Advances in medical diagnosis, treatment, and care (AMDTC) book series,
Journal Year:
2024,
Volume and Issue:
unknown, P. 29 - 52
Published: Dec. 17, 2024
Tumor
formation
and
progression
are
caused
by
neoplastic
cells,
which
take
advantage
of
interfere
with
cellular
processes
that
control
growth,
survival,
division.
New
research
emphasizes
the
critical
role
tumor
microenvironment
(TME)
in
cancer
initiation
metastasis,
even
though
genetic
epigenetic
changes
well-known
malignant
transformation.
The
influences
metagenesis,
angiogenesis,
immune
tolerance,
helps
cells
proliferate
rapidly.
It
also
plays
a
origin,
progression,
invasion
cancer.
With
variety
roles,
including
matrix
deposition
remodeling,
extensive
reciprocal
signaling
connections
crosstalk
invading
leukocytes,
cancer-associated
fibroblasts
(CAFs)
an
essential
part
microenvironment.
This
chapter
reveals
origins
CAFs
heterogeneity
CAF
function,
wherein
it
is
preferable
to
preserve
some
antitumorigenic
properties.
Frontiers in Oncology,
Journal Year:
2024,
Volume and Issue:
14
Published: July 2, 2024
The
biophysical
and
biomechanical
properties
of
the
extracellular
matrix
(ECM)
are
crucial
in
processes
cell
differentiation
proliferation.
However,
it
is
unclear
to
what
extent
tumor
cells
influenced
by
changes
surrounding
microenvironment
how
this
response
varies
between
different
forms,
over
course
progression.
entire
ensemble
genes
encoding
ECM
associated
proteins
called
matrisome.
In
cancer,
evolves
become
highly
dysregulated,
rigid,
fibrotic,
serving
both
pro-tumorigenic
anti-tumorigenic
roles.
Tumor
desmoplasia
characterized
a
dramatic
increase
α-smooth
muscle
actin
expressing
fibroblast
deposition
hard
containing
collagen,
fibronectin,
proteoglycans,
hyaluronic
acid
common
many
solid
tumors.
review,
we
described
role
inflammation
inflammatory
cytokines,
desmoplastic
remodeling,
state
transition
driven
forces
signaling
pathways
mechanotransduction
as
potential
targeted
therapies,
focusing
on
impact
qualitative
quantitative
variations
regulation
development,
hypothesizing
presence
matrisome
drivers,
acting
alongside
cell-intrinsic
oncogenic
some
stages
neoplastic
progression
contexts,
such
pancreatic
carcinoma,
breast
lung
cancer
mesothelioma.
Antibiotics,
Journal Year:
2024,
Volume and Issue:
13(2), P. 184 - 184
Published: Feb. 13, 2024
Bacterial
biofilms,
enigmatic
communities
of
microorganisms
enclosed
in
an
extracellular
matrix,
still
represent
open
challenge
many
clinical
contexts,
including
orthopedics,
where
biofilm-associated
bone
and
joint
infections
remain
the
main
cause
implant
failure.
This
study
explores
scenario
biofilm
infections,
with
a
focus
on
those
related
to
orthopedic
implants,
highlighting
recently
emerged
substantial
aspects
pathogenesis
their
potential
repercussions
clinic,
as
well
progress
gaps
that
exist
diagnostics
management
these
infections.
The
classic
mechanisms
through
which
biofilms
form
more
proposed
new
ones
are
depicted.
ways
bacteria
hide,
become
impenetrable
antibiotics,
evade
immune
defenses,
creating
reservoirs
difficult
detect
reach,
delineated,
such
bacterial
dormancy
within
entry
into
host
cells,
penetration
canaliculi.
New
findings
formation
components
presented.
article
also
delves
emerging
critical
concept
immunometabolism,
key
function
cells
interferes
with.
growing
metabolomics
diagnosis
therapy
is
highlighted,
referring
latest
research.
Cancer Drug Resistance,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 8, 2025
Metabolic
reprogramming
within
the
tumor
microenvironment
(TME)
plays
a
critical
role
in
driving
drug
resistance
gastrointestinal
cancers
(GI),
particularly
through
pathways
of
fatty
acid
oxidation
and
glycolysis.
Cancer
cells
often
rewire
their
metabolism
to
sustain
growth
reshape
TME,
creating
conditions
such
as
nutrient
depletion,
hypoxia,
acidity
that
impair
antitumor
immune
responses.
Immune
TME
also
undergo
metabolic
alterations,
frequently
adopting
immunosuppressive
phenotypes
promote
progression
reduce
efficacy
therapies.
The
competition
for
essential
nutrients,
glucose,
between
cancer
compromises
functions
effector
cells,
T
cells.
Additionally,
by-products
like
lactate
kynurenine
further
suppress
activity
populations,
including
regulatory
M2
macrophages.
Targeting
glycolysis
presents
new
opportunities
overcome
improve
therapeutic
outcomes
GI
cancers.
Modulating
these
key
has
potential
reinvigorate
exhausted
shift
toward
phenotypes,
enhance
effectiveness
immunotherapies
other
treatments.
Future
strategies
will
require
continued
research
into
metabolism,
development
novel
inhibitors,
clinical
trials
evaluating
combination
Identifying
validating
biomarkers
be
crucial
patient
stratification
treatment
monitoring.
Insights
may
have
broader
implications
across
multiple
types,
offering
avenues
improving
treatment.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(5), P. 2750 - 2750
Published: Feb. 27, 2024
Inflammation
is
a
key
contributor
to
both
the
initiation
and
progression
of
tumors,
it
can
be
triggered
by
genetic
instability
within
as
well
lifestyle
dietary
factors.
The
inflammatory
response
plays
critical
role
in
epigenetic
reprogramming
tumor
cells,
cells
that
comprise
microenvironment.
Cells
microenvironment
acquire
phenotype
promotes
immune
evasion,
progression,
metastasis.
We
will
review
mechanisms
pathways
involved
interaction
between
inflammation,
nutrition,
limitations
current
therapies,
discuss
potential
future
therapeutic
approaches.
Current Issues in Molecular Biology,
Journal Year:
2025,
Volume and Issue:
47(2), P. 90 - 90
Published: Jan. 31, 2025
Chimeric
antigen
receptor-T
(CAR-T)
cell
therapy
has
demonstrated
impressive
efficacy
in
the
treatment
of
blood
cancers;
however,
its
effectiveness
against
solid
tumors
been
significantly
limited.
The
differences
arise
from
a
range
difficulties
linked
to
tumors,
including
an
unfriendly
tumor
microenvironment,
variability
within
and
barriers
CAR-T
infiltration
longevity
at
location.
Research
shows
that
reasons
for
decreased
cells
treating
are
not
well
understood,
highlighting
ongoing
need
strategies
address
these
challenges.
Current
frequently
incorporate
combinatorial
therapies
designed
boost
functionality
enhance
their
capacity
effectively
target
tumors.
However,
remain
testing
phase
necessitate
additional
validation
assess
potential
benefits.
CAR-NK
(natural
killer),
CAR-iNKT
(invariant
natural
killer
T),
CAR-M
(macrophage)
emerging
as
promising
Recent
studies
highlight
construction
optimization
cells,
emphasizing
overcome
unique
challenges
posed
by
such
hypoxia
metabolic
barriers.
This
review
focuses
on
CAR
Immunology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 27, 2024
ABSTRACT
Cancer
is
a
complex
and
heterogeneous
disease
characterised
by
uncontrolled
cell
growth
proliferation.
One
hallmark
of
cancer
cells
their
ability
to
undergo
metabolic
reprogramming,
which
allows
them
sustain
rapid
survival.
This
reprogramming
creates
an
immunosuppressive
microenvironment
that
facilitates
tumour
progression
evasion
the
immune
system.
In
this
article,
we
review
mechanisms
underlying
in
discuss
how
these
alterations
contribute
establishment
microenvironment.
We
also
explore
potential
therapeutic
strategies
targeting
vulnerabilities
enhance
immune‐mediated
anti‐tumour
responses.
Trial
Registration
ClinicalTrials.gov
identifier:
NCT02044861,
NCT03163667,
NCT04265534,
NCT02071927,
NCT02903914,
NCT03314935,
NCT03361228,
NCT03048500,
NCT03311308,
NCT03800602,
NCT04414540,
NCT02771626,
NCT03994744,
NCT03229278,
NCT04899921