Regulatory mechanisms and potential therapeutic targets in precancerous lesions of gastric cancer: A comprehensive review
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
177, С. 117068 - 117068
Опубликована: Июль 16, 2024
Precancerous
lesions
of
gastric
cancer
(PLGC)
represent
a
critical
pathological
stage
in
the
transformation
from
normal
mucosa
to
(GC).
The
global
incidence
PLGC
has
been
rising
over
past
few
decades,
with
trend
towards
younger
onset
ages.
Increasing
evidence
suggests
that
early
prevention
and
treatment
can
effectively
reverse
malignant
development
mucosal
epithelial
cells.
However,
there
is
currently
lack
effective
therapeutic
drugs
methods.
Recent
years
have
witnessed
substantial
advancements
research,
elucidation
novel
regulatory
mechanisms
offering
promising
avenues
for
clinical
intervention
drug
development.
This
review
aims
delineate
potential
targets
diagnosis
GC
while
exploring
innovative
approaches
management.
article
focuses
on
elucidating
inflammatory
microenvironment,
bile
acids
(BA),
glycolysis,
autophagy,
apoptosis,
ferroptosis,
cellular
senescence.
We
pay
particular
attention
PLGC,
goal
providing
insights
theoretical
basis
research
PLGC.
Язык: Английский
Gastric Intestinal Metaplasia: Challenges and the Opportunity for Precision Prevention
Cancers,
Год журнала:
2023,
Номер
15(15), С. 3913 - 3913
Опубликована: Авг. 1, 2023
GIM
is
a
persistent,
premalignant
lesion
whereby
gastric
mucosa
replaced
by
metaplastic
resembling
intestinal
tissue,
arising
in
the
setting
of
chronic
inflammation,
particularly
context
Helicobacter
pylori.
While
overall
rates
progression
to
adenocarcinoma
are
low,
estimated
at
from
0.25
2.5%,
there
features
that
confer
much
higher
risk
and
warrant
follow-up.
In
this
review,
we
collate
summarise
current
knowledge
regarding
pathogenesis
GIM,
clinical,
endoscopic
histologic
factors
for
cancer.
We
examine
state-of-practice
with
regard
diagnosis
management
which
varies
widely
published
guidelines
practice.
consider
emerging
evidence
population
studies,
artificial
intelligence
molecular
markers,
will
guide
future
models
care.
The
ultimate
goal
increase
detection
early
dysplasia/neoplasia
can
be
cured
while
avoiding
unnecessary
surveillance
very
low-risk
individuals.
Язык: Английский
Сharacterization of the immune microenvironment’s cellular composition and its influence on gene expression during metaplastic changes of the gastric mucosa epithelium
Morphology,
Год журнала:
2024,
Номер
161(4), С. 53 - 65
Опубликована: Июнь 17, 2024
BACKGROUND:
Intestinal
metaplasia
of
the
gastric
mucosa
epithelium
in
chronic
atrophic
gastritis
is
considered
a
precancerous
condition;
however,
it
potentially
reversible.
The
study
regulation
mechanisms
metaplastic
epithelial
changes
may
help
understanding
carcinogenesis
and
cancer
prevention.
AIM:
To
determine
whether
microenvironment
related
to
development
patients
with
by
assessing
gene
expression
cellular
composition
immune
infiltrates.
MATERIALS
AND
METHODS:
In
this
retrospective
cohort
study,
alternative
hypothesis
was
that
differed
between
cases
without
epithelium.
Biopsy
specimens
(n=38)
obtained
during
endoscopic
examination
from
five
stomach
sites
(2
antrum,
2
body,
1
corner)
unspecified
etiology
results
RNA
sequencing
biopsy
registered
NCBI
open
database
(n=12)
were
analyzed.
Histological
analysis,
histochemical
staining
methods,
immunohistochemical
morphometric,
statistical,
bioinformatic
analyses
performed.
RESULTS:
proportion
macrophages,
T-cytotoxic
lymphocytes,
plasmocytes
increased
samples
A
correlation
found
lymphocytes
risk
for
metaplasia.
It
number
B
cells,
macrophages
M2,
T-regulatory
cells
NK-cells
are
associated
increase
six
genes
most
specific
intestinal-type
CONCLUSION:
significant
difference
mucosal
indicates
potential
influence
on
progression
pathological
process
along
Correa
cascade.
One
be
their
as
an
epigenetic
factor.
Язык: Английский
Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Ноя. 7, 2024
Background
Gastric
intestinal
metaplasia
is
a
common
pathological
feature
in
patients
with
Helicobacter
pylori
(
H.
)
infection.
Rabeprazole
was
widely
used
as
the
first-line
regimen
for
infectious
treatment.
The
objective
of
this
study
to
explore
mechanism
rabeprazole
gastric
Methods
Real-time
PCR,
Western
blotting
(WB)
and
ROS
analysis
were
conducted
confirm
that
could
induce
ferroptosis
suppress
metaplasia.
Cellular
fraction,
luciferase
chromatin
immunoprecipitation
(ChIP)
identify
underlying
modulated
ferroptosis.
Results
Herein,
we
found
treatment
led
inhibit
CDX2
MUC2
expression,
alleviating
metaplasia,
which
attributed
enhanced
characterized
by
decreased
GPX4
expression.
Inhibition
ferrostatin-1
(Fer-1)
reverse
expression
caused
rabeprazole.
Mechanically,
CREB
phosphorylation
nuclear
translocation,
further
binding
promoter,
reducing
transactivity.
Moreover,
endogenous
PKA
interacted
CREB,
interaction
drastically
destroyed
response
Most
importantly,
observed
pylori-
infected
comparison
HC
control.
Conclusion
These
findings
suggested
induced
reduce
epithelial
cells
through
PKA/CREB
cascade
signaling,
implying
targeting
be
promising
strategy
improving
during
-infected
patients.
Язык: Английский