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parallels with cancer drug resistance

Posted by suihuang on 27 Aug 2014 at 14:49 GMT

It is fascinating that this confluence of fitness features, nicely described here, has exact parallels in cancer cells: (i) non-genetic resistance to drugs (persistor state), (ii) slower proliferation of the persistors; (iii) inherent association of resistance with increased pathogeneicity (cancer stem cell -like properties), (iv) cooperation between non-genetically heterogeneous subpopulations (albeit more directly, via growth factors secreted by subpopuations) .

see: http://www.ncbi.nlm.nih.g...

The key point, not emphasized here is that the non-genetic nature (absence of mutation) and population level fitness will shall make us rethink details of Darwinian evolution dynamics. Yet cancer biologists still resort to the simple mutation/selection (of individual cell) scheme to explain resistance.

One difference in cancer cells is that the slower proliferation of the tolerant state in mammalian cell is not simply the consequence of the burden of expressing the resistance conferring protein but may have deeper roots in populations and is a adaptive trait itself. But Why?.

No competing interests declared.

RE: parallels with cancer drug resistance

rolir replied to suihuang on 03 Sep 2014 at 10:37 GMT

Many thanks for these insightful comments. Readers who are interested in the connection that Dr Huang makes might be interested in reading the following PLOS Biology Essay by Steve Frank and Marsha Rich Rosner:

Competing interests declared: I'm a PLOS Biology editor and author of this Synopsis.