Lung Cancer Targets and Therapy,
Journal Year:
2024,
Volume and Issue:
Volume 15, P. 29 - 40
Published: March 1, 2024
This
study
aimed
to
investigate
the
effectiveness
and
tolerability
of
anlotinib
plus
PD-1
blockades
in
patients
with
previously
immunotherapy
treated
advanced
non-small-cell
lung
cancer
(NSCLC).
A
total
67
NSCLC
who
received
clinical
practice
were
screened
retrospectively.
All
used
this
approved
China
consisted
sintilimab,
camrelizumab,
tislelizumab
pembrolizumab.
Effectiveness
safety
assessed,
all
followed
up
regularly.
Clinical
significance
between
response
status
previous
immune-related
treatment
regimens
therapeutic
outcomes
was
further
explored.
The
best
overall
among
suggested
that
a
partial
observed
16
patients,
stable
disease
noted
41
progressive
found
10
which
yielded
an
objective
rate
23.9%
(95%
CI:
14.3-35.9%)
control
85.1%
74.3-92.6%).
Prognostic
indicated
median
progression-free
survival
(PFS)
6.1
months
2.37-9.83)
(OS)
16.5
10.73-22.27).
Exploratory
analysis
highlighted
intolerant
(17
patients)
might
have
superior
prognosis
(median
OS:
22.3
vs
12.5
months,
P=0.024).
Additionally,
adverse
reactions
any
grades
during
administration
62
(92.5%),
31
(46.3%)
had
≥grade
3
reactions.
Most
common
fatigue,
hypertension,
diarrhea
hepatotoxicity.
Anlotinib
demonstrated
promising
tolerable
NSCLC.
Those
benefit
significantly
from
blockades.
conclusion
should
be
confirmed
future
studies.
Experimental Hematology and Oncology,
Journal Year:
2022,
Volume and Issue:
11(1)
Published: April 23, 2022
During
the
course
of
tumorigenesis
and
subsequent
metastasis,
malignant
cells
gradually
diversify
become
more
heterogeneous.
Consequently,
tumor
mass
might
be
infiltrated
by
diverse
immune-related
components,
including
cytokine/chemokine
environment,
cytotoxic
activity,
or
immunosuppressive
elements.
This
immunological
heterogeneity
is
universally
presented
spatially
varies
temporally
along
with
evolution
therapeutic
intervention
across
almost
all
solid
tumors.
The
anti-tumor
immunity
shows
a
profound
association
progression
disease
responsiveness
to
treatment,
particularly
in
realm
immunotherapy.
Therefore,
an
accurate
understanding
essential
for
development
effective
therapies.
Facilitated
multi-regional
-omics
sequencing,
single
cell
longitudinal
liquid
biopsy
approaches,
recent
studies
have
demonstrated
potential
investigate
complexity
tumors
its
clinical
relevance
Here,
we
aimed
review
mechanism
underlying
immune
microenvironment.
We
also
explored
how
assessments
facilitate
personalized
Pharmaceutics,
Journal Year:
2023,
Volume and Issue:
15(4), P. 1143 - 1143
Published: April 4, 2023
Cancer
immunotherapy
is
a
type
of
treatment
that
harnesses
the
power
immune
systems
patients
to
target
cancer
cells
with
better
precision
compared
traditional
chemotherapy.
Several
lines
have
been
approved
by
US
Food
and
Drug
Administration
(FDA)
led
remarkable
success
in
solid
tumors,
such
as
melanoma
small-cell
lung
cancer.
These
immunotherapies
include
checkpoint
inhibitors,
cytokines,
vaccines,
while
chimeric
antigen
receptor
(CAR)
T-cell
has
shown
responses
hematological
malignancies.
Despite
these
breakthrough
achievements,
response
variable
among
patients,
only
small
percentage
gained
from
this
treatment,
depending
on
histological
tumor
other
host
factors.
develop
mechanisms
avoid
interacting
circumstances,
which
an
adverse
effect
how
effectively
they
react
therapy.
arise
either
due
intrinsic
factors
within
or
microenvironment
(TME).
When
scenario
used
therapeutic
setting,
term
“resistance
immunotherapy”
applied;
“primary
resistance”
denotes
failure
respond
start,
“secondary
relapse
following
initial
immunotherapy.
Here,
we
provide
thorough
summary
internal
external
underlying
resistance
Furthermore,
variety
are
briefly
discussed,
along
recent
developments
employed
prevent
relapses
focus
upcoming
initiatives
improve
efficacy
for
patients.
Angiogenesis,
Journal Year:
2024,
Volume and Issue:
27(3), P. 333 - 349
Published: April 6, 2024
Abstract
Sustained
angiogenesis
stands
as
a
hallmark
of
cancer.
The
intricate
vascular
tumor
microenvironment
fuels
cancer
progression
and
metastasis,
fosters
therapy
resistance,
facilitates
immune
evasion.
Therapeutic
strategies
targeting
vasculature
have
emerged
transformative
for
treatment,
encompassing
anti-angiogenesis,
vessel
normalization,
endothelial
reprogramming.
Growing
evidence
suggests
the
dynamic
regulation
by
infiltrating
myeloid
cells,
such
macrophages,
myeloid-derived
suppressor
cells
(MDSCs),
neutrophils.
Understanding
these
regulatory
mechanisms
is
pivotal
in
paving
way
successful
vasculature-targeted
treatments.
interventions
aimed
to
disrupt
cell-mediated
may
reshape
overcome
resistance
radio/chemotherapy
immunotherapy.
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Nov. 21, 2024
Metabolic
alterations,
a
hallmark
of
cancer,
enable
tumor
cells
to
adapt
their
environment
by
modulating
glucose,
lipid,
and
amino
acid
metabolism,
which
fuels
rapid
growth
contributes
treatment
resistance.
In
primary
breast
metabolic
shifts
such
as
the
Warburg
effect
enhanced
lipid
synthesis
are
closely
linked
chemotherapy
failure.
Similarly,
metastatic
lesions
often
display
distinct
profiles
that
not
only
sustain
but
also
confer
resistance
targeted
therapies
immunotherapies.
The
review
emphasizes
two
major
aspects:
mechanisms
driving
in
both
how
unique
environments
sites
further
complicate
treatment.
By
targeting
vulnerabilities
at
stages,
new
strategies
could
improve
efficacy
existing
provide
better
outcomes
for
cancer
patients.
Journal of Hematology & Oncology,
Journal Year:
2025,
Volume and Issue:
18(1)
Published: Jan. 13, 2025
The
tumor
microenvironment
(TME)
is
integral
to
cancer
progression,
impacting
metastasis
and
treatment
response.
It
consists
of
diverse
cell
types,
extracellular
matrix
components,
signaling
molecules
that
interact
promote
growth
therapeutic
resistance.
Elucidating
the
intricate
interactions
between
cells
TME
crucial
in
understanding
progression
challenges.
A
critical
process
induced
by
epithelial-mesenchymal
transition
(EMT),
wherein
epithelial
acquire
mesenchymal
traits,
which
enhance
their
motility
invasiveness
progression.
By
targeting
various
components
TME,
novel
investigational
strategies
aim
disrupt
TME's
contribution
EMT,
thereby
improving
efficacy,
addressing
resistance,
offering
a
nuanced
approach
therapy.
This
review
scrutinizes
key
players
emphasizing
avenues
therapeutically
components.
Moreover,
article
discusses
implications
for
resistance
mechanisms
highlights
current
toward
modulation
along
with
potential
caveats.
Science Advances,
Journal Year:
2024,
Volume and Issue:
10(9)
Published: Feb. 28, 2024
Cancer
immunity
is
subjected
to
spatiotemporal
regulation
by
leukocyte
interaction
with
neoplastic
and
stromal
cells,
contributing
immune
evasion
immunotherapy
resistance.
Here,
we
identify
a
distinct
mesenchymal-like
population
of
endothelial
cells
(ECs)
that
form
an
immunosuppressive
vascular
niche
in
glioblastoma
(GBM).
We
reveal
spatially
restricted,
Twist1/SATB1-mediated
sequential
transcriptional
activation
mechanism,
through
which
tumor
ECs
produce
osteopontin
promote
macrophage
(Mφ)
phenotypes.
Genetic
or
pharmacological
ablation
Twist1
reverses
Mφ-mediated
immunosuppression
enhances
T
cell
infiltration
activation,
leading
reduced
GBM
growth
extended
mouse
survival,
sensitizing
chimeric
antigen
receptor
immunotherapy.
Thus,
these
findings
uncover
restricted
mechanism
controlling
suggest
targeting
may
offer
attractive
opportunities
for
optimizing
cancer
Arthritis Research & Therapy,
Journal Year:
2025,
Volume and Issue:
27(1)
Published: Jan. 20, 2025
Advances
in
treatment
have
swiftly
alleviated
systemic
inflammation
of
Takayasu's
arteritis
(TAK),
while
subclinical
vascular
and
the
ensuing
arterial
remodeling
continue
to
present
unresolved
challenges
TAK.
The
phenotypic
switching
smooth
muscle
cells
(VSMC)
is
regarded
as
first
step
pathology
contributes
remodeling.
Exosomes
facilitate
transfer
exchange
proteins
specific
nucleic
acids,
thereby
playing
a
significant
role
intercellular
communication.
Little
known
about
modulatory
serum
exosomes
VSMC
Serum
isolated
from
TAK
patients
were
co-cultured
with
identify
exosomes.
transfected
miR-199a-5p
mimic
inhibitor.
CCK8
assays
EdU
performed
measure
proliferative
ability.
migration
was
evaluated
by
scratch
transwell
assays.
flow
cytometry
employed
apoptosis
VSMC.
Dual-luciferase
reporter
assay,
RNA
immunoprecipitation
assay
fluorescence
situ
hybridization
utilized
validate
target
gene
miR-199a-5p.
correlational
analysis
conducted
among
exosome
miRNA,
MMP2,
TIMP2
clinical
parameters
patients.
coculture
mediated
dedifferentiation
Through
gain-
loss-of-function
approaches,
over-expression
significantly
increased
expression
marker
genes
inhibited
proliferation
migration,
whilst
opposite
effect
observed
when
endogenous
knocked
down.
overexpression
suppressed
apoptosis.
Further,
MMP2
serves
functional
correlation
analyses
revealed
an
inverse
between
Vasculitis
Damage
Index
level
or
which
requires
validation
larger
cohort.
Our
study
indicated
that
miR-199a-5p/MMP2
pathway
played
inhibiting
decreased
secretion
may
potentially
prompt
intimal
infiltration
inflammatory
within
wall,
offering
novel
therapeutic
opportunity
tackling
both
responses
neointimal
overgrowth
associated
damage.
Moreover,
derived
possess
potential
future
biomarkers
for
injury.