1234567890xyz
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#1
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What kind of gene would be passed down to mean that cancer is genentic? What would that gene do/code for?
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macpatgh-Sheldon
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Hi,
Some genes code for proteins that protect against cancer to a certain extent - so having the recessive alleles of such genes confers a higher preponderance to develop cancer.

In addition, some genes [sometimes through a mutation] can actually cause certain types of cancer e.g. the "Philadelphia gene" results in chronic myelocytic leukaemia {CML - cancer of the myeloid series of leukocytes [white blood cells]]; a mutation of chromosome 13 can [rarely] lead to retinoblastoma [type of tumour in the eye, seen mostly in young people].

M.
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Jpw1097
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(Original post by 1234567890xyz)
What kind of gene would be passed down to mean that cancer is genentic? What would that gene do/code for?
I think you’re confusing genetic and hereditary. Fundamentally, cancer is caused by genetic (or epigenetic) mutations. These mutations can occur in tumour suppressor genes or (proto-oncogenes). Tumour suppressor genes (e.g. TP53) are usually genes involved in DNA repair and regulation of cell cycle checkpoints. Proto-oncogenes are usually genes that code for receptors and proteins (e.g. Ras, RAF) involved in signalling pathways that promote cell survival and proliferation. These mutations usually cause these proteins to become constitutively active (i.e. always on) so that the pathway is always activating, promoting cell survival and proliferation.

Having said that, you certainly can inherit mutations and germline variants that predispose you to cancer. For example, individuals who inherit mutations in BRCA1/2 are at increased risk of breast, ovarian, prostate and pancreatic cancer amongst others.
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1234567890xyz
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(Original post by Jpw1097)
I think you’re confusing genetic and hereditary. Fundamentally, cancer is caused by genetic (or epigenetic) mutations. These mutations can occur in tumour suppressor genes or (proto-oncogenes). Tumour suppressor genes (e.g. TP53) are usually genes involved in DNA repair and regulation of cell cycle checkpoints. Proto-oncogenes are usually genes that code for receptors and proteins (e.g. Ras, RAF) involved in signalling pathways that promote cell survival and proliferation. These mutations usually cause these proteins to become constitutively active (i.e. always on) so that the pathway is always activating, promoting cell survival and proliferation.

Having said that, you certainly can inherit mutations and germline variants that predispose you to cancer. For example, individuals who inherit mutations in BRCA1/2 are at increased risk of breast, ovarian, prostate and pancreatic cancer amongst others.
Thank you - so if you inherit mutations, is it not inevitable that you'll get cancer?
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Jpw1097
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(Original post by 1234567890xyz)
Thank you - so if you inherit mutations, is it not inevitable that you'll get cancer?
In most cases, no. Often individuals can inherit a mutated copy of the gene, but they still have the other allele. They may develop cancer if they acquire a mutation in the other allele.

There are some mutations which, if you inherit, you will almost certainly develop cancer. An example is the condition familial adenomatous polyposis, caused by a mutation in the APC gene, which causes colorectal cancer by age 40.
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Kallisto
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(Original post by 1234567890xyz)
What kind of gene would be passed down to mean that cancer is genentic? What would that gene do/code for?
Are you talking about a genetic defect or heredity? in terms of the first a genetic defect is caused by mutations they can influence the tumor suppressor genes and DNA repair enzymes negatively and the cell regulation can't stop the spread of tumor cells what lead to cancer.
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chazwomaq
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I would interpret OP's question as follows: "If cancer is heritable, why hasn't it been selected out as it causes mortality."

First, cancer is heritable. Twin studies show that many types of cancer are influenced by inherited genes. For example: https://www.ncbi.nlm.nih.gov/pmc/art...0and%20Finland.

Second, the evolutionary logic is correct - selection should remove deleterious genes. However, if the cancer only kicks in at older age after reproduction has typically occurred, then the genes can still be passed on. This is why childhood cancers are rare and they become increasingly common with age. In fact, many people who die old from non-cancer causes have multiple tumours; they just never caused any problems and so were never diagnosed.

Thirdly and most importantly, you have to take the gene's eye view to understand cancer. When a cell mutates it is not longer genetically identical to the rest of the body, and the cancer gene's interest is no longer aligned to the rest of the cells. Thus selection will favour its spread even though that could eventually kill its host. This is the selfish gene action. So actually, what we should expect is for cancer to be rampant, occurring all the time, because evolution works fundamentally at the level of the genes, not the organism. The real question is why is cancer so rare.

However, from the rest of the cells' perspective, it is in their interest to oppose the cancerous cells, and they do this via the action of tumour suppressor genes (p53 was the first and best known). Essentially each cell "polices" all the others to suppress tumours. It is only rare failure of the tumour suppressor system that results in tumours growing enough to cause problems.

Then there are animals where cancer is very rare like naked mole rats (the world's ugliest mammal).

Further reading:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660034/
http://www.bbc.co.uk/earth/story/201...cer-inevitable
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chazwomaq
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I'm not sure it's as simple as size being inversely related to cancer, as small naked mole rats are cancer resistant . Some species (like elephants) have lots of tumour suppressor genes, which gives a proximate answer to your question. But that just begs the question. Why do these species has many tumour suppressor genes? I don't know enough to give a full answer but here is some reading:

http://www.bbc.co.uk/earth/story/201...snt-get-cancer
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Jpw1097
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#9
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It's certainly a possibility. In theory, it is possible to use gene editing (e.g. CRISPR-Cas9) to inactivate oncogenes and replace lost tumour suppressor genes. However, it would be technically challenging. Delivering the vector into the tumour cells would be difficult, and you'd have to ensure that all tumour cells take up the vector. If not, the tumour cells that did not undergo gene editing will outcompete those that did.
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