Indus journal of bioscience research.,
Год журнала:
2024,
Номер
3(1), С. 868 - 880
Опубликована: Дек. 31, 2024
This
research
sought
to
explore
the
role
of
epigenetic
changes
in
cancer
initiation
and
progression,
therapeutic
potential
modulators,
i.e.,
DNMT
inhibitors
HDAC
inhibitors,
expression
levels
non-coding
RNAs,
miRNAs,
controlling
cells.
The
used
a
quantitative
method,
structured
questionnaires
regression
analysis
determine
biology.
validated
that
65%
respondents
were
familiar
with
DNA
methylation,
60%
histone
modification,
55%
gene-editing
technologies
like
CRISPR.
Chi-Square
presence
significant
disparity
awareness
among
demographic
groups,
p-values
0.02
0.05
for
methylation
by
age
modification
medical
specialty,
respectively.
Regression
significantly
caused
cell
apoptosis
(β
=
0.55,
p
0.0002)
suppressed
migration
-0.30,
0.02),
while
also
0.47,
0.005)
promoted
inhibition
-0.25,
0.03).
test
miRNAs
further
correlations
between
miR-21
type
(χ²
10.4,
0.02)
miR-34a
12.1,
0.01).
These
results
suggest
therapies
miRNA-based
behavior
enhancing
efficacy.
study
highlights
modifications
cancer,
urging
on
optimization.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
174, С. 116559 - 116559
Опубликована: Апрель 10, 2024
Breast
cancer
comprises
a
substantial
proportion
of
diagnoses
in
women
and
is
primary
cause
cancer-related
mortality.
While
hormone-responsive
cases
generally
have
favorable
prognosis,
the
aggressive
nature
triple-negative
breast
presents
challenges,
with
intrinsic
resistance
to
established
treatments
being
persistent
issue.
The
complexity
intensifies
emergence
acquired
resistance,
further
complicating
management
cancer.
Epigenetic
changes,
encompassing
DNA
methylation,
histone
RNA
modifications,
non-coding
RNAs,
are
acknowledged
as
crucial
contributors
heterogeneity
unique
epigenetic
landscape
harbored
by
each
cellular
component
within
tumor
microenvironment
(TME)
adds
great
diversity
intricate
regulations
which
influence
therapeutic
responses.
TME,
sophisticated
ecosystem
non-cellular
elements
interacting
cells,
establishes
an
immunosuppressive
fuels
processes
such
growth,
angiogenesis,
extracellular
matrix
remodeling.
These
factors
contribute
challenging
conditions
treatment
fostering
hypoxic
environment,
inducing
metabolic
stress,
creating
physical
barriers
drug
delivery.
This
article
delves
into
complex
connections
between
response,
underlying
vital
interactions
TME.
To
restore
sensitivity
treatment,
it
emphasizes
need
for
combination
therapies
considering
changes
specific
individual
members
Recognizing
pivotal
role
epigenetics
comprehending
specificities
TME
essential
devising
more
effective
strategies.
development
reliable
biomarkers
patient
stratification
will
facilitate
tailored
precise
approaches.
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.
Epigenomes,
Год журнала:
2025,
Номер
9(1), С. 5 - 5
Опубликована: Фев. 5, 2025
Genomic
and
epigenomic
instability
are
defining
features
of
cancer,
driving
tumor
progression,
heterogeneity,
therapeutic
resistance.
Central
to
this
process
epigenetic
echoes,
persistent
dynamic
modifications
in
DNA
methylation,
histone
modifications,
non-coding
RNA
regulation,
chromatin
remodeling
that
mirror
underlying
genomic
chaos
actively
influence
cancer
cell
behavior.
This
review
delves
into
the
complex
relationship
between
these
illustrating
how
they
collectively
shape
genome,
affect
repair
mechanisms,
contribute
evolution.
However,
dynamic,
context-dependent
nature
changes
presents
scientific
ethical
challenges,
particularly
concerning
privacy
clinical
applicability.
Focusing
on
lung
we
examine
specific
patterns
function
as
biomarkers
for
distinguishing
subtypes
monitoring
disease
progression
relapse.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(23), С. 13165 - 13165
Опубликована: Дек. 7, 2024
Breast
cancer
is
a
significant
health
challenge
worldwide
and
the
most
frequently
diagnosed
among
women
globally.
This
review
provides
comprehensive
overview
of
breast
biology,
genomics,
microbial
dysbiosis,
focusing
on
its
various
subtypes
racial
differences.
primarily
classified
into
carcinomas
sarcomas,
with
constituting
cases.
Epidemiology
risk
factors
are
important
for
public
intervention.
Staging
grading,
based
TNM
Nottingham
grading
systems,
respectively,
crucial
to
determining
clinical
outcome
treatment
decisions.
Histopathological
include
in
situ
invasive
carcinomas,
such
as
ductal
carcinoma
(IDC)
lobular
(ILC).
The
explores
molecular
subtypes,
including
Luminal
A,
B,
Basal-like
(Triple
Negative),
HER2-enriched,
delves
cancer's
histological
progression
patterns.
Recent
research
findings
related
nuclear
mitochondrial
genetic
alterations,
epigenetic
reprogramming,
role
microbiome
dysbiosis
differences
also
reported.
an
update
current
diagnostics
modalities.
Frontiers in Oncology,
Год журнала:
2024,
Номер
14
Опубликована: Окт. 16, 2024
The
p53
is
a
crucial
tumor
suppressor
and
transcription
factor
that
participates
in
apoptosis
senescence.
It
can
be
activated
upon
DNA
damage
to
regulate
the
expression
of
series
genes.
Previous
studies
have
demonstrated
some
specific
lncRNAs
are
part
TP53
regulatory
network.
To
enhance
our
understanding
relationship
between
P53
cancers,
we
review
localization,
structure,
function
related
mechanisms
pathway
or
serve
as
transcriptional
targets.
Frontiers in Oncology,
Год журнала:
2024,
Номер
14
Опубликована: Дек. 18, 2024
Triple-negative
breast
cancer
(TNBC)
is
a
highly
aggressive
and
clinically
challenging
subtype
of
cancer,
lacking
the
expression
estrogen
receptor
(ER),
progesterone
(PR),
HER2/neu.
The
absence
these
receptors
limits
therapeutic
options
necessitating
exploration
novel
treatment
strategies.
Epigenetic
modifications,
which
include
DNA
methylation,
histone
microRNA
(miRNA)
regulation,
play
pivotal
role
in
TNBC
pathogenesis
represent
promising
targets.
This
review
delves
into
potential
epigenetic
interventions
TNBC,
with
focus
on
miRNA
therapeutics.
We
examine
methylation
gene
silencing
within
development
inhibitors
designed
to
reactivate
silenced
tumor
suppressor
genes.
Histone
through
deacetylation
acetylation
particular,
are
critical
regulating
expression.
explore
efficacy
deacetylase
(HDACi),
have
shown
promise
reversing
aberrant
patterns,
thereby
restoring
normal
function,
suppressing
growth.
Furthermore,
highlights
dual
miRNAs
as
both
oncogenes
suppressors
discusses
mimics
modulating
regulatory
molecules
inhibit
progression.
By
integrating
therapies,
we
propose
multifaceted
approach
target
underlying
mechanisms
that
drive
synergistic
use
inhibitors,
HDACi,
miRNA-based
therapies
offers
avenue
for
personalized
strategies,
aiming
enhance
clinical
outcome
patients
TNBC.
Health Sciences,
Год журнала:
2024,
Номер
35(5), С. 213 - 214
Опубликована: Авг. 1, 2024
Karcinomos
in
situ,
įskaitant
lobulinę
karcinomą
situ
(LCIS)
ir
duktalinę
(DCIS)
vystymasis
susijęs
su
sudėtingais
molekuliniais
mechanizmais,
kurie
prisideda
prie
šių
neinvazinių
krūties
pažeidimų
atsiradimo
progresavimo.
Straipsnyje
nagrinėjami
molekuliniai
mechanizmai,
lemiantys
karcinomos
vystymąsi,
jie
gali
skirtis
priklausomai
nuo
carcinoma
konkretaus
potipio
išsivystymo
aplinkybių.
Aiškus
molekulinių
mechanizmų,
susijusių
vėžinių
ląstelių
vystymusi,
supratimas
galėtų
padėti
nustatyti
koreguoti
genetines
mutacijas,
kad
būtų
galima
valdyti
dalijimosi
sutrikimus.
