Russian Family Doctor,
Год журнала:
2024,
Номер
28(4), С. 39 - 49
Опубликована: Дек. 15, 2024
Multifactorial
diseases
pose
a
growing
challenge
to
global
healthcare
due
their
rapidly
increasing
prevalence,
high
mortality
rates,
and
significant
contribution
disability
among
the
working-age
population.
Intensive
research
aimed
at
improving
early
diagnosis,
prevention,
treatment
has
underscored
critical
role
of
epigenetic
changes,
which
influence
gene
expression
without
altering
primary
DNA
sequence.
This
article
provides
an
overview
mechanisms
involved
in
regulation,
including
methylation,
post-translational
histone
modifications,
non-coding
microRNAs
silencing.
Epigenetic
factors
serve
as
bridge
between
genome
environmental
influences.
Environmental
risk
factors—shaped
by
lifestyle,
behavior,
ecological
exposures,
psycho-emotional
stress—play
phenotypic
manifestations
overall
human
health.
The
reversibility
regulating
can
lead
both
beneficial
adverse
health
outcomes.
continuous
development
new
technologies
positions
epigenetics
promising
field
for
functional
research,
with
potential
fundamentally
transform
therapeutic
approaches
multifactorial
diseases.
Biomolecules,
Год журнала:
2025,
Номер
15(1), С. 71 - 71
Опубликована: Янв. 6, 2025
The
tumor
microenvironment
(TME)
plays
a
pivotal
role
in
neoplastic
initiation
and
progression.
Epigenetic
machinery,
governing
the
expression
of
core
oncogenes
suppressor
genes
transformed
cells,
significantly
contributes
to
development
at
both
primary
distant
sites.
Recent
studies
have
illuminated
how
epigenetic
mechanisms
integrate
external
cues
downstream
signals,
altering
phenotype
stromal
cells
immune
cells.
This
remolds
area
surrounding
ultimately
fostering
an
immunosuppressive
microenvironment.
Therefore,
correcting
TME
by
targeting
modifications
holds
substantial
promise
for
cancer
treatment.
review
synthesizes
recent
research
that
elucidates
impact
specific
regulations-ranging
from
DNA
methylation
histone
chromatin
remodeling-on
within
TME.
Notably,
we
highlight
their
functional
roles
either
promoting
or
restricting
We
also
discuss
potential
applications
agents
treatment,
envisaging
ability
normalize
ecosystem.
aims
assist
researchers
understanding
dynamic
interplay
between
epigenetics
TME,
paving
way
better
therapy.
Clinical and Molecular Hepatology,
Год журнала:
2025,
Номер
31(2), С. 563 - 576
Опубликована: Янв. 14, 2025
Hepatocellular
carcinoma
(HCC)
exhibits
high
de
novo
recurrence
rates
post-resection.
Current
post-surgery
prediction
methods
are
limited,
emphasizing
the
need
for
reliable
biomarkers
to
assess
risk.
We
aimed
develop
methylation-based
markers
classifying
HCC
patients
and
predicting
their
risk
of
post-surgery.
In
this
retrospective
cohort
study,
we
analyzed
data
from
who
underwent
surgical
resection
in
Korea,
excluding
those
with
within
one
year
Using
Infinium
Methylation
EPIC
array
on
140
samples
discovery
cohort,
classified
into
low-
high-risk
groups
based
methylation
profiles.
Distinctive
were
identified
through
random
forest
analysis.
These
validated
cancer
genome
atlas
(n=217),
Validation
1
(n=63)
experimental
using
a
methylation-sensitive
high-resolution
melting
(MS-HRM)
assay
2
(n=63).
The
low-risk
group
(methylation
1;
MG1)
showed
average
0.73
(95%
confidence
interval
[CI]
0.69-0.77)
23.5%
rate,
while
(MG2)
had
an
0.17
CI
0.14-0.20)
44.1%
rate
(P<0.03).
confirmed
applicability
across
diverse
populations,
showing
accuracy
probability
(area
under
curve
96.8%).
MS-HRM
its
effectiveness
95.5%
sensitivity,
89.7%
specificity,
92.2%
accuracy.
effectively
by
risk,
enhancing
potentially
offering
personalized
management
strategies.
Pharmaceuticals,
Год журнала:
2025,
Номер
18(2), С. 207 - 207
Опубликована: Фев. 3, 2025
Breast
cancer
is
the
most
common
malignancy
affecting
women,
manifesting
as
a
heterogeneous
disease
with
diverse
molecular
characteristics
and
clinical
presentations.
Recent
studies
have
elucidated
role
of
epigenetic
modifications
in
pathogenesis
breast
cancer,
including
drug
resistance
efflux
characteristics,
offering
potential
new
diagnostic
prognostic
markers,
treatment
efficacy
predictors,
therapeutic
agents.
Key
include
DNA
cytosine
methylation
covalent
modification
histone
proteins.
Unlike
genetic
mutations,
reprogramming
landscape
epigenome
promising
targeted
therapy
for
reversal
resistance.
Epidrugs,
which
target
modifications,
can
provide
novel
options
by
reversing
acquired
to
treatment.
Currently,
approach
involves
combination
therapies
consisting
epidrugs
immune
checkpoint
inhibitors.
This
review
examines
aberrant
regulation
initiation
progression,
focusing
on
related
estrogen
signaling,
resistance,
epithelial–mesenchymal
transition
(EMT).
It
existing
drugs
treating
agents
that
modify
DNA,
inhibitors
acetyltransferases,
deacetylases,
methyltransferases,
demethyltransferases.
also
delves
into
ongoing
combining
other
addresses
upcoming
obstacles
this
field.
Current Oncology,
Год журнала:
2025,
Номер
32(2), С. 88 - 88
Опубликована: Фев. 5, 2025
Members
of
the
DNA
methyltransferase
(DNMT)
family
have
been
recognized
as
major
epigenetic
regulators
altered
gene
expression
during
tumor
development.
They
establish
and
maintain
methylation
CpG
island
promoter
non-CpG
region
genome.
The
abnormal
status
suppressor
genes
(TSGs)
has
associated
with
tumorigenesis,
leading
to
genomic
instability,
improper
silence,
immune
evasion.
DNMT1
helps
preserve
patterns
replication,
whereas
DNMT3
is
responsible
for
de
novo
methylation,
creating
new
patterns.
Altered
significantly
supports
growth
by
changing
FDA-approved
DNMT
inhibitors
reverse
hypermethylation-induced
repression
improve
therapeutic
outcomes
cancer.
Recent
studies
indicate
that
combining
chemotherapies
immunotherapies
can
synergistic
effects,
especially
in
aggressive
metastatic
tumors.
Improving
treatment
schedules,
increasing
isoform
specificity,
reducing
toxicity,
utilizing
genome-wide
analyses
CRISPR-based
editing
create
personalized
therapies
tailored
individual
patient
needs
are
promising
strategies
enhancing
outcomes.
This
review
discusses
interaction
between
DNMT1,
its
binding
partners,
connection
tumors,
how
these
processes
contribute
development,
inhibitors’
advancements
pharmacological
properties.
Journal of Experimental & Clinical Cancer Research,
Год журнала:
2025,
Номер
44(1)
Опубликована: Фев. 18, 2025
Abstract
Background
Co-targeting
of
immune
checkpoint
inhibitors
(ICI)
CTLA-4
and
PD-1
has
recently
become
the
new
first-line
standard
care
therapy
pleural
mesothelioma
(PM)
patients,
with
a
significant
improvement
overall
survival
(OS)
over
conventional
chemotherapy.
The
analysis
by
tumor
histotype
demonstrated
greater
efficacy
ICI
compared
to
chemotherapy
in
non-epithelioid
(non-E)
vs.
epithelioid
(E)
PM,
although
some
E
PM
patients
also
benefit
from
treatment.
This
evidence
suggests
that
molecular
features,
beyond
histotype,
could
be
relevant
improve
PM.
Among
these,
DNA
methylation
emerges
as
promising
factor
explore,
due
its
potential
role
driving
phenotype
cancer
cells.
Therefore,
we
utilized
panel
cultured
cells
different
provide
preclinical
supporting
landscape,
along
pharmacologic
modulation,
prospectively
patients.
Methods
methylome
profile
(EPIC
array)
distinct
(
n
=
5)
non-E
9)
cell
lines
was
analyzed,
followed
integrated
their
associated
transcriptomic
(Clariom
S
array),
before
after
vitro
treatment
hypomethylating
agent
(DHA)
guadecitabine.
most
variable
methylated
probes
were
selected
calculate
score
(CIMP
index)
for
each
line
at
baseline.
Genes
differentially
expressed
(DE)
(DM)
then
gene
ontology
analysis.
Results
CIMP
index
stratified
into
two
classes,
(hyper-methylated;
7)
LOW
(hypo-methylated;
7),
regardless
or
histotype.
Integrated
transcriptome
analyses
revealed
exhibited
substantial
number
hyper-methylated,
silenced
genes,
which
negatively
impacted
Treatment
DHA
reverted
methylation-driven
immune-compromised
enhanced
constitutive
immune-favorable
Conclusion
study
highlighted
relevance
shaping
classification
cells,
independent
histological
subtypes.
identified
shifting
towards
an
state
highlights
evaluation
phase
I/II
clinical
trials
investigating
epigenetic-based
combinations
reverse
resistance
mechanisms.
Clinical & Translational Oncology,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 22, 2025
Abstract
Increasing
knowledge
of
the
immunosuppressive
tumor
microenvironment
in
cancer-related
processes
has
led
to
developing
novel
immune-based
therapies
that
have
changed
cancer
treatment
paradigm.
In
microenvironment,
plethora
soluble
factors
secreted
by
cells
interacts
with
immune
and
non-immune
components
deliver
signals
necessary
for
progression.
Accordingly,
targeting
tumor-derived
inducing
this
become
an
appealing
therapeutic
potential
advancing
treatment.
CCL20,
a
chemokine
best
known
induce
leucocyte
migration
response
pathological
inflammatory
conditions,
been
implicated
proliferation,
angiogenesis,
metastasis,
immunosuppression,
resistance.
Notably,
CCL20
its
receptor
CCR6
are
important
interactions.
This
review
discusses
interaction
between
CCL20–CCR6
axis
how
these
interactions
promote
Also,
outline
studies
utilizing
combination
other
standard
treatments
shed.
Comptes Rendus Biologies,
Год журнала:
2025,
Номер
348(G1), С. 43 - 53
Опубликована: Фев. 25, 2025
Cancer
is
one
of
the
leading
causes
mortality
worldwide.
Known
since
antiquity,
its
understanding
has
evolved
over
time
and
significantly
advanced
with
new
technologies
past
four
decades.
initiation
currently
admitted
to
be
explainable
by
somatic
mutation
theory,
which
postulates
that
DNA
mutations
altering
function
oncogenes
tumor
suppressor
genes
initiate
cancer.
In
addition
these
mutations,
epigenetic
alterations,
heritably
change
gene
expression
without
sequence,
also
play
a
key
role.
Recent
data
suggests
components
regulate
all
aspects
progression,
including
cancer
initiation.
These
discoveries
prompt
reevaluation
prevention
treatment
strategies.
Le
est
une
des
principales
de
mortalité
mondiale.
Connu
depuis
l'Antiquité,
sa
compréhension
évolué
au
fil
du
temps
et
progressé
énormément
grâce
aux
nouvelles
durant
les
quatre
dernières
décennies.
L'initiation
aujourd'hui
expliquée
par
la
théorie
somatiques,
suggérant
que
d'ADN
altérant
fonction
d'oncogènes
gènes
suppresseurs
tumeurs
initieraient
le
Outre
ces
altérations
épigénétiques,
qui
changent
l'expression
manière
héritable
sans
changement
séquence
d'ADN,
jouent
cependant
aussi
un
rôle
clé.
Des
données
récentes
suggèrent
composantes
épigénétiques
régulent
tous
progression
tumorale,
y
compris
l'initiation
cancers.
Ces
découvertes
amènent
à
revisiter
somatiques
revoir
stratégies
prévention
traitement
