deaths, originate from the lung, liver, stomach, colorectum, breast,
esophagus, pancreas, and prostate (2014 World Cancer Report), all
of which requiring EMT/METs in their developmental ontogeny
and being derived (except for the mammary gland) from the endoderm germ layer [1], suggesting that human cancer incidence/
mortality preferentially affects endoderm-derived epithelial structures. It is therefore not surprising that both developmental and
cancer biologists have become increasingly interested in applying
the EMT/MET concept in their respective research and in trying to
uncover common regulators for both physiological (developmental) and pathological (disease) EMT/METs [2, 3].
A common theme emerged from such studies in recent years
concerns the issue of EMT/MET diversity as it has become increasingly clear that in both development and cancer, a complete transition of E to M or M to E is rare [4]. Most EMT/MET phenomena
involve transitions that partially overlap with the full spectrum
between full epithelium and full mesenchyme (Fig. 2). With such
observations came questions of whether diverse EMT/METs could
have a standardized definition with a conserved set of regulators
and, if not, whether comparison between developmental and cancer
EMT/METs (or between any two EMT/METs) is meaningful [5].
Answer to these questions will come from advancement in
related fields of cellular, molecular, biophysical, bioinformatic,
and computational research that will place precise quantitative
values to each EMT/MET descriptor [6, 7]. For example, both
epithelial and mesenchymal cells are polarized, and their polarity is
Fig. 1 Number of EMT-related publications by year, from 1980 to June 2019, based on Web of Science search
30
Sofiane Hamidi et al.
esophagus, pancreas, and prostate (2014 World Cancer Report), all
of which requiring EMT/METs in their developmental ontogeny
and being derived (except for the mammary gland) from the endoderm germ layer [1], suggesting that human cancer incidence/
mortality preferentially affects endoderm-derived epithelial structures. It is therefore not surprising that both developmental and
cancer biologists have become increasingly interested in applying
the EMT/MET concept in their respective research and in trying to
uncover common regulators for both physiological (developmental) and pathological (disease) EMT/METs [2, 3].
A common theme emerged from such studies in recent years
concerns the issue of EMT/MET diversity as it has become increasingly clear that in both development and cancer, a complete transition of E to M or M to E is rare [4]. Most EMT/MET phenomena
involve transitions that partially overlap with the full spectrum
between full epithelium and full mesenchyme (Fig. 2). With such
observations came questions of whether diverse EMT/METs could
have a standardized definition with a conserved set of regulators
and, if not, whether comparison between developmental and cancer
EMT/METs (or between any two EMT/METs) is meaningful [5].
Answer to these questions will come from advancement in
related fields of cellular, molecular, biophysical, bioinformatic,
and computational research that will place precise quantitative
values to each EMT/MET descriptor [6, 7]. For example, both
epithelial and mesenchymal cells are polarized, and their polarity is
Fig. 1 Number of EMT-related publications by year, from 1980 to June 2019, based on Web of Science search
30
Sofiane Hamidi et al.