Frontiers in Oncology,
Journal Year:
2020,
Volume and Issue:
10
Published: Dec. 9, 2020
A
higher
incidence
of
colorectal
cancer
(CRC)
is
found
in
males
compared
to
females.
Young
women
(18-44
years)
with
CRC
have
a
better
survival
outcome
men
the
same
age
or
older
(over
50
years),
indicating
global
sexual
dimorphism
rates
and
survival.
This
suggests
protective
role
for
sex
steroid
hormone
estrogen
development.
Key
proliferative
pathways
tumorigenesis
exhibit
dimorphism,
which
confer
females
through
regulated
genes
cell
signaling.
Estrogen
regulates
activity
class
Kv
channels
(KCNQ1:KCNE3),
control
fundamental
ion
transport
functions
colon
epithelial
mesenchymal
transition
bi-directional
interactions
Wnt/β-catenin
signalling
pathway.
also
modulates
responses
hypoxia
Cancers,
Journal Year:
2019,
Volume and Issue:
11(7), P. 1017 - 1017
Published: July 20, 2019
Colorectal
cancer
(CRC)
is
a
leading
cause
of
death
worldwide.
It
includes
different
subtypes
that
differ
in
their
clinical
and
prognostic
features.
In
the
past
decade,
addition
to
conventional
adenoma-carcinoma
model,
an
alternative
multistep
mechanism
carcinogenesis,
namely
"serrated
pathway",
has
been
described.
Approximately,
15
30%
all
CRCs
arise
from
neoplastic
serrated
polyps,
heterogeneous
group
lesions
are
histologically
classified
into
three
morphologic
categories:
hyperplastic
sessile
adenomas/polyps,
traditional
adenomas/polyps.
Serrated
polyps
characterized
by
genetic
(BRAF
or
KRAS
mutations)
epigenetic
(CpG
island
methylator
phenotype
(CIMP))
alterations
cooperate
initiate
drive
malignant
transformation
normal
colon
mucosa
then
CRC.
The
high
heterogeneity
renders
diagnostic
pathological
interpretation
difficult.
Hence,
novel
biomarkers
required
for
better
classification
management
CRCs.
To
date,
several
molecular
have
associated
with
polyp-CRC
sequence.
addition,
gut
microbiota
emerging
as
contributor
to/modulator
pathway.
This
review
summarizes
state
art
genetic,
signatures
CRCs,
together
implications.
The Journal of Immunology,
Journal Year:
2019,
Volume and Issue:
202(10), P. 3065 - 3075
Published: April 12, 2019
Although
multidisciplinary
treatment
is
widely
applied
in
colorectal
cancer
(CRC),
the
prognosis
of
patients
with
advanced
CRC
remains
poor.
Immunotherapy
blocking
programmed
cell
death
ligand
1
(PD-L1)
a
promising
approach.
Binding
transmembrane
protein
PD-L1
expressed
by
tumor
cells
or
microenvironment
to
its
receptor
(PD-1)
induces
immunosuppressive
signals
and
reduces
proliferation
T
cells,
which
an
important
mechanism
immune
escape
key
issue
immunotherapy.
However,
regulation
expression
poorly
understood
CRC.
Fibroblast
growth
factor
(FGF)
(FGFR)
2
causes
tyrosine
kinase
domains
initiate
cascade
intracellular
binding
FGFs
dimerization
(pairing
receptors),
involved
tumorigenesis
progression.
In
this
study,
we
showed
that
FGFR2
were
frequently
overexpressed
CRC,
was
significantly
associated
lymph
node
metastasis,
clinical
stage,
poor
survival.
current
positively
correlated
Tumor-derived-activated
induced
via
JAK/STAT3
signaling
pathway
human
(SW480
NCI-H716),
apoptosis
Jurkat
cells.
also
promoted
xenograft
mouse
model
The
results
our
study
reveal
novel
thus
providing
theoretical
basis
for
reversing
tolerance
overexpression
Frontiers in Oncology,
Journal Year:
2020,
Volume and Issue:
10
Published: Dec. 9, 2020
A
higher
incidence
of
colorectal
cancer
(CRC)
is
found
in
males
compared
to
females.
Young
women
(18-44
years)
with
CRC
have
a
better
survival
outcome
men
the
same
age
or
older
(over
50
years),
indicating
global
sexual
dimorphism
rates
and
survival.
This
suggests
protective
role
for
sex
steroid
hormone
estrogen
development.
Key
proliferative
pathways
tumorigenesis
exhibit
dimorphism,
which
confer
females
through
regulated
genes
cell
signaling.
Estrogen
regulates
activity
class
Kv
channels
(KCNQ1:KCNE3),
control
fundamental
ion
transport
functions
colon
epithelial
mesenchymal
transition
bi-directional
interactions
Wnt/β-catenin
signalling
pathway.
also
modulates
responses
hypoxia
