Deleted Journal,
Journal Year:
2024,
Volume and Issue:
32(4), P. 200871 - 200871
Published: Sept. 2, 2024
Some
cancer
types
including
bladder,
cervical,
and
uterine
cancers
are
characterized
by
frequent
mutations
in
EP300
that
encode
histone
acetyltransferase
p300.
This
enzyme
can
act
both
as
a
tumor
suppressor
oncogene.
In
this
review,
we
describe
the
role
of
p300
initiation
progression
regarding
aberrations
have
been
identified
TGCA
Pan-Cancer
Atlas
studies
also
discuss
possible
anticancer
strategies
target
mutated
cancers.
Copy
number
alterations,
truncating
mutations,
abnormal
transcriptions
affect
abundance
activity
associated
with
several
pathological
features
such
grading,
metastases,
patient
survival.
Elevated
correlates
higher
mRNA
level
other
epigenetic
factors
chromatin
remodeling
enzymes
co-operate
creating
permissive
conditions
for
malignant
transformation,
growth
metastases.
The
status
expression
be
considered
prognostic
marker
immunotherapy
efficacy,
followed
an
increased
PDL-1.HAT
activators
CTB
or
YF2
applied
p300-deficient
patients,
whereas
natural
synthetic
inhibitors
activity,
well
dual
HAT/bromodomain
PROTAC
degradation
p300,
may
serve
fight
against
p300-fueled
cancers.Graphical
abstract
Cancer
is
a
fatal
genetic
disease
involving
unregulated
cell
growth
and
proliferation
with
varying
underlying
complexities
including
immune
evasion,
treatment
resistance
recurrence,
optimized
required
for
proper
cure.
Molecular
studies
have
revealed
that
tumors
are
extremely
heterogeneous
in
nature,
leading
to
the
complexity
of
cancer
development,
which
ultimately
linked
its
machinery.
It
would
require
effective
targeting
dysregulated
molecular
mechanisms
factors,
regulatory
proteins,
adhesion
molecules,
molecules
system
mainly
driven
by
alterations
tumor
suppressor
genes
oncogenes
may
vary
among
different
types.
Importantly,
patients
same
type
respond
differently
available
treatments,
indicating
need
patient-specific
options.
Thus,
in-depth
genomic
patients’
needed
fully
understand
determinants
initiation
progression
targeted
therapy.
Precision
oncology
has
evolved
as
form
therapy
focused
on
profiling
identify
involved
manifestation
tailored
individualized
disease.
Accordingly,
there
been
great
developments
formulation
production
anticancer
agents
recent
years
owing
advances
technologies
enabling
precise
oncogenic
pathways
progression.
This
article
aims
briefly
explain
foundations
frontiers
precision
context
advancements
tools
techniques
associated
process
assess
scope
importance
realizing
intended
goals.
Cancers,
Journal Year:
2025,
Volume and Issue:
17(2), P. 234 - 234
Published: Jan. 13, 2025
The
complex
signaling
network
within
the
breast
tumor
microenvironment
is
crucial
for
its
growth,
metastasis,
angiogenesis,
therapy
escape,
stem
cell
maintenance,
and
immunomodulation.
An
array
of
secretory
factors
their
receptors
activate
downstream
cascades
regulating
cancer
progression
metastasis.
Among
various
pathways,
EGFR,
ER,
Notch,
Hedgehog
pathways
have
recently
been
identified
as
in
terms
proliferation,
survival,
differentiation,
maintenance
CSCs,
failure.
These
mediate
such
MAPK,
including
MEK/ERK
that
promote
common
pro-oncogenic
signaling,
whereas
dysregulation
PI3K/Akt,
Wnt/β-catenin,
JAK/STAT
activates
key
oncogenic
events
drug
resistance,
CSC
enrichment,
metabolic
reprogramming.
Additionally,
these
orchestrate
an
intricate
interplay
between
stromal
cells,
immune
cells.
Metabolic
reprogramming
adaptations
contribute
to
aggressive
are
unresponsive
therapy.
Herein,
recent
insights
into
novel
operating
TME
aid
advancement
emphasized
current
developments
practices
targeting
enhance
treatment
efficacy
reviewed.
Authorea (Authorea),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 9, 2025
Cancer
is
a
fatal
genetic
disease
involving
unregulated
cell
growth
and
proliferation
with
varying
underlying
complexities
including
immune
evasion,
treatment
resistance
recurrence,
optimized
required
for
proper
cure.Molecular
studies
have
revealed
that
tumors
are
extremely
heterogeneous
in
nature,
leading
to
the
complexity
of
cancer
development,
which
ultimately
linked
its
machinery.It
would
require
effective
targeting
dysregulated
molecular
mechanisms
factors,
regulatory
proteins,
adhesion
molecules,
molecules
system
mainly
driven
by
alterations
tumor
suppressor
genes
oncogenes
may
vary
among
different
types.Importantly,
patients
same
type
respond
differently
available
treatments,
indicating
need
patient-specific
options.Thus,
in-depth
genomic
patients'
needed
fully
understand
determinants
initiation
progression
targeted
therapy.Precision
oncology
has
evolved
as
form
therapy
focused
on
profiling
identify
involved
manifestation
tailored
individualized
disease.Accordingly,
there
been
great
developments
formulation
production
anticancer
agents
recent
years
owing
advances
technologies
enabling
precise
oncogenic
pathways
progression.This
article
aims
briefly
explain
foundations
frontiers
precision
context
advancements
tools
techniques
associated
process
assess
scope
importance
realizing
intended
goals.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 27, 2025
Precision
medicine
has
revolutionized
the
treatment
of
colorectal
cancer
by
enabling
a
personalized
approach
tailored
to
each
patient's
unique
genetic
characteristics.
Genomic
profiling
allows
for
identification
specific
mutations
in
genes
such
as
KRAS,
BRAF,
and
PIK3CA,
which
play
crucial
role
cell
signaling
pathways
that
regulate
proliferation,
apoptosis,
differentiation.
This
information
enables
doctors
select
targeted
therapies
inhibit
molecular
pathways,
maximizing
effectiveness
minimizing
side
effects.
also
facilitates
adaptive
monitoring
tumor
progression,
allowing
adjustments
therapy
maintain
effectiveness.
While
challenges
high
costs,
limited
access
genomic
technology,
need
more
representative
data
diverse
populations
remain,
collaboration
between
researchers,
medical
practitioners,
policymakers,
pharmaceutical
industry
is
ensure
precision
becomes
standard
care
accessible
all.
With
continued
advances
support,
potential
improve
outcomes,
reduce
morbidity
mortality
rates,
enhance
quality
life
patients
worldwide.
Molecular Biology and Evolution,
Journal Year:
2022,
Volume and Issue:
39(7)
Published: July 1, 2022
Abstract
The
p53
tumor
suppressor
is
a
transcription
factor
with
roles
in
cell
development,
apoptosis,
oncogenesis,
aging,
and
homeostasis
response
to
stresses
infections.
tightly
regulated
by
the
MDM2
E3
ubiquitin
ligase.
p53–MDM2
pathway
has
coevolved,
remaining
largely
conserved,
whereas
TP53
gene
morphed
into
various
isoforms.
Studies
on
prevertebrate
ancestral
homologs
revealed
transition
from
an
environmentally
induced
mechanism
activating
system
involving
signaling.
evolution
of
this
depends
structural
changes
interacting
protein
motifs.
Elephants
such
as
Loxodonta
africana
constitute
ideal
models
investigate
coevolution
they
are
large
long-living
well
having
20
copies
isoformic
sequences
expressing
variety
BOX-I
MDM2-binding
Collectively,
these
isoforms
would
enhance
sensitivity
cellular
stresses,
DNA
damage,
presumably
accounting
for
strong
cancer
defenses
other
adaptations
favoring
healthy
aging.
Here
we
molecular
combining
silico
modeling
vitro
assays
explore
functional
aspects
retaining
interaction,
forming
distinct
pools
methodology
used
demonstrates,
first
time
that
docking
simulations
can
be
elephant
Our
observations
elucidate
mechanistic
regulation,
facilitate
understanding
complex
signaling,
suggest
testable
hypotheses
referencing
Peto’s
Paradox.