Genes & Development,
Journal Year:
2021,
Volume and Issue:
35(7-8), P. 433 - 448
Published: April 1, 2021
p53
is
an
important
tumor
suppressor,
and
the
complexities
of
function
in
regulating
cancer
cell
behaviour
are
well
established.
Many
cancers
lose
or
express
mutant
forms
p53,
with
evidence
that
type
alteration
affecting
may
differentially
impact
development
progression.
It
also
clear
addition
to
cell-autonomous
functions,
status
affects
way
cells
interact
each
other.
In
this
review,
we
briefly
examine
different
mutations
focus
on
how
heterogeneity
can
affect
relationships
between
within
a
tumor.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: June 18, 2024
Abstract
Tumorigenesis
is
a
multistep
process,
with
oncogenic
mutations
in
normal
cell
conferring
clonal
advantage
as
the
initial
event.
However,
despite
pervasive
somatic
and
expansion
tissues,
their
transformation
into
cancer
remains
rare
event,
indicating
presence
of
additional
driver
events
for
progression
to
an
irreversible,
highly
heterogeneous,
invasive
lesion.
Recently,
researchers
are
emphasizing
mechanisms
environmental
tumor
risk
factors
epigenetic
alterations
that
profoundly
influencing
early
malignant
evolution,
independently
inducing
mutations.
Additionally,
evolution
tumorigenesis
reflects
multifaceted
interplay
between
cell-intrinsic
identities
various
cell-extrinsic
exert
selective
pressures
either
restrain
uncontrolled
proliferation
or
allow
specific
clones
progress
tumors.
by
which
induce
both
intrinsic
cellular
competency
remodel
stress
facilitate
not
fully
understood.
In
this
review,
we
summarize
genetic,
epigenetic,
external
events,
effects
on
co-evolution
transformed
cells
ecosystem
during
initiation
evolution.
A
deeper
understanding
earliest
molecular
holds
promise
translational
applications,
predicting
individuals
at
high-risk
developing
strategies
intercept
transformation.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: July 29, 2024
Amino
acid
metabolism
plays
a
pivotal
role
in
tumor
microenvironment,
influencing
various
aspects
of
cancer
progression.
The
metabolic
reprogramming
amino
acids
cells
is
intricately
linked
to
protein
synthesis,
nucleotide
modulation
signaling
pathways,
regulation
cell
metabolism,
maintenance
oxidative
stress
homeostasis,
and
epigenetic
modifications.
Furthermore,
the
dysregulation
also
impacts
microenvironment
immunity.
can
act
as
molecules
that
modulate
immune
function
tolerance
within
reshaping
anti-tumor
response
promoting
evasion
by
cells.
Moreover,
influence
behavior
stromal
cells,
such
cancer-associated
fibroblasts,
regulate
ECM
remodeling
promote
angiogenesis,
thereby
facilitating
growth
metastasis.
Understanding
intricate
interplay
between
crucial
significance.
Expanding
our
knowledge
multifaceted
roles
holds
significant
promise
for
development
more
effective
therapies
aimed
at
disrupting
dependencies
modulating
enhance
responses
inhibit
Cells,
Journal Year:
2025,
Volume and Issue:
14(2), P. 143 - 143
Published: Jan. 19, 2025
Brain
plasticity
is
at
the
basis
of
many
cognitive
functions,
including
learning
and
memory.
It
includes
several
mechanisms
synaptic
extrasynaptic
changes,
neurogenesis,
formation
elimination
synapses.
The
transmission
involves
expression
immediate
early
genes
(IEGs)
that
regulate
neuronal
activity,
thereby
supporting
In
addition,
IEGs
are
involved
in
regulation
brain
cells’
metabolism,
proliferation,
survival,
establishment
multicellular
ensembles,
and,
presumably,
cell
competition
tissue.
this
review,
we
analyze
current
understanding
role
(c-Fos,
c-Myc,
Arg3.1/Arc)
controlling
physiological
pathological
conditions,
aging
neurodegeneration.
This
work
might
inspire
new
gene
therapy
strategies
targeting
to
plasticity,
potentially
prevent
or
mitigate
neurodegenerative
diseases.
