Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Dec. 23, 2024
In
recent
decades,
immunometabolism
in
cancers
has
emerged
as
an
interesting
target
for
treatment
development.
Indeed,
the
tumor
microenvironment
(TME)
unique
characteristics
such
hypoxia
and
limitation
of
nutrients
availability
lead
to
a
switch
metabolic
pathways
both
TME
cells
order
support
their
adaptation
grow.
Glioblastoma
(GBM),
most
frequent
aggressive
primary
brain
adults,
been
extensively
studied
multiple
aspects
regarding
its
immune
population,
but
research
focused
on
remains
limited.
Here,
we
provide
overview
myeloid
with
specific
focus
GBM
other
tumors,
before
describing
current
therapeutic
strategies
targeting
pathways.
The
main
composing
include
tumor-associated
macrophages
(TAMs),
which
comprise
peripheral
local
microglia,
well
myeloid-derived
suppressor
cells.
involved
cell
remodeling
encompass
tricarboxylic
acid
cycle
(TCA
cycle),
lipid,
glucose
amino
metabolism
hypoxia.
Developing
treatments
that
these
growth
is
promising
increasing
field.
It
includes
drug-repurposing
development
innovative
therapies.
We
finally
all
clinical
trials
neuro-oncology
involving
modifying
preclinical
rationale
drugs
already
evaluated
within
potential
candidates
future
trials.
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.
Seminars in Cancer Biology,
Journal Year:
2024,
Volume and Issue:
101, P. 58 - 73
Published: May 27, 2024
Cancer
is
daunting
pathology
with
remarkable
breadth
and
scope,
spanning
genetics,
epigenetics,
proteomics,
metalobomics
cell
biology.
Cellular
senescence
represents
a
stress-induced
essentially
irreversible
fate
associated
aging
various
age-related
diseases,
including
malignancies.
Senescent
cells
are
characterized
of
morphologic
alterations
metabolic
reprogramming,
develop
highly
active
secretome
termed
as
the
senescence-associated
secretory
phenotype
(SASP).
Since
first
discovery,
has
been
understood
an
important
barrier
to
tumor
progression,
its
induction
in
pre-neoplastic
limits
carcinogenesis.
Paradoxically,
senescent
arising
microenvironment
(TME)
contribute
augmented
therapeutic
resistance.
In
this
article,
we
define
typical
forms
commonly
observed
within
TME
how
functionally
remodel
their
surrounding
niche,
affect
immune
responses
promote
cancer
evolution.
Furthermore,
highlight
recently
emerging
pipelines
senotherapies
particularly
senolytics,
which
can
selectively
deplete
from
affected
organs
vivo
impede
progression
by
restoring
securing
anticancer
efficacies.
Together,
co-targeting
normal
but
counterparts
holds
potential
achieve
increased
benefits
restrained
disease
relapse
future
clinical
oncology.
Frontiers in Oncology,
Journal Year:
2025,
Volume and Issue:
15
Published: March 5, 2025
Multiple
myeloma
(MM)
is
a
complex
hematological
malignancy
characterized
by
the
clonal
expansion
of
plasma
cells
in
bone
marrow.
Emerging
studies
have
emphasized
importance
lipid
metabolism,
which
closely
associated
with
survival,
proliferation,
and
drug
resistance
tumor
cells.
The
hypoxic
environment
marrow
(BM)
contributes
to
metabolic
reprogramming
MM
cells,
including
alterations
metabolite
levels,
changes
enzyme
activity,
shifts.
Cancer
possess
ability
adapt
their
metabolism
order
fulfill
continuously
increasing
energy
demands.
In
this
review,
we
will
discuss
during
development
MM,
reciprocal
interactions
microenvironment.
Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
30(1)
Published: Aug. 23, 2024
Abstract
Mitochondria,
responsible
for
cellular
energy
synthesis
and
signal
transduction,
intricately
regulate
diverse
metabolic
processes,
mediating
fundamental
biological
phenomena
such
as
cell
growth,
aging,
apoptosis.
Tumor
invasion
metastasis,
key
characteristics
of
malignancies,
significantly
impact
patient
prognosis.
cells
frequently
exhibit
abnormalities
in
mitochondria,
including
alterations
dynamics
changes
the
expression
relevant
genes
associated
transduction
pathways.
Recent
investigations
unveil
further
insights
into
mitochondrial
abnormalities,
revealing
their
active
involvement
tumor
proliferation,
resistance
to
chemotherapy,
a
crucial
role
metastasis.
This
paper
comprehensively
outlines
latest
research
advancements
structure
function.
Emphasis
is
placed
on
summarizing
genome
(mutations),
activation
mitochondrial-to-nuclear
signaling,
within
all
linked
processes
In
conclusion,
discusses
unresolved
scientific
questions
this
field,
aiming
provide
theoretical
foundation
novel
perspectives
developing
innovative
strategies
targeting
metastasis
based
biology.
Graphical
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(20), P. 11185 - 11185
Published: Oct. 17, 2024
Cancer
stem
cells
(CSCs),
or
tumor-initiating
(TICs),
are
small
subpopulations
(0.0001-0.1%)
of
cancer
that
crucial
for
relapse
and
therapy
resistance.
The
elimination
each
CSC
is
essential
achieving
long-term
remission.
Metabolic
reprogramming,
particularly
lipids,
has
a
significant
impact
on
drug
efficacy
by
influencing
diffusion,
altering
membrane
permeability,
modifying
mitochondrial
function,
adjusting
the
lipid
composition
within
CSCs.
These
changes
contribute
to
development
chemoresistance
in
various
cancers.
intricate
relationship
between
metabolism
resistance
CSCs
an
emerging
area
research,
as
different
species
play
roles
multiple
stages
autophagy.
However,
link
autophagy
context
regulation
remains
unclear.
Understanding
interplay
reprogramming
could
lead
new
approaches
enhancing
therapies
reducing
tumorigenicity
these
cells.
In
this
review,
we
explore
latest
findings
CSCs,
including
role
key
regulatory
enzymes,
inhibitors,
contribution
maintaining
homeostasis.
recent
may
provide
critical
insights
identifying
novel
pharmacological
targets
effective
anticancer
treatment.
iScience,
Journal Year:
2024,
Volume and Issue:
27(9), P. 110810 - 110810
Published: Sept. 1, 2024
Downstream
interferon
signaling
through
the
type
I
(IFN)
receptor,
IFNAR,
is
crucial
for
proper
production
of
IFNs
in
mounting
anti-tumor
immune
responses.
Our
study
investigates
role
IFN
glioblastoma
(GBM)
tumor
microenvironment
by
leveraging
single-cell
RNA
sequencing
to
analyze
tumor-infiltrating
lymphocytes.
We
investigate
how
within
myeloid
compartment
contributes
crosstalk
with
T
cells
microenvironment.
Through
use
Gl261
murine
GBM
model,
we
find
that
lack
response
results
enhanced
PD-L1
interactions
among
cells,
thereby
affecting
cell
functionality.
Additionally,
also
characterize
anti-PD1
treatment
induces
transcriptional
changes
tumor-associated
monocytes
and
macrophages
analyzing
intercellular
communication
networks
propose
checkpoint
blockade
therapy
could
possibly
relieve
some
immunosuppression
derived
from
production.
