Italian researchers working in Texas
have discovered the driver of aggressive tumours like that of
the pancreas, saying that the key is in how cells transform
themselves.
A key mechanism underlying the aggressiveness of tumors has been
discovered, and in particular of pancreatic cancer, which is
currently a particularly difficult form to treat.
The 'driver' of aggressiveness lies in the transformation that
tumor cells can undergo, which, by completely changing
'appearance' and transitioning from the status of epithelial
cells to mesenchymal cells, make the tumor 'nastier' and capable
of proliferating quickly, as happens in the case of pancreatic
cancer.
The study could open the door to new treatments capable of
selectively targeting cells with mesenchymal characteristics and
thus depriving the tumor of its main driver.
The discovery, published in the journal Nature, is down to
Italian researchers from the MD Anderson Cancer Center in
Houston, USA, from the Università Cattolica del Sacro Cuore, and
their teachers, Giampaolo Tortora and Alessandro Sgambato.
Researchers from the IRCCS San Raffaele in Milan also took part
in the study.
Tumor cells, the study highlighted, can therefore transition
from the state of epithelial cells (present in internal organs,
body cavities but also on the surface of the skin) to
mesenchymal cells (primitive, non-specialized cells that can
transform into different types of cells in the body), capable of
escaping various types of control, and it is precisely this
transformation that makes the tumor more aggressive.
The epithelial-mesenchymal transition is typical of many tumors,
but is more pronounced in pancreatic tumors. An important
discovery that has potential practical implications, says
Tortora, director of the Comprehensive Cancer Center of
Fondazione Policlinico Gemelli Irccs.
"For example, the future identification of some biomarkers that
identify this plasticity of the tumor cell, to exploit it in
diagnostic-therapeutic terms, so as to be able to intervene
promptly, for example by modifying the therapy. What we are
learning will almost certainly have implications for many other
tumors in which this transformation is a way acquired by the
tumor to escape control and therapies".
This study, adds Sgambato, vice dean of the Faculty of Medicine
and Surgery of the Università Cattolica del Sacro Cuore, "is
very significant and offers us the opportunity to look with new
eyes at a very aggressive pathology such as pancreatic cancer,
paving the way for the development of new diagnostic-therapeutic
approaches useful not only for this but also for other tumor
pathologies".
Until now, Luigi Perelli, the first author of the study,
explained to ANSA, "it was not clear whether the transition from
epithelial to mesenchymal provided advantages to the tumor or
not. In the new research we discovered that not only is it
important, but in the case of pancreatic cancer it plays a key
role in its aggressiveness".
Furthermore, the transition from epithelial to mesenchymal has
several consequences: on the one hand, it gives rise to tumor
cells with a greater capacity for diffusion, on the other it
generates instability in the genome of tumor cells which
translates into a greater heterogeneity of the cells that make
up the tumor.
The result is a greater ability of the tumor to adapt to
unfavorable conditions and therapies.
As if that were not enough, "this transformation, which in other
tumors occurs in an advanced stage, in pancreatic cancer occurs
almost immediately.
This explains the extreme difficulty in identifying an effective
treatment for this tumor", adds Perelli.
"Our work is fundamental for clarifying the evolutionary models
underlying the aggressive clinical behavior of pancreatic
cancer", comments the coordinator of the work, Giannicola
Genovese.
These findings, he concludes, "add another layer to our
understanding of tumor heterogeneity and the complexity of the
cancer microenvironment, providing crucial new information for
the treatment of this devastating disease."
ALL RIGHTS RESERVED © Copyright ANSA