The Legacy of Mesenchymal Stem Cells in Vindicating the Clonal Evolution Model of Cancer

Organogenesis and tumorigenesis seem to be following
a set pretty similar instructions and pathways and tumors,
like any other organ, can be seen as the summation of
many different cell types. However, unlike normal tissues,
intercellular networks in cancer show high degrees
of robustness and plasticity, employing other cellular
networks in favor of their own growth1. The integrated
hallmarks of cancer were first described by Hanahan and
Weinberg in 20002, and was updated in 2011 by the same
scientists3. They have described 10 hallmarks including:
1) self-sufficiency in growth signals, 2) not responding to
antigrowth signals, 3) unlimited proliferation, 4) resisting
apoptosis, 5) genomic instability, 6) angiogenesis, 7)
deregulated metabolism, 8) inflammation, 9) escaping
immune destruction, and 10) tissue invasion and
metastasis3, all of which have stood the test of time as
being integral components of most forms of neoplasms.
These unifying hallmarks are a reflection of the network
structure of human cells dictating which genetic/epigenetic
alterations are viable and in favor of tumor formation
and progression. Among all the theories trying to explain
the origins and hallmarks of cancer since Hippocrates4,
clonal evolution and the stem cell hypothesis are the two
theories that explain hallmarks of cancer the best5. For
the purpose of this editorial our focus will be on the clonal
evolution theory.