International Journal of Clinical Oncology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Sept. 18, 2024
Abstract
Background
Genome
DNA
methylation
profiling
is
a
promising
yet
costly
method
for
cancer
classification,
involving
substantial
data.
We
developed
an
ensemble
learning
model
to
identify
types
using
profiles
from
limited
number
of
CpG
sites.
Methods
Analyzing
data
890
samples
across
10
the
TCGA
database,
we
utilized
ANOVA
and
Gain
Ratio
select
most
significant
sites,
then
employed
Gradient
Boosting
reduce
these
just
100
Results
This
approach
maintained
high
accuracy
multiple
machine
models,
with
classification
rates
between
87.7%
93.5%
methods
including
Extreme
Boosting,
CatBoost,
Random
Forest.
effectively
minimizes
features
needed
without
losing
performance,
helping
classify
primary
organs
uncover
subgroups
within
specific
cancers
like
breast
lung.
Conclusions
Using
gradient
boosting
feature
selector
shows
potential
streamlining
methylation-based
classification.
Pharmaceuticals,
Journal Year:
2025,
Volume and Issue:
18(2), P. 207 - 207
Published: Feb. 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.
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.
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: April 21, 2025
Abstract
Aberrant
methylation
of
the
EphA7
promoter
has
been
observed
in
cervical
cancer
(CC);
however,
its
precise
function
and
role
CC
remain
largely
unknown.
In
this
study,
we
investigated
molecular
mechanisms
carcinogenesis.
First,
our
results
indicated
that
reactivation
expression
via
a
CRISPR
demethylation
tool
(dCas9-Tet1)
had
antitumor
effects.
It
restrained
tumor
proliferation
invasion
while
promoting
apoptosis
PI3K/AKT
signaling
pathway
both
CaSki
SiHa
cells.
The
upstream
interacting
factors
were
subsequently
captured
by
CRISPR-mediated
pull-down
situ,
result
revealed
SP1
MAZ
interacted
with
EphA7.
However,
perturbation
was
associated
SP1/DNMT1
but
not
MAZ.
Furthermore,
17-β-estradiol
(E2)
can
upregulate
through
axis.
A
rescue
experiment
interference
could
restore
effect
E2
on
increasing
upregulating
estrogen
receptor
expression.
addition,
reduced
half-maximal
inhibitory
concentration
(IC
50
)
cisplatin
paclitaxel.
Pooled
analysis
hypermethylation
positively
correlated
purity
negatively
immune
cell
infiltration,
cytotoxic
T
lymphocyte
(CTL)
checkpoint
(IC)
activity,
significantly
mutational
burden
(TMB),
microsatellite
instability
(MSI)
presence
single
nucleotide
variant
(SNV)
neoantigens,
suggesting
better
prognosis
for
patients
hypomethylation
high
Collectively,
these
findings
indicate
targeted
restoration
endogenous
dCas9-Tet1
are
promising
therapeutic
approaches
favorable
patients.
Biomolecules,
Journal Year:
2025,
Volume and Issue:
15(1), P. 71 - 71
Published: Jan. 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,
Journal Year:
2025,
Volume and Issue:
31(2), P. 563 - 576
Published: Jan. 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.
Current Oncology,
Journal Year:
2025,
Volume and Issue:
32(2), P. 88 - 88
Published: Feb. 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.