In the molecular biology of the cell (6th ed), it is stated that:

Some cancers seem to be organized in a similar way: they consist of rare cancer stem cells capable of dividing indefinitly, toghether with much lager numbers of dividing transit amplifying cells that are derived from the ancer stem cells but haave a limited capacity for self-renewal. These non-stem cells appear to constitute the great majority of the cell population of some tumorus (p.1121).

Although in an earlier segment, however, we can read that:

Human cancer cells avoid replicative cell senescense in one of two ways. They can maintain the activity of telomerase as they proliferate, so that their telomeres do not shorten or become uncapped, or they can evolve an alternate mechamism based on homologous recombination (called ALT) for elongating their chromosome ends. Regardless of strategy usedd, the result is that the cancer cells continue to proliferate under conditions when normal cells would stop (p.1100).

How do we interpret these two passages? Are some cancer cells incapable of lenghtening their telomeres, and is it these types of tumours that can't persist without cancer stem cells? Or are cancer stem cells beneficial in some other way to the tumour (such that a tumour stem cell might differentiate into several types of tumour cells, which might be suitable for different environments)?

I understand that having cancer stem cells that proliferate at a slower pace than regular cancer cells might be beneficial for withstanding things like chemotherapy. But what's being emphaphized is not their capacity for survival, but their greater ability at self renewal?

  • 2
    $\begingroup$ Be careful with thinking that tumors have wants and needs; these are descriptions of what happens, not statements of how things need to be. $\endgroup$
    – Bryan Krause
    Commented Nov 9, 2021 at 16:50
  • $\begingroup$ Sure, I could have rephrased that in another way ("Why tumour cells which aren't stem cells have a limited capacity for self-renewal?"), $\endgroup$
    – Magnus
    Commented Nov 9, 2021 at 20:18
  • 1
    $\begingroup$ Isn't that a tautology? $\endgroup$
    – Bryan Krause
    Commented Nov 9, 2021 at 20:23

2 Answers 2


This is like asking why there are multiple forms/mechanisms of dementia when "one would suffice".

To save this from being just a trivial comment, note that the mechanism of elongation differs between cancer types, likely depending on the types of cells involved:

Despite being present in a minority of cancers overall, the prevalence of ALT in cancers is not uniform, with cells of mesenchymal origin being more likely to rely on ALT for telomere elongation. Indeed, certain cancers, such as osteosarcomas and cancers of the central nervous system, have rates of ALT positivity approaching 90%, eluding to possible mechanistic reasons for ALT development. The most likely cause of this distribution is that, in contrast to cells of epithelial origin, cells of mesenchymal origin are more likely to have more stringently regulated telomerase expression, reducing the potential for telomerase-mediated telomere maintenance.

  • $\begingroup$ Are tumors cells vulnerable, as healthy stem cells, to DNA alteration? $\endgroup$ Commented Apr 30, 2023 at 16:16

My professor claims that cells go into senescence due to multiple reasons, and that many cells stop dividing after a set number of divisions, despite having ample telomeres and no appreciable DNA damage. He claimed that tumours (counterintuitively) often work in this very same way, so that cancer cells need to be able to differentiate back into cancer stem cells for the cycle to reset itself.

I'm not really qualified to determine who is right. I'll post this answer and let people vote for what's more reasonable.


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