Breast Cancer Research,
Journal Year:
2025,
Volume and Issue:
27(1)
Published: March 26, 2025
Blood
DNA
methylation
(DNAm)
profiles
have
been
used
to
show
that
changes
in
circulating
leukocyte
composition
occur
during
breast
cancer
development,
suggesting
peripheral
immune
system
alterations
are
markers
of
risk.
DNAm
recently
predict
plasma
protein
concentrations
("Protein
EpiScores"),
but
their
associations
with
risk
not
examined
detail.
Whole
blood
were
obtained
for
a
case-cohort
sample
participants
the
Sister
Study
and
calculate
109
Protein
EpiScores.
Of
4,479
women
included,
2,151
(48%)
diagnosed
within
15
years
baseline
draw
(median
time
diagnosis:
8.6
years;
1,673
invasive
478
ductal
carcinomas
situ).
EpiScores
incidence
estimated
using
weighted
Cox
regression
models,
overall
stratified
by
participant
characteristics.
RARRES2,
IGFBP4,
CCL21
positively
associated
(hazard
ratios
from
1.17
1.24),
while
those
F7,
SELL,
CXCL9,
CD48,
IL19
inversely
0.82
0.86)
(all
FDR
<
0.10).
Eight
response-related
(CXCL9,
FCGR3B,
CXCL11,
CCL21,
CRTAM,
VCAM1,
GZMA)
cancers
five
enrollment.
EpiScore
consistently
stronger
estrogen
receptor-negative
tumors.
Several
EpiScores,
including
many
related
response,
risk,
highlighting
novel
development.
Journal of Cancer,
Journal Year:
2023,
Volume and Issue:
14(5), P. 850 - 873
Published: Jan. 1, 2023
Programmed
death-1
is
a
protein
found
on
the
surface
of
immune
cells
that
can
interact
with
its
ligand,
programmed
death-ligand
1
(PD-L1),
which
expressed
plasma
membrane,
secreted
cellular
exosomes,
in
cell
nuclei,
or
as
circulating
soluble
protein.
This
interaction
lead
to
escape
cancer
patients.
In
clinical
settings,
PD-L1
plays
an
important
role
tumor
disease
diagnosis,
determining
therapeutic
effectiveness,
and
predicting
patient
prognosis.
inhibitors
are
also
essential
components
immunotherapy.
Thus,
detection
levels
crucial,
especially
era
precision
therapy.
recent
years,
innovations
have
been
made
traditional
immunoassay
methods
development
new
immunoassays
for
detection.
review
aims
summarize
research
progress
technology
highlight
applications
PD-L1.
Cancer Science,
Journal Year:
2023,
Volume and Issue:
115(2), P. 347 - 356
Published: Dec. 21, 2023
Abstract
Circulating
miRNAs
(cirmiRNAs)
can
be
packaged
into
the
exosomes,
participating
in
intercellular
communication,
which
affects
malignant
progression
and
therapy
resistance
of
triple‐negative
breast
cancer
(TNBC).
Currently,
immune
checkpoint
inhibitors
that
regulate
T‐cell
function,
especially
antibodies
against
programmed
cell
death
1
(PD‐1)
or
its
ligand
PD‐L1,
are
emerging
as
new
promising
for
TNBC
patients.
However,
only
very
limited
patients
showed
complete
partial
response
to
anti‐PD‐1
treatment.
Dysfunction
CD8
+
T
cells
is
one
key
reasons
escape
TNBC.
The
regulation
exosome‐derived
cirmiRNAs
on
deserves
more
investigation.
Here,
cirmiR‐20a‐5p
level
was
significantly
upregulated
plasma
culture
supernatant
cells.
High
abundance
correlated
with
a
worse
prognosis
secreted
form
exosomes
by
Exosomal
internalized
resulted
dysfunction
T.
A
mechanism
study
uncovered
targeted
nuclear
protein
ataxia‐telangiectasia
(NPAT)
decreased
NPAT
expression
An
vivo
xenograft
mouse
model
conferred
treatment
resistance.
Collectively,
these
findings
indicated
released
via
exosome
promotes
growth
leads
immunosuppression
inducing
dysfunction.
This
suggests
targeting
might
novel
strategy
overcoming
immunotherapy.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Dec. 13, 2024
Triple-negative
breast
cancer
(TNBC)
is
an
aggressive
subtype
of
characterized
by
the
absence
progesterone
and
estrogen
receptors
low
(or
absent)
HER2
expression.
TNBC
accounts
for
15-20%
all
cancers.
It
associated
with
younger
age,
a
higher
mutational
burden,
increased
risk
recurrence
mortality.
Standard
treatment
primarily
relies
on
cytotoxic
agents,
such
as
taxanes,
anthracyclines,
platinum
compounds
both
early
advanced
stages
disease.
Several
targeted
therapies,
including
bevacizumab
sunitinib,
have
failed
to
demonstrate
significant
clinical
benefit
in
TNBC.
The
emergence
immune
checkpoint
inhibitors
(ICI)
has
revolutionized
treatment.
By
stimulating
system,
ICIs
induce
durable
anti-tumor
response
across
various
solid
tumors.
particularly
promising
target
due
levels
tumor-infiltrating
lymphocytes
(TIL),
PD-L1
expression,
which
generates
tumor-specific
neoantigens
that
activate
cells.
administered
monotherapy
yields
only
modest
response;
however,
rates
significantly
improve
when
are
combined
tumors
expressing
PD-L1.
Pembrolizumab
approved
use
combination
standard
chemotherapy.
However,
more
research
needed
identify
potent
biomarkers,
better
elucidate
synergism
other
agents.
In
this
review,
we
explore
challenges
immunotherapy
TNBC,
examining
mechanisms
tumor
progression
mediated
cells
within
microenvironment,
signaling
pathways
involved
primary
acquired
resistance.
Finally,
provide
comprehensive
overview
ongoing
trials
underway
investigate
novel
immune-targeted
therapies
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(11), P. 6224 - 6224
Published: June 5, 2024
Breast
cancers
(BCs)
are
solid
tumors
composed
of
heterogeneous
tissues
consisting
cancer
cells
and
an
ever-changing
tumor
microenvironment
(TME).
The
TME
includes,
among
other
non-cancer
cell
types,
immune
influencing
the
context
tissues.
In
particular,
cross
talk
their
interactions
with
dramatically
influence
BC
dissemination,
immunoediting,
outcomes
therapies.
Tumor-infiltrating
lymphocytes
(TILs),
tumor-associated
macrophages
(TAMs),
myeloid-derived
suppressor
(MDSCs)
represent
prominent
populations
breast
TMEs,
they
have
important
roles
in
immunoescape
dissemination.
Therefore,
this
article
we
review
features
TILs,
TAMs,
MDSCs
BCs.
Moreover,
highlight
mechanisms
by
which
these
remodel
lead
to
metastasis.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(7), P. 3950 - 3950
Published: April 2, 2024
IL-1α
is
a
dual
function
cytokine
that
affects
inflammatory
and
immune
responses
plays
pivotal
role
in
cancer.
The
effects
of
intracellular
on
the
development
triple
negative
breast
cancer
(TNBC)
mice
were
assessed
using
CRISPR/Cas9
system
to
suppress
expression
4T1
cells.
Knockout
cells
modified
multiple
genes,
including
downregulation
cytokines
chemokines
involved
recruitment
tumor-associated
pro-inflammatory
Orthotopical
injection
knockout
(KO)
into
BALB/c
led
significant
decrease
local
tumor
growth
lung
metastases,
compared
wild-type
(4T1/WT)
Neutrophils
myeloid-derived
suppressor
abundant
tumors
developing
after
4T1/WT
cells,
whereas
more
antigen-presenting
observed
microenvironment
KO
This
switch
correlated
with
increased
infiltration
CD3+CD8+
NKp46+cells.
Engraftment
immunodeficient
NOD.SCID
resulted
rapid
growth,
metastasis
comparison
engraftment
Our
results
suggest
TNBC
progression
by
modulating
interplay
between
immunosuppressive
vs.
cytotoxic
Stem Cell Research & Therapy,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: April 25, 2024
Abstract
Background
Triple-negative
breast
cancer
(TNBC)
is
the
most
lethal
subtype
of
and,
despite
its
adverse
effects,
chemotherapy
standard
systemic
treatment
option
for
TNBC.
Since,
it
utmost
importance
to
consider
combination
different
agents
achieve
greater
efficacy
and
curability
potential,
MSC
secretome
a
possible
innovative
alternative.
Methods
In
present
study,
we
proposed
investigate
anti-tumor
effect
chemical
agent
(paclitaxel)
with
complex
biological
product,
derived
from
human
Uterine
Cervical
Stem
cells
(CM-hUCESC)
in
Results
The
paclitaxel
CM-hUCESC
decreased
cell
proliferation
invasiveness
tumor
induced
apoptosis
vitro
(MDA-MB-231
and/or
primary
cells).
was
confirmed
mouse
xenograft
model
showing
that
both
products
has
significant
reducing
growth.
Also,
pre-conditioning
hUCESC
sub-lethal
dose
enhances
reduced
significantly
growth
even
allows
diminish
vivo.
This
part
due
action
extracellular
vesicles
(EVs)
soluble
factors,
such
as
TIMP-1
−
2.
Conclusions
conclusion,
our
data
demonstrate
synergistic
on
TNBC
opens
an
opportunity
reduce
chemotherapeutic
agents,
which
may
decrease
chemotherapy-related
toxicity.
Abstract
Breast
cancer
(BC)
is
one
of
the
most
diagnosed
cancers
in
women.
Based
on
histological
characteristics,
they
are
classified
as
non-invasive,
or
situ
(tumors
located
within
milk
ducts
lobules)
and
invasive.
BC
may
develop
from
carcinomas
over
time.
Determining
prognosis
predicting
response
to
treatment
essential
tools
manage
this
disease
reduce
its
incidence
mortality,
well
promote
personalized
therapy
for
patients.
However,
half
cases
not
associated
with
known
risk
factors.
In
addition,
some
patients
resistance
relapse.
Therefore,
it
necessary
identify
new
biomarkers
strategies
that
improve
existing
therapies.
regard,
role
microbiome
being
researched
could
play
a
carcinogenesis
efficacy
This
review
aims
describe
specific
patterns
BC.
For
this,
literature
search
was
carried
out
PubMed
database
using
MeSH
terms
“Breast
Neoplasms”
“Gastrointestinal
Microbiome”,
including
29
publications.
Most
studies
have
focused
characterizing
gut
breast
tissue
Likewise,
animal
models
vitro
investigated
impact
microbiota
(GM)
treatments
effects
tumor
cells
were
included.
results
included
articles,
be
an
imbalance
GM.
varied
depending
molecular
type,
stage
grade
cancer,
menopause,
menarche,
body
mass
index,
physical
activity.
microbial
profile
identified
biomarker.
On
other
hand,
suggest
GM
influence
microorganisms
bacterial
metabolites
therapies
development.
Cell Biochemistry and Function,
Journal Year:
2024,
Volume and Issue:
42(3)
Published: March 29, 2024
Nucleic
acid
vaccines
(NAVs)
have
the
potential
to
be
economical,
safe,
and
efficacious.
Furthermore,
just
chosen
antigen
in
pathogen
is
target
of
immune
responses
brought
on
by
NAVs.
Triple-negative
breast
cancer
(TNBC)
treatment
shows
great
promise
for
nucleic
acid-based
vaccines,
such
as
DNA
(as
plasmids)
RNA
messenger
[mRNA]).
Moreover,
offer
a
compelling
approach
that
can
elicit
targeted
long-lasting
against
tumor
antigens.
Bacterial
plasmids
encode
antigens
immunostimulatory
molecules
serve
foundation
vaccines.
In
1990s,
plasmid
encoding
influenza
A
nucleoprotein
triggered
protective
cytotoxic
T
lymphocyte
(CTL)
response,
marking
first
instance
vaccine-mediated
immunity.
Similarly,
vitro
transcribed
mRNA
was
successfully
used
animals
1990.
At
point,
mice
were
given
an
injection
gene
sequence,
researchers
saw
production
protein.
We
begin
this
review
summarizing
our
existing
knowledge
Next,
we
addressed
NAV
delivery,
emphasizing
need
increase
efficacy
TNBC.
Cancers,
Journal Year:
2024,
Volume and Issue:
16(19), P. 3250 - 3250
Published: Sept. 24, 2024
Triple-negative
breast
cancer
(TNBC)
lacks
the
expression
of
estrogen
receptors
(ERs),
human
epidermal
growth
factor
receptor
2
(HER2),
and
progesterone
(PRs).
TNBC
has
poorest
prognosis
among
subtypes
is
more
likely
to
respond
immunotherapy
due
its
higher
PD-L1
a
greater
percentage
tumor-infiltrating
lymphocytes.
Immunotherapy
revolutionized
treatment,
especially
with
FDA’s
approval
pembrolizumab
(Keytruda)
combined
chemotherapy
for
advanced
cases,
opening
new
avenues
treating
this
deadly
disease.
Although
can
significantly
improve
patient
outcomes
in
subset
patients,
achieving
desired
response
rate
all
remains
an
unmet
clinical
goal.
Strategies
that
enhance
responses
immune
checkpoint
blockade,
including
combining
chemotherapy,
molecularly
targeted
therapy,
or
radiotherapy,
may
rates
outcomes.
In
review,
we
provide
short
background
on
explore
different
types
strategies
are
currently
being
evaluated
TNBC.
Additionally,
review
why
combination
be
beneficial,
overview
strategies,
discuss
novel
immunotherapeutic
opportunities
approved
near
future
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 14, 2025
ABSTRACT
The
non-receptor
tyrosine
kinase
PTK6
is
expressed
in
70%
of
triple
negative
breast
cancers
(TNBC)
and
an
oncogenic
driver
epithelial-mesenchymal
transition
(EMT).
EMT
promotes
metastasis
immune
evasion
TNBC.
Therefore,
targeting
drivers
could
reverse
these
properties
lead
to
more
favorable
outcomes.
Treatment
TNBC
tumors
with
a
small
molecule
inhibitor
(P21d)
suppressed
their
growth
vivo
.
Tumor
inhibition
by
P21d
dependent
on
induced
response
because:
1)
observed
immunocompetent,
but
not
immunodeficient,
mice;
2)
increases
tumor-infiltrating
CD8
+
T
NK
cells
decreases
immunosuppressive
myeloid-derived
suppressor
cells;
3)
tumor
abrogated
co-treatment
or
cell-depleting
antibodies.
These
effects
cytotoxic
TILs
are
phenocopied
the
knockdown
tumoral
SNAIL,
which
supports
as
mechanism
for
enhanced
anti-tumor
response.
RNA
sequencing
(RNA-seq)
profiling
P21d-treated
also
revealed
changes
consistent
activation
identified
CXCL10
critical
chemokine
intratumorally
that
recruitment
NK/CD8+
site,
leading
inhibition.
Our
study
highlights
novel
microenvironmental
functions
important
consequences
new
immunotherapeutic
approaches