Discover Oncology,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: April 17, 2025
Abstract
Triple-negative
breast
cancer
(TNBC)
is
an
aggressive
malignancy
characterized
by
limited
therapeutic
options
and
poor
prognosis.
Despite
advancements
in
precision
oncology,
conventional
chemotherapy
remains
the
cornerstone
of
TNBC
treatment,
often
accompanied
debilitating
side
effects
suboptimal
outcomes.
This
review
presents
a
comprehensive
analysis
clinical
trials
on
targeted
therapies,
aiming
to
establish
novel,
evidence-based
treatment
strategy
exclusively
leveraging
molecularly
agents.
By
integrating
patient-specific
genetic
profiles
with
responses
observed
across
various
trial
phases,
this
approach
seeks
optimize
efficacy
while
minimizing
toxicity.
The
proposed
therapy
combinations
hold
significant
potential
revolutionize
offering
paradigm
shift
toward
medicine
improved
patient
Journal of Hematology & Oncology,
Journal Year:
2023,
Volume and Issue:
16(1)
Published: Aug. 28, 2023
Triple-negative
breast
cancer
(TNBC),
a
highly
aggressive
subtype
of
cancer,
negatively
expresses
estrogen
receptor,
progesterone
and
the
human
epidermal
growth
factor
receptor
2
(HER2).
Although
chemotherapy
is
main
form
treatment
for
patients
with
TNBC,
effectiveness
TNBC
still
limited.
The
search
more
effective
therapies
urgent.
Multiple
targeted
therapeutic
strategies
have
emerged
according
to
specific
molecules
signaling
pathways
expressed
in
TNBC.
These
include
PI3K/AKT/mTOR
inhibitors,
Notch
poly
ADP-ribose
polymerase
antibody-drug
conjugates.
Moreover,
immune
checkpoint
example,
pembrolizumab,
atezolizumab,
durvalumab,
are
widely
explored
clinic.
We
summarize
recent
advances
therapy
immunotherapy
aim
serving
as
reference
development
individualized
future.
Journal of Translational Medicine,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Jan. 3, 2024
Abstract
Breast
cancer
(BC)
is
a
multifaceted
disease
characterized
by
distinct
molecular
subtypes
and
varying
responses
to
treatment.
In
BC,
the
phosphatidylinositol
3-kinase
(PI3K)
pathway
has
emerged
as
crucial
contributor
development,
advancement,
resistance
This
review
article
explores
implications
of
PI3K
in
predictive,
preventive,
personalized
medicine
for
BC.
It
emphasizes
identification
predictive
biomarkers,
such
PIK3CA
mutations,
utility
profiling
guiding
treatment
decisions.
The
also
discusses
potential
targeting
preventive
strategies
customization
therapy
based
on
tumor
stage,
subtypes,
genetic
alterations.
Overcoming
inhibitors
exploring
combination
therapies
are
addressed
important
considerations.
While
this
field
holds
promise
improving
patient
outcomes,
further
research
clinical
trials
needed
validate
these
approaches
translate
them
into
practice.
Graphical
Discover Nano,
Journal Year:
2024,
Volume and Issue:
19(1)
Published: March 7, 2024
Abstract
Breast
cancer
is
a
complex
and
heterogeneous
disease,
encompassing
various
subtypes
characterized
by
distinct
molecular
features,
clinical
behaviors,
treatment
responses.
Categorization
of
based
on
the
presence
or
absence
estrogen
receptor
(ER),
progesterone
(PR),
human
epidermal
growth
factor
2
(HER2),
leading
to
such
as
luminal
A,
B,
HER2-positive,
triple-negative
breast
(TNBC).
TNBC,
comprising
around
20%
all
cancers,
lacks
expression
ER,
PR,
HER2
receptors,
rendering
it
unresponsive
targeted
therapies
presenting
significant
challenges
in
treatment.
TNBC
associated
with
aggressive
behavior,
high
rates
recurrence,
resistance
chemotherapy.
Tumor
initiation,
progression,
are
attributed
stem
cells
(BCSCs),
which
possess
self-renewal,
differentiation,
tumorigenic
potential.
Surface
markers,
self-renewal
pathways
(Notch,
Wnt,
Hedgehog
signaling),
apoptotic
protein
(Bcl-2),
angiogenesis
inhibition
(VEGF
inhibitors),
immune
modulation
(cytokines,
checkpoint
inhibitors)
among
key
targets
discussed
this
review.
However,
targeting
BCSC
subpopulation
presents
challenges,
including
off-target
effects,
low
solubility,
bioavailability
anti-BCSC
agents.
Nanoparticle-based
offer
promising
approach
target
cellular
processes
implicated
survival
BSCS
TNBC.
In
review,
we
explore
nanocarrier-based
approaches
for
BCSCs
aiming
overcome
these
improve
outcomes
patients.
These
nanoparticle-based
therapeutic
strategies
hold
promise
addressing
gap
delivering
while
minimizing
systemic
toxicity
enhancing
efficacy.
Graphical
abstract
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: Jan. 5, 2024
Abstract
Breast
cancer
is
the
second
leading
cause
of
death
in
women
worldwide,
with
triple-negative
breast
(TNBC)
having
worst
prognosis.
Although
there
are
numerous
studies
on
TNBC,
no
effective
treatment
for
it,
and
it
still
a
major
problem
today.
Studies
PIWI-interacting
RNAs
(piRNAs)
increasing
investigating
mechanism
piRNAs
proliferation
metastasis
TNBC
may
lead
to
new
potential
targets.
Here,
we
identified
novel
piRNA,
piR-YBX1,
which
was
downregulated
compared
matched
normal
tissue.
Overexpression
piR-YBX1
significantly
inhibited
proliferation,
migration,
invasion
ability
cells
both
vivo
vitro.
Mechanistically,
could
bind
directly
mRNA
Y-box
binding
protein
1
(
YBX1
)
overexpression
levels,
while
function
be
partly
rescued
by
YBX1.
In
addition,
RAF1
key
molecule
MAPK
signaling
pathway,
p-MEK
p-ERK1/2,
can
reverted
conclusion,
our
findings
discovered
that
piR-YBX1/YBX1/MAPK
axis
suppresses
therefore
has
an
therapeutic
agent
cancer.
Journal of Experimental & Clinical Cancer Research,
Journal Year:
2024,
Volume and Issue:
43(1)
Published: May 31, 2024
RNA
modifications
of
transfer
RNAs
(tRNAs)
are
critical
for
tRNA
function.
Growing
evidence
has
revealed
that
related
to
various
disease
processes,
including
malignant
tumors.
However,
the
biological
functions
methyltransferase-like
1
(METTL1)-regulated
m7G
in
breast
cancer
(BC)
remain
largely
obscure.
The
role
METTL1
BC
progression
were
examined
by
cellular
loss-
and
gain-of-function
tests
xenograft
models
both
vitro
vivo.
To
investigate
change
modification
mRNA
translation
efficiency
BC,
m7G-methylated
immunoprecipitation
sequencing
(m7G
MeRIP-seq),
Ribosome
profiling
(Ribo-seq),
polysome-associated
performed.
Rescue
assays
conducted
decipher
underlying
molecular
mechanisms.
methyltransferase
complex
components
WD
repeat
domain
4
(WDR4)
down-regulated
tissues
at
protein
levels.
Functionally,
inhibited
cell
proliferation,
cycle
progression,
relying
on
its
enzymatic
activity.
Mechanistically,
increased
levels
19
tRNAs
modulate
growth
arrest
DNA
damage
45
alpha
(GADD45A)
retinoblastoma
(RB1)
a
codon-dependent
manner
associated
with
m7G.
Furthermore,
vivo
experiments
showed
overexpression
enhanced
anti-tumor
effectiveness
abemaciclib,
cyclin-dependent
kinases
6
(CDK4/6)
inhibitor.
Our
study
uncovered
crucial
tumor-suppressive
METTL1-mediated
promoting
GADD45A
RB1
mRNAs,
selectively
blocking
G2/M
phase
cycle.
These
findings
also
provided
promising
strategy
improving
therapeutic
benefits
CDK4/6
inhibitors
treatment
patients.
Journal of Advanced Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: April 1, 2024
Triple-negative
breast
cancer
(TNBC)
represents
the
most
aggressive
subtype
of
with
an
extremely
dismal
prognosis
and
few
treatment
options.
As
a
desmoplastic
tumor,
TNBC
tumor
cells
are
girdled
by
stroma
composed
cancer-associated
fibroblasts
(CAFs)
their
secreted
stromal
components.
The
rapidly
proliferating
cells,
together
stroma,
exert
additional
solid
tissue
pressure
on
vasculature
surrounding
tissues,
severely
obstructing
therapeutic
agent
from
deep
intratumoral
penetration,
resulting
in
metastasis
resistance.
Journal of Experimental & Clinical Cancer Research,
Journal Year:
2024,
Volume and Issue:
43(1)
Published: June 27, 2024
Abstract
Background
Triple-negative
breast
cancer
(TNBC)
is
characterized
by
its
high
metastatic
potential,
which
results
in
poor
patient
survival.
Cancer-associated
fibroblasts
(CAFs)
are
crucial
facilitating
TNBC
metastasis
via
induction
of
mitochondrial
biogenesis.
However,
how
to
inhibit
CAF-conferred
biogenesis
still
needed
explore.
Methods
We
investigated
using
wound
healing
and
cell
invasion
assays,
3D-culture,
anoikis
detection,
NOD/SCID
mice.
Mitochondrial
was
detected
MitoTracker
green
FM
staining,
quantification
DNA
levels,
blue-native
polyacrylamide
gel
electrophoresis.
The
expression,
transcription,
phosphorylation
peroxisome-proliferator
activated
receptor
coactivator
1α
(PGC-1α)
were
western
blotting,
chromatin
immunoprecipitation,
dual-luciferase
reporter
assay,
quantitative
polymerase
chain
reaction,
liquid
chromatography-tandem
mass
spectrometry.
prognostic
role
PGC-1α
evaluated
the
Kaplan–Meier
plotter
database
clinical
tissue
samples.
Results
demonstrated
that
indicated
lymph
node
metastasis,
tumor
thrombus
formation,
survival
patients,
it
induced
CAFs,
functioned
as
an
inducer
TNBC.
Shikonin
impeded
CAF-induced
nuclear
localization,
interaction
with
estrogen-related
alpha
(ERRα),
thereby
inhibiting
PGC-1α/ERRα-targeted
genes.
Mechanistically,
downregulation
mediated
synthase
kinase
3β-induced
at
Thr295,
associated
neural
precursor
expressed
developmentally
downregulated
4e1
recognition
subsequent
degradation
ubiquitin
proteolysis.
Mutation
Thr295
negated
suppressive
effects
shikonin
on
CAF-stimulated
vitro
vivo.
Conclusions
Our
findings
indicate
a
viable
target
for
blocking
disrupting
biogenesis,
merits
potential
treatment
inhibitor
through
targeting
PGC-1α.
