MedComm,
Journal Year:
2023,
Volume and Issue:
4(3)
Published: May 28, 2023
Tumor
suppressor
p53
can
transcriptionally
activate
downstream
genes
in
response
to
stress,
and
then
regulate
the
cell
cycle,
DNA
repair,
metabolism,
angiogenesis,
apoptosis,
other
biological
responses.
has
seven
functional
domains
12
splice
isoforms,
different
subtypes
play
roles.
The
activation
inactivation
of
are
finely
regulated
associated
with
phosphorylation/acetylation
modification
ubiquitination
modification,
respectively.
Abnormal
is
closely
related
occurrence
development
cancer.
While
targeted
therapy
signaling
pathway
still
its
early
stages
only
a
few
drugs
or
treatments
have
entered
clinical
trials,
new
ongoing
trials
expected
lead
widespread
use
signaling-targeted
cancer
treatment
future.
TRIAP1
novel
inhibitor
apoptosis.
homolog
yeast
mitochondrial
intermembrane
protein
MDM35,
which
tumor-promoting
role
by
blocking
mitochondria-dependent
apoptosis
pathway.
This
work
provides
systematic
overview
recent
basic
research
progress
proposes
that
an
important
therapeutic
target
signaling.
Nanomedicine Nanotechnology Biology and Medicine,
Journal Year:
2024,
Volume and Issue:
56, P. 102732 - 102732
Published: Jan. 8, 2024
Among
the
tumor
suppressor
genes,
TP53
is
most
frequently
mutated
in
human
cancers,
and
mutations
are
missense
causing
production
of
mutant
p53
(mutp53)
proteins.
not
only
results
loss
function
(LOH)
as
a
transcription
factor
suppressor,
but
also
gain
wild-type
(WTp53)-independent
oncogenic
functions
that
enhance
cancer
metastasis
progression
(Yamamoto
Iwakuma,
2018;
Zhang
et
al.,
2022).
has
extensively
been
studied
therapeutic
target
well
for
drug
development
therapies,
however
with
limited
success.
Achieving
targeted
therapies
restoration
WTp53
depletion
or
repair
will
have
far
reaching
implication
treatment
therapies.
This
review
briefly
discusses
role
mutation
potential
restoring
through
advances
mRNA
nanomedicine.
Heliyon,
Journal Year:
2024,
Volume and Issue:
10(6), P. e27655 - e27655
Published: March 1, 2024
Cancer
is
a
complex
disease
that
caused
by
multiple
genetic
factors.
Researchers
have
been
studying
protein
domain
mutations
to
understand
how
they
affect
the
progression
and
treatment
of
cancer.
These
can
significantly
impact
development
spread
cancer
changing
structure,
function,
signalling
pathways.
As
result,
there
growing
interest
in
these
be
used
as
prognostic
indicators
for
prognosis.
Recent
studies
shown
provide
valuable
information
about
severity
patient's
response
treatment.
They
may
also
predict
resistance
targeted
therapy
The
clinical
implications
are
significant,
regarded
essential
biomarkers
oncology.
However,
additional
techniques
approaches
required
characterize
changes
domains
their
functional
effects.
Machine
learning
other
computational
tools
offer
promising
solutions
this
challenge,
enabling
prediction
on
structure
function.
Such
predictions
aid
interpretation
information.
Furthermore,
genome
editing
like
CRISPR/Cas9
has
made
it
possible
validate
significance
mutants
more
efficiently
accurately.
In
conclusion,
hold
great
promise
predictive
Overall,
considerable
research
still
needed
better
define
molecular
heterogeneity
resolve
challenges
remain,
so
full
potential
realized.
Biomolecules,
Journal Year:
2025,
Volume and Issue:
15(5), P. 621 - 621
Published: April 25, 2025
The
tumor
microenvironment
(TME)
plays
a
crucial
role
in
the
development,
progression,
and
metastasis
of
oral
squamous
cell
carcinoma
(OSCC).
TME
comprises
various
cellular
acellular
components,
including
immune
cells,
stromal
cytokines,
extracellular
matrix,
microbiome,
all
which
dynamically
interact
with
cells
to
influence
their
behavior.
Immunosuppression
is
key
feature
OSCC
TME,
regulatory
T
(Tregs),
myeloid-derived
suppressor
(MDSCs),
tumor-associated
macrophages
(TAMs)
contributing
an
environment
that
allows
evade
surveillance
supports
angiogenesis.
microbiome
also
pivotal
pathogenesis,
as
dysbiosis,
or
imbalances
microbiota,
can
lead
chronic
inflammation,
promotes
carcinogenesis
through
production
pro-inflammatory
cytokines
reactive
oxygen
species
(ROS).
Pathogens
like
Porphyromonas
gingivalis
Fusobacterium
nucleatum
have,
hence,
been
implicated
OSCC-driven
they
induce
activate
oncogenic
pathways,
modulate
responses.
In
this
review,
we
discuss
how
interplay
between
immunosuppression
microbiome-driven
inflammation
creates
tumor-promoting
OSCC,
leading
treatment
resistance
poor
patient
outcomes,
explore
potential
therapeutic
implication
better
understanding
etiology
molecular
changes.
Discover Oncology,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 21, 2025
Abstract
Aging
is
an
inevitable
physiological
process
in
organisms,
and
the
development
of
tumors
closely
associated
with
cellular
senescence.
This
article
initially
examines
role
senescence
tumorigenesis,
emphasizing
correlation
between
telomere
length—a
marker
senescence—and
tumor
risk.
Concurrently,
study
explores
expression
levels
senescence-associated
markers,
such
as
p16,
p53,
mTOR,
context
development.
Additionally,
investigates
impact
on
organismal
senescence,
including
effects
immune
system
function
metabolic
processes.
Ultimately,
discussion
potential
application
anti-aging
strategies
therapy
considers
possibility
utilizing
mechanisms
a
novel
therapeutic
approach
for
tumors.
research
provides
insights
into
complex
interplay
development,
suggesting
future
preventative
measures
interventions.
