immune system less 'tuned' for the full spectrum of challenges it faces (like clearing early cancers). It's an adaptive dynamic system with nonlinear effects, not a simple pool of fixed exhaustible capability.
  - rsync 9y ago
    "Removing mild, survivable challenges from the environment could thus leave the immune system less 'tuned' for the full spectrum of challenges it faces" Exactly. You want to protect people from, say, Rubella ... but I think we should proceed with caution with things like the cold and the flu ...
agumonkey 9y ago
Cue the senescence guys who aim to fix accumulated damages there.
- ShabbosGoy 9y ago
  Ultimately, I think it comes down to metabolism. As you age, your metabolism slows. Coenzymes like NAD+[0] are depleted. [0] https://www.nature.com/articles/nrneph.2017.5 https://www.nature.com/articles/nrneph.2017.5
  - glibgil 9y ago
    Right, so just back up a step and stop the metabolism from slowing
    - bluetwo 9y ago
      Medicinal Cocaine?
    - shrimp_emoji 9y ago
      Or cut the knot. Upload mind to digital facsimile. Die, per nature's capricious designs. Robo-you lives smugly without any of this nonsense and can be resurrected if the power cuts out and sent across the stars at light speed with no need for fuel or supplies--breathes ... to somewhere without air.
      - agumonkey 9y ago
        I don't get why people go after these virtual things
- glibgil 9y ago
  I mean, it bears repeating on account of the fact that senolytic treatments make a lot of other health problems seem like not even worth understanding
lisper 9y ago
One immediate problem with the hypothesis that cancer is caused by the loss of T cells with age is the fact that HIV also destroys T cells, and it is associated with increased risk of some types of cancer. But the cancers associated with HIV are different from those associated with aging. In particular, Kaposi sarcoma occurs 500 times more in HIV patients than the general population. So there must be something else going on besides just the loss of T cells.
- sungam 9y ago
  Agree. No doubt immunosenescence contributes to the increased rate of malignancy at older ages but the spectrum of cancers seen in immunosupressed individuals does not that match seen in the elderly.
- cma 9y ago
  Kaposi sarcoma is associated with Kaposi's sarcoma-associated herpesvirus even in the HIV cases though. It might be that losing the amount of T cells you lose with HIV or immunosuppression has a different effect than just losing some fraction of them with age with respect to that virus.
ransom1538 9y ago
I always think of these two monkeys[i] when I consider slowing down my age. [i] http://www.slate.com/articles/health_and_science/medical_examiner/2012/08/calorie_restriction_and_longevity_monkey_study_shows_hunger_doesn_t_increase_longevity_but_type_of_food_does_.html http://www.slate.com/articles/health_and_science/medical_exa...
- baxtr 9y ago
  This is really great! Thanks for the link. I think you should post it to HN
- musha68k 9y ago
  Thanks for sharing – always those poor monkeys though... An even stronger data point to me would be the actual people of Okinawa who are (were?) among the healthiest and oldest in the world. In addition to having a high quality diet and a rich social life in general, they are practicing “hara hachi bu” – the confucian tradition of always eating only until “about 80% full”. https://en.m.wikipedia.org/wiki/Hara_hachi_bun_me https://en.m.wikipedia.org/wiki/Hara_hachi_bun_me
- mysterypie 9y ago
  It's an interesting well-written article, but you realize that their main point was that it contradicts the earlier calorie-restriction study: "The Nature authors found no increase in lifespan; the calorically restricted animals lived no longer, statistically, than their well-fed cousins." They try to reconcile the studies: maybe it's the natural-ingredient foods vs the refined foods, maybe it's the generous diet vs the more-than-generous free-feeding, or conceding that the monkey's don't live longer, but they live healthier. IMO, the best paragraph from the article was this: "Many of us simply roll our eyes and click away when yet another medical study contradicts the last study—so what else is new? Coffee’s bad for you, until it’s good for you—and so is red wine. Antioxidants are essential, or they’re useless. And so on." Other than some very basic common sense things -- like don't eat rat poison -- I never find that these kinds of studies lead to correct and actionable information about how to slow down aging or how to lead your life. And it's extremely frustrating to even try.
sungam 9y ago
How do you account for the observation that incidence of cancer in young, immunosupressed individuals (e.g. solid organ transplant recipients), whilst increased, is no way comparable to that seen in elderly individuals?
- reasonattlm 9y ago
  Other age-related cell and tissue damage that raises the risk of cells becoming cancerous, or reduces the effectiveness of internal-to-the-cell controls that can shut down and destroy cancerous cells, would be the other variable, I'd imagine.
  - sungam 9y ago
    I think far more likely that the predominant variable is the expansion of mutant clones over time to occupy large fractions of the stem cell reservoir.
    - reasonattlm 9y ago
      Possibly so, which is a phenomenon that might explain how stochastic nuclear mutation at its given rates can possibly cause widespread enough harm to be significant. There is an interesting recent paper on that subject: https://doi.org/10.1371/journal.pgen.1007108 https://doi.org/10.1371/journal.pgen.1007108 "Recent single-cell studies point to the possibility that essentially all cells have unshared mutations in their genomes. In view of this extensive genetic diversity, it is perhaps not surprising that mutations that confer a proliferative advantage are readily detected as clonal populations of increasing abundance and size in the elderly. These clonal populations might lead to loss of organismal health through the functional decline of tissue and/or the promotion of disease processes, such as cancer. In this review, we summarize recent research that supports the notion that aberrant clonal expansion (ACE) resulting from cancer-associated mutations are common in noncancerous tissue and accumulate with age. We propose ACE to be a previously underappreciated aging phenotype that is universal in most organisms, affects multiple tissues, and likely helps explain why aging is the biggest risk factor for cancer."
HumanDrivenDev 9y ago
Really? I figured as we age our cancer rates will plummet while our immune systems only strengthen, which is why the leading cause of the death in the elderly is extreme sports.
- eliben 9y ago
  The alternative hypothesis was the "two-hit" idea of multiple changes accumulating in DNA over time, so it's not a trivial topic to study.
- acct1771 9y ago
  Extreme sports like "the stairs".
- josephv 9y ago
  I'm with you, upvoted for voicing the absurdity of the title. The article, which I refuse to read completely, seems like mediocre pop health science and this website has devolved into giving it, at this point at least 16 hours of frontpage time. I'll summarize it: "We don't understand cancer but we'll keep throwing shit at the wall until something sticks, and we're going to write up a bunch of shit and you shits read it so we can pay for throwing more shit."
kazinator 9y ago
The link between cancer and the immune system (the latter's role in defending against the former) is not all that clear. Here is a cancer.com (American Cancer Society) article on the relationship between AIDS and cancer. Source: https://www.cancer.org/cancer/cancer-causes/infectious-agents/hiv-infection-aids/hiv-aids-and-cancer.html https://www.cancer.org/cancer/cancer-causes/infectious-agent... Firstly, they say that "In fact, some types of cancer occur so often in people with AIDS that they are considered AIDS-defining conditions". But that's only certain specific cancers. Then there are some other cancers that occur often with AIDS but are not "AIDS-defining". And then there is the kicker: "Of course, as people with HIV are now living longer, they are also developing other cancers that are not clearly linked to HIV but are more common in older people, such as breast, colorectal, and prostate cancer.". So, these cancers go up in AIDS survivors due to age, even though those people have immune systems that were already shot years before. So much for a tidy hypothesis about aging -> lower immune system -> cancer, I suppose. As for why those afflicted with AIDS get certain cancers, one explanation (also given in above page) is that some cancers are caused by viral infections. Weakened defense against viral infections, increased cancer of that type.
Thriptic 9y ago
Isn't this a bit of an oversimplification? It's not like if you knock out p53 and something else you instantly get a metastatic tumor. Granted if you remove key tumor suppressor genes your probability of mutations persisting skyrockets, but that in itself doesn't create a dangerous tumor. You need many more mutations than 2 to be able to acquire the functionality to grow, persist, escape the local environment, and establish a foot hold in a new environment. Here is the classic review paper on tumor formation: http://www.cell.com/abstract/S0092-8674(11)00127-9 http://www.cell.com/abstract/S0092-8674(11)00127-9
samstave 9y ago
What are white blood cell counts in someone who is sixty vs one who is eighteen? Is this where the blood transfusion concept is strong? What is the oxygen-carrying-capacity of hemoglobin in old blood vs young blood?
thrownaway954 9y ago
I was told once (by who I don't remember): Live long enough and you will eventually get cancer. To me it's a no-brainer. You get old, cells break down, immune system isn't what it use to be, increasing the risk of that rouge new cell becoming cancerous.
commandlinefan 9y ago
I worked for a cancer research startup a few years ago - I was just doing IT stuff, but I worked with a lot of oncologist/cancer research types. One of the things that they often said was that every living organism will develop cancer eventually, but most things die of other causes before that happens.
- ngvrnd 9y ago
  it seems plausible or maybe even likely that everyone develops cancer many times, or at least the beginnings of it, but the immune system kills it over and over. Until it doesn't.
moosekaka 9y ago
Obligatory link to yesterdays topic https://gravityandlevity.wordpress.com/2009/07/08/your-body-wasnt-built-to-last-a-lesson-from-human-mortality-rates/ https://gravityandlevity.wordpress.com/2009/07/08/your-body-...

313 points by okket 9y ago

throwaway521 9y ago

I-T-S A P-A-T-H-O-G-E-N Read Paul Ewald and Gregory Cochran

reasonattlm 9y ago
https://en.wikipedia.org/wiki/Immunosurveillance https://en.wikipedia.org/wiki/Immunosurveillance "Cancer immunosurveillance is a process by which an organism's immune system recognizes transformed cells in order to inhibit the growth of neoplastic tissue. It comprises the first phase of immunoediting and is also known as the elimination phase."

reasonattlm 9y ago

Paper: https://doi.org/10.1073/pnas.1714478115 https://doi.org/10.1073/pnas.1714478115 Which is a suggestive model, by the way, not direct evidence. The best direct evidence would be to restore the pace of immune cell creation - such as via regeneration of the thymus (via FOXN1, or BMP4, or tissue engineering), cell therapy to replace or increase the pool of hematopoietic stem cells, etc. - and then see what happens. This sort of thing is five years out; there are people working on it, though more of those and more funding would certainly be a good thing. It would certainly be possible to push forward a startup today based on thymic regeneration or hematopoietic stem cell transplantation; the science is more or less ready for it. -------- T cells develop from hematopoietic stem cells as part of the lymphoid lineage and have the ability to detect foreign antigens and neoantigens arising from cancer cells. In the thymus, lymphoid progenitors commit to a specific T cell receptor and undergo selection events that screen against self-reactivity. Cells that pass these selection gates then leave the thymus, clonally expanding to form the patrolling naive T cell pool. The vast majority of vertebrates experience thymic involution (or atrophy) in which thymic epithelial tissue is replaced with adipose tissue, resulting in decreasing T cell export from the thymus. In humans, this is thought to begin as early as 1 year of age. The rate of thymic T cell production is estimated to decline exponentially over time with a half-life of ∼15.7 years. Declining production of new naive T cells is thought to be a significant component of immunosenescence, the age-related decline in immune system function. With the recent successes of T cell-based immunotherapies, it is timely to assess how thymic involution may affect cancer and infectious disease incidence. It is clear from epidemiological data that incidence of infectious disease and cancer increases dramatically with age, and, specifically, that many cancer incidence curves follow an apparent power law. The simplest model to account for this assumes that cancer initiation is the result of a gradual accumulation of rare "driver" mutations in one single cell. Furthermore, the fitting of this power law model (PLM) can be used to estimate the number of such mutations. Exponential curves have also been used to fit cancer incidence data, resulting in worse fits than the PLM overall. Nevertheless, it is worth noting that exponential rates close to the declining curve for thymic T cell production can be seen to emerge from the incidence data, indicating the relevance of the thymic involution timescale. While the PLM fits well, it does not account for changes in the immune system with age. To better determine the processes underlying carcinogenesis, we asked whether an alternative model, based only on age-related changes in immune system function, might partly or entirely explain cancer incidence. Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data. Our hypothesis and results add to the understanding of infectious disease and cancer incidence, suggesting in the latter case that immunosenescence, rather than gradual accumulation of mutations, serves as the predominant reason for an increase in cancer incidence with age for many cancers. For future therapies, including preventative therapies, strengthening the functionality of the aging immune system appears to be more feasible than limiting genetic mutations, which raises hope for effective new treatments. -------

truculation 9y ago

If the immune system has finite resources, would reducing the lifetime drain on those resources by infectious diseases delay the age at which we can expect get cancer? For example, curing the common cold and/or developing a universal flu vaccine.

vibrio 9y ago
I'm not sure 'finite' is the right way to think about it. I'd be more inclined to think of infections acting to 'Exercise' the immune system, similar to how jogging keeps your heart healthy, rather than using up a limited number of immune cells.
Retric 9y ago
Reducing immune system load is fairly straightforward, low dose antibiotics is one approach that significantly reduces the effort put forth by the immune system. However, it does not seem to make a significant difference in lifespans.
gojomo 9y ago
Via mechanisms similar to either the hygiene hypothesis or hormesis, it's possible those might backfire. This is highly speculative, but: * the hygiene hypothesis suggests that allergies and auto-immune disorders can arise from having insufficient immune-system challenges, especially when young. Lacking the calibration from an 'expected' or 'optimal' level of dirt/allergens/infectious-diseases, the immune system starts doing unwanted self-destructive things. * hormesis is the observation that almost everything bad for you also turns out to be good in very-tiny exposures – radiation, poisons, cancer-causing chemicals, etc. It's as if tiny doses trigger beneficial self-repairs to occur even beyond the direct damage received, even as larger doses overwhelm that mechanism. Removing mild, survivable challenges from the environment could thus leave the immune system less 'tuned' for the full spectrum of challenges it faces (like clearing early cancers). It's an adaptive dynamic system with nonlinear effects, not a simple pool of fixed exhaustible capability.
- rsync 9y ago
  "Removing mild, survivable challenges from the environment could thus leave the immune system less 'tuned' for the full spectrum of challenges it faces" Exactly. You want to protect people from, say, Rubella ... but I think we should proceed with caution with things like the cold and the flu ...

agumonkey 9y ago

Cue the senescence guys who aim to fix accumulated damages there.

ShabbosGoy 9y ago
Ultimately, I think it comes down to metabolism. As you age, your metabolism slows. Coenzymes like NAD+[0] are depleted. [0] https://www.nature.com/articles/nrneph.2017.5 https://www.nature.com/articles/nrneph.2017.5
- glibgil 9y ago
  Right, so just back up a step and stop the metabolism from slowing
  - bluetwo 9y ago
    Medicinal Cocaine?
  - shrimp_emoji 9y ago
    Or cut the knot. Upload mind to digital facsimile. Die, per nature's capricious designs. Robo-you lives smugly without any of this nonsense and can be resurrected if the power cuts out and sent across the stars at light speed with no need for fuel or supplies--breathes ... to somewhere without air.
    - agumonkey 9y ago
      I don't get why people go after these virtual things
glibgil 9y ago
I mean, it bears repeating on account of the fact that senolytic treatments make a lot of other health problems seem like not even worth understanding

lisper 9y ago

One immediate problem with the hypothesis that cancer is caused by the loss of T cells with age is the fact that HIV also destroys T cells, and it is associated with increased risk of some types of cancer. But the cancers associated with HIV are different from those associated with aging. In particular, Kaposi sarcoma occurs 500 times more in HIV patients than the general population. So there must be something else going on besides just the loss of T cells.

sungam 9y ago
Agree. No doubt immunosenescence contributes to the increased rate of malignancy at older ages but the spectrum of cancers seen in immunosupressed individuals does not that match seen in the elderly.
cma 9y ago
Kaposi sarcoma is associated with Kaposi's sarcoma-associated herpesvirus even in the HIV cases though. It might be that losing the amount of T cells you lose with HIV or immunosuppression has a different effect than just losing some fraction of them with age with respect to that virus.

ransom1538 9y ago

I always think of these two monkeys[i] when I consider slowing down my age. [i] http://www.slate.com/articles/health_and_science/medical_examiner/2012/08/calorie_restriction_and_longevity_monkey_study_shows_hunger_doesn_t_increase_longevity_but_type_of_food_does_.html http://www.slate.com/articles/health_and_science/medical_exa...

baxtr 9y ago
This is really great! Thanks for the link. I think you should post it to HN
musha68k 9y ago
Thanks for sharing – always those poor monkeys though... An even stronger data point to me would be the actual people of Okinawa who are (were?) among the healthiest and oldest in the world. In addition to having a high quality diet and a rich social life in general, they are practicing “hara hachi bu” – the confucian tradition of always eating only until “about 80% full”. https://en.m.wikipedia.org/wiki/Hara_hachi_bun_me https://en.m.wikipedia.org/wiki/Hara_hachi_bun_me
mysterypie 9y ago
It's an interesting well-written article, but you realize that their main point was that it contradicts the earlier calorie-restriction study: "The Nature authors found no increase in lifespan; the calorically restricted animals lived no longer, statistically, than their well-fed cousins." They try to reconcile the studies: maybe it's the natural-ingredient foods vs the refined foods, maybe it's the generous diet vs the more-than-generous free-feeding, or conceding that the monkey's don't live longer, but they live healthier. IMO, the best paragraph from the article was this: "Many of us simply roll our eyes and click away when yet another medical study contradicts the last study—so what else is new? Coffee’s bad for you, until it’s good for you—and so is red wine. Antioxidants are essential, or they’re useless. And so on." Other than some very basic common sense things -- like don't eat rat poison -- I never find that these kinds of studies lead to correct and actionable information about how to slow down aging or how to lead your life. And it's extremely frustrating to even try.

sungam 9y ago

How do you account for the observation that incidence of cancer in young, immunosupressed individuals (e.g. solid organ transplant recipients), whilst increased, is no way comparable to that seen in elderly individuals?

reasonattlm 9y ago
Other age-related cell and tissue damage that raises the risk of cells becoming cancerous, or reduces the effectiveness of internal-to-the-cell controls that can shut down and destroy cancerous cells, would be the other variable, I'd imagine.
- sungam 9y ago
  I think far more likely that the predominant variable is the expansion of mutant clones over time to occupy large fractions of the stem cell reservoir.
  - reasonattlm 9y ago
    Possibly so, which is a phenomenon that might explain how stochastic nuclear mutation at its given rates can possibly cause widespread enough harm to be significant. There is an interesting recent paper on that subject: https://doi.org/10.1371/journal.pgen.1007108 https://doi.org/10.1371/journal.pgen.1007108 "Recent single-cell studies point to the possibility that essentially all cells have unshared mutations in their genomes. In view of this extensive genetic diversity, it is perhaps not surprising that mutations that confer a proliferative advantage are readily detected as clonal populations of increasing abundance and size in the elderly. These clonal populations might lead to loss of organismal health through the functional decline of tissue and/or the promotion of disease processes, such as cancer. In this review, we summarize recent research that supports the notion that aberrant clonal expansion (ACE) resulting from cancer-associated mutations are common in noncancerous tissue and accumulate with age. We propose ACE to be a previously underappreciated aging phenotype that is universal in most organisms, affects multiple tissues, and likely helps explain why aging is the biggest risk factor for cancer."

HumanDrivenDev 9y ago

Really? I figured as we age our cancer rates will plummet while our immune systems only strengthen, which is why the leading cause of the death in the elderly is extreme sports.

eliben 9y ago
The alternative hypothesis was the "two-hit" idea of multiple changes accumulating in DNA over time, so it's not a trivial topic to study.
acct1771 9y ago
Extreme sports like "the stairs".
josephv 9y ago
I'm with you, upvoted for voicing the absurdity of the title. The article, which I refuse to read completely, seems like mediocre pop health science and this website has devolved into giving it, at this point at least 16 hours of frontpage time. I'll summarize it: "We don't understand cancer but we'll keep throwing shit at the wall until something sticks, and we're going to write up a bunch of shit and you shits read it so we can pay for throwing more shit."

kazinator 9y ago

The link between cancer and the immune system (the latter's role in defending against the former) is not all that clear. Here is a cancer.com (American Cancer Society) article on the relationship between AIDS and cancer. Source: https://www.cancer.org/cancer/cancer-causes/infectious-agents/hiv-infection-aids/hiv-aids-and-cancer.html https://www.cancer.org/cancer/cancer-causes/infectious-agent... Firstly, they say that "In fact, some types of cancer occur so often in people with AIDS that they are considered AIDS-defining conditions". But that's only certain specific cancers. Then there are some other cancers that occur often with AIDS but are not "AIDS-defining". And then there is the kicker: "Of course, as people with HIV are now living longer, they are also developing other cancers that are not clearly linked to HIV but are more common in older people, such as breast, colorectal, and prostate cancer.". So, these cancers go up in AIDS survivors due to age, even though those people have immune systems that were already shot years before. So much for a tidy hypothesis about aging -> lower immune system -> cancer, I suppose. As for why those afflicted with AIDS get certain cancers, one explanation (also given in above page) is that some cancers are caused by viral infections. Weakened defense against viral infections, increased cancer of that type.

Thriptic 9y ago

Isn't this a bit of an oversimplification? It's not like if you knock out p53 and something else you instantly get a metastatic tumor. Granted if you remove key tumor suppressor genes your probability of mutations persisting skyrockets, but that in itself doesn't create a dangerous tumor. You need many more mutations than 2 to be able to acquire the functionality to grow, persist, escape the local environment, and establish a foot hold in a new environment. Here is the classic review paper on tumor formation: http://www.cell.com/abstract/S0092-8674(11)00127-9 http://www.cell.com/abstract/S0092-8674(11)00127-9

samstave 9y ago

What are white blood cell counts in someone who is sixty vs one who is eighteen? Is this where the blood transfusion concept is strong? What is the oxygen-carrying-capacity of hemoglobin in old blood vs young blood?

thrownaway954 9y ago

I was told once (by who I don't remember): Live long enough and you will eventually get cancer. To me it's a no-brainer. You get old, cells break down, immune system isn't what it use to be, increasing the risk of that rouge new cell becoming cancerous.

commandlinefan 9y ago

I worked for a cancer research startup a few years ago - I was just doing IT stuff, but I worked with a lot of oncologist/cancer research types. One of the things that they often said was that every living organism will develop cancer eventually, but most things die of other causes before that happens.

ngvrnd 9y ago
it seems plausible or maybe even likely that everyone develops cancer many times, or at least the beginnings of it, but the immune system kills it over and over. Until it doesn't.

moosekaka 9y ago

Obligatory link to yesterdays topic https://gravityandlevity.wordpress.com/2009/07/08/your-body-wasnt-built-to-last-a-lesson-from-human-mortality-rates/ https://gravityandlevity.wordpress.com/2009/07/08/your-body-...