4
$\begingroup$

If a certain set of cells or tissue are undergoing a lot of reproduction and repair cycles for some reason, does this inevitably lead to cancerous growths? If the mutation rate exceeds the normal 'background' mutation rate for the tissue will these extra mutations eventually cause cancer?

As user Luke said below; does an increased rate of replication increase the rate of mutations.

$\endgroup$
  • $\begingroup$ This is too broad. Can you please narrow your question down? $\endgroup$ – Chris Jan 22 '15 at 6:46
  • $\begingroup$ If with any type of cells a 'group' of them in a tissue or an organ, say; if they all go through a lot of dividing and reproducing , more than they would if 'healthy' would more mutations occur than 'expected if 'healthy' cells. If a culture of cells in a petri dish are 'made' to reproduce a lot more than they 'usually would ,would more mutations occur as the reproduction rate increases? $\endgroup$ – 201044 Jan 22 '15 at 7:03
  • 1
    $\begingroup$ it is desperately unclear what you are trying to ask $\endgroup$ – rg255 Jan 22 '15 at 15:20
  • 2
    $\begingroup$ So is your question "Does increased replication rate lead to a higher likelihood of mutation?" $\endgroup$ – Luke Jan 23 '15 at 14:28
  • 2
    $\begingroup$ @201044 I voted to reopen your question, because I think it deserves an answer. However, answering aggressively ("Why do I bother trying?") to users likely to be the only ones who may help you is not a good idea. We are a small community, so there are few specialists on a given topic, and if they ask you to clarify, either comply or get closed. $\endgroup$ – Raoul Jan 31 '15 at 19:16
3
$\begingroup$

Increased cell turnover indirectly leads to cancer. Below is a direct quote from Human Molecular Genetics, 2ed. Chapter 9: Instability of the human genome: mutation and DNA repair.

Mutations can be induced in our DNA by exposure to a variety of mutagens occurring in our external environment or to mutagens generated in the intracellular environment. In the case of radiation-induced mutation, for example, Dubrova et al. 1996 reported that the normal germline mutation rate for hypervariable minisatellite loci was doubled as a consequence of heavy exposure to the radiaoctive fallout from the Chernobyl accident. However, under normal circumstances by far the greatest source of mutations is from endogenous mutation, notably spontaneous errors in DNA replication and repair. During an average human lifetime there are an estimated 10^17 cell divisions: about 2 × 10^14 divisions are required to generate the approximately 10^14 cells in the adult, and additional mitoses are required to permit cell renewal in the case of certain cell types, notably epithelial cells (see Cairns, 1975). As each cell division requires the incorporation of 6 × 10^9 new nucleotides, error-free DNA replication in an average lifetime would require a DNA replication-repair process with an accuracy great enough so that the correct nucleotide was inserted on the growing DNA strands on each of about 6 × 10^26 occasions.

Such a level of DNA replication fidelity is impossible to sustain; indeed, the observed fidelity of replication of DNA polymerases is very much less than this and uncorrected replication errors occur with a frequency of about 10^-9 to 10^-11 per incorporated nucleotide (see Cooper et al., 1995). As the coding DNA of an average human gene is about 1.7 kb, coding DNA mutations will occur spontaneously with an average frequency of about 1.7 × 10^-6 -1.7 × 10^-8 per gene per cell division. Thus, during the approximately 10^16 mitoses undergone in an average human lifetime, each gene will be a locus for about 10^8-10^10 mutations (but for any one gene, only a tiny minority of cells will carry a mutation). In many cases, a deleterious gene mutation in a somatic cell will be inconsequential: the mutation may cause lethality for that single cell, but will not have consequences for other cells. However, in some cases, the mutation may lead to an inappropriate continuation of cell division, causing cancer (see Chapter 18).

Here is another great paper that specifically addresses your question, linking increased cell division with the accumulation of both significant and insignificant mutations, which over time, lead to an accumulation of mutations needed for cancer to develop.

$\endgroup$
  • $\begingroup$ tl;dr answer: The probability of mutation for each cell division remains more or less the same. So the absolute number of cell divisions will determine the absolute number of mutations. So higher cell divsion rate - higher turn over - means higher risk of mutation - which translates to higher chance of cancer $\endgroup$ – One Face Feb 1 '15 at 7:26
  • 1
    $\begingroup$ Yes, essentially, until repair mechanisms have mutations that make them less effective in which case more absolute number of mutations would accumulate per future cell division. $\endgroup$ – Anne Feb 1 '15 at 18:34
  • $\begingroup$ Could a lot of acquired mutations in a cell's genome somehow 'distort' the cell's ability to 'self-destruct'? ( thereby 'making it 'non-mortal') $\endgroup$ – 201044 Feb 14 '15 at 5:21
  • $\begingroup$ Yes, that is essentially a cancer. $\endgroup$ – Anne Feb 16 '15 at 2:59
  • $\begingroup$ Would mutations in the repair mechanisms of a cell make it 'noticeable' to the immune system? $\endgroup$ – 201044 Mar 31 '15 at 5:24

Your Answer

By clicking “Post Your Answer”, you agree to our terms of service, privacy policy and cookie policy

Not the answer you're looking for? Browse other questions tagged or ask your own question.