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CANCER STEM CELLS AND
ONCOLOGY RESEARCH
11th International Conference on
Journal of Medical Oncology and Therapeutics | Volume 3
CIRCULATING
EPITHELIOID CELLS
AND PERSONALIZED
MEDICINE: THE GOOD,
THE BAD AND THE UGLY
AND MANY OTHERS
Alexia Lopresti, Daniel Birnbaum,
Claire Acquaviva and Emilie Mamessier
Centre de Recherche en Cancérologie de Marseille, France
When tissues are damaged, such as during inflammation
or cancer, epithelial cells circulates in the blood at low
frequencies. Circulating epithelioid cells (CECs) represent
a non-invasive way to access to information on distant
damaged tissue sites. Recent technologies now allow the
detection of CECs with a very high sensitivity. However,
not all CECs are informative. In the case of cancer, only a
minority of these CECs is at risk to give rise to metastases,
and is thus the actual population to identify. We develop
new models for Personalized Oncology. We search for
markers related to tumor evolution and drug resistance
in CECs, and more specifically in true Circulating tumor
cells (CTCs) from breast and colorectal tumors. Using
histological (count, morphology) and phenotypical (multi-
color staining) analyses, we identified several types of
CECs in the blood of cancer patients: normal epithelial
cells (most certainly collateral damage), epithelioid cells
of unknown significance, isolated tumor cells at different
degree of epithelial-to-mesenchymal transition (EMT)
stages, and tumor micro-emboli. We established the
multidrug resistance phenotype and stemness status of
these cells. The data were correlated to patients’ clinical
information and response to treatment. Our results show
that specific subsets of CTCs, rather than the unselected
population, should be considered and characterized, if
one wants to use CTCs as a window for patient’s tumor
heterogeneity and/or evolution. This makes more complex
a situation already difficult due to limited number of
available cells, but which should be workable now in the
single-cell era.
J Med Oncl Ther 2018, Volume 3
POLYPLOID GIANT
CANCER CELLS MAY
REPRESENT A SOMATIC
EQUIVELANT OF
BLASTOMERE
Jinsong Liu and Na Niu
The University of Texas, USA
It is now generally accepted that all mature somatic
cells retain the capability to be reprogrammed (or
dedifferentiated) to pluripotent state. However, it remains
unclear how the endogenous developmental pathway is
activatedforsuchareprogramming.Wehaverecentlyshown
that chemotherapy drug paclitaxel (PTX) can induce cancer
cells undergo senescence and lead the formation of a big
monster cells, refer as polyploid giant cancer cells (PGCCs).
PGCCs bypass the spindle checkpoint and replicate the
DNA without cell division. PGCCs show time- and space-
dependent activation of expression of reprogramming
factors OCT4, NANOG, and SOX2; lack expression of Xist;
and are capable of de-differentiation. The parental cancer
cells are reprogrammed via formation of PGCCs which can
give a birth of diploid resistance cancer cells via budding.
This division mode recapitulates that of blastomere-to-
morula stage embryo and facilitates the dedifferentiation
toward the blastomere stage embryonic stem cells. PGCCs
use an evolutionarily conserved embryonic program
used to reprogram zygote to new embryonic state for for
disease relapse and thus represent a somatic equivalent
of blastomere. Here, we provide a model on how PGCCs
divide and how they achieve the dedifferention, named
the blastomere model for cancer and disease relapse.
This new conceptual paradigm, which integrates different
tumors along bidirectional developmental hierarchy, should
facilitate our understanding of cancer origin and to guide
our efforts for therapeutic intervention.