Frontiers in Oncology,
Journal Year:
2024,
Volume and Issue:
14
Published: March 25, 2024
Altered
lipid
metabolism
is
a
well-recognized
feature
of
solid
cancers,
including
colorectal
cancer.
In
cancer,
upregulation
contributes
to
initiation,
progression,
and
metastasis;
thus,
aberrant
poor
patient
outcome.
The
inactivating
mutation
APC
,
vital
tumor
suppressor
in
the
Wnt
signaling
pathway,
key
event
that
occurs
early
majority
cancer
cases.
potential
crosstalk
between
APC-driven
poorly
understood.
This
review
collectively
highlights
summarizes
limited
understanding
mutations
Wnt/beta-catenin
metabolism.
interconnection
inactivation
activates
which
causes
transcriptome,
epigenetic,
microbiome
changes
promote
initiation
progression.
Furthermore,
downstream
effects
this
collaborative
effort
are
enhanced
stemness,
cellular
proliferation,
prooncogenic
signaling,
survival.
Understanding
mechanistic
link
alterations
may
foster
identification
new
therapeutic
targets
enable
development
more
efficacious
strategies
for
prevention
and/or
treatment
Cancer Discovery,
Journal Year:
2024,
Volume and Issue:
14(10), P. 1783 - 1809
Published: Oct. 4, 2024
Abstract
Cancer
is
a
complex
disease
in
which
several
molecular
and
cellular
pathways
converge
to
foster
the
tumoral
phenotype.
Notably,
latest
iteration
of
cancer
hallmarks,
“nonmutational
epigenetic
reprogramming”
was
newly
added.
However,
epigenetics,
much
like
genetics,
broad
scientific
area
that
deserves
further
attention
due
its
multiple
roles
initiation,
progression,
adaptive
nature.
Herein,
we
present
detailed
examination
hallmarks
affected
human
cancer,
elucidating
genes
involved,
dissecting
disrupted
landscapes
for
DNA
methylation,
histone
modifications,
chromatin
architecture
define
disease.
Significance:
characterized
by
constant
evolution,
spanning
from
initial
premalignant
stages
advanced
invasive
disseminated
stages.
It
pathology
able
adapt
survive
amidst
hostile
microenvironments
diverse
treatments
implemented
medical
professionals.
The
more
fixed
setup
genetic
structure
cannot
fully
provide
transformed
cells
with
tools
but
rapid
plastic
nature
changes
ready
task.
This
review
summarizes
ecological
success
our
bodies.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Aug. 14, 2024
Non-genetic
mechanisms
have
recently
emerged
as
important
drivers
of
anticancer
drug
resistance.
Among
these,
the
tolerant
persister
(DTP)
cell
phenotype
is
attracting
more
and
attention
giving
a
predominant
non-genetic
role
in
cancer
therapy
The
DTP
characterized
by
quiescent
or
slow-cell-cycle
reversible
state
subpopulation
inert
specialization
to
stimuli,
which
tolerates
exposure
some
extent
through
interaction
multiple
underlying
recovering
growth
proliferation
after
withdrawal,
ultimately
leading
treatment
resistance
recurrence.
Therefore,
targeting
cells
anticipated
provide
new
opportunities
for
patients,
although
our
current
knowledge
these
remains
limited.
In
this
review,
we
comprehensive
overview
formation
characteristics
cells,
investigate
potential
drugs
(including
preclinical
drugs,
novel
use
old
natural
products)
based
on
different
medicine
models,
discuss
necessity
feasibility
anti-DTP
therapy,
related
application
forms,
future
issues
that
will
need
be
addressed
advance
emerging
field
towards
clinical
applications.
Nonetheless,
understanding
functions
may
enable
us
develop
effective
improve
outcomes
patients.
Trends in Cell Biology,
Journal Year:
2023,
Volume and Issue:
34(6), P. 451 - 464
Published: Nov. 15, 2023
Non-genetic
alterations
can
produce
changes
in
a
cell's
phenotype.
In
cancer,
these
phenomena
influence
fitness
by
conferring
access
to
heritable,
beneficial
phenotypes.
Herein,
we
argue
that
current
discussions
of
'phenotypic
plasticity'
cancer
evolution
ignore
salient
feature
the
original
definition:
namely,
it
occurs
response
an
environmental
change.
We
suggest
noise'
be
used
distinguish
non-genetic
phenotype
occur
independently
from
environment.
discuss
conceptual
and
methodological
techniques
identify
during
evolution.
propose
distinction
will
guide
efforts
define
mechanisms
change,
accelerate
translational
work
manipulate
phenotypes
through
treatment,
and,
ultimately,
improve
patient
outcomes.
Cells,
Journal Year:
2023,
Volume and Issue:
12(8), P. 1124 - 1124
Published: April 10, 2023
Reprogramming
energy
production
from
mitochondrial
respiration
to
glycolysis
is
now
considered
a
hallmark
of
cancer.
When
tumors
grow
beyond
certain
size
they
give
rise
changes
in
their
microenvironment
(e.g.,
hypoxia,
mechanical
stress)
that
are
conducive
the
upregulation
glycolysis.
Over
years,
however,
it
has
become
clear
can
also
associate
with
earliest
steps
tumorigenesis.
Thus,
many
oncoproteins
most
commonly
involved
tumor
initiation
and
progression
upregulate
Moreover,
recent
considerable
evidence
been
reported
suggesting
upregulated
itself,
through
its
enzymes
and/or
metabolites,
may
play
causative
role
tumorigenesis,
either
by
acting
itself
as
an
oncogenic
stimulus
or
facilitating
appearance
mutations.
In
fact,
several
induced
have
shown
be
early
tumorigenesis:
glycolysis-induced
chromatin
remodeling,
inhibition
premature
senescence
induction
proliferation,
effects
on
DNA
repair,
O-linked
N-acetylglucosamine
modification
target
proteins,
antiapoptotic
effects,
epithelial–mesenchymal
transition
autophagy,
angiogenesis.
this
article
we
summarize
and,
following,
propose
mechanistic
model
aimed
at
explaining
how
such
role.
Journal of Xenobiotics,
Journal Year:
2023,
Volume and Issue:
13(3), P. 323 - 385
Published: July 18, 2023
Recent
European
data
facilitate
an
epidemiological
investigation
of
the
controversial
cannabis-cancer
relationship.
Of
particular
concern
were
prior
findings
associating
high-dose
cannabis
use
with
reproductive
problems
and
potential
genetic
impacts.
Cancer
incidence
age-standardised
to
world
population
was
obtained
from
Information
System
2000-2020
many
national
cancer
registries.
Drug
Monitoring
Centre
for
Drugs
Addiction.
Alcohol
tobacco
consumption
sourced
WHO.
Median
household
income
taken
World
bank.
rates
in
high-cannabis-use
countries
significantly
higher
than
elsewhere
(β-estimate
=
0.4165,
p
3.54
×
10-115).
Eighteen
forty-one
cancers
(42,675
individual
rates)
associated
exposure
at
bivariate
analysis.
Twenty-five
linked
inverse-probability-weighted
multivariate
models.
Temporal
lagging
panel
models
intensified
these
effects.
In
multivariable
models,
a
more
powerful
correlate
or
alcohol.
Reproductive
toxicity
evidenced
by
involvement
testis,
ovary,
prostate
breast
because
some
myeloid
lymphoid
leukaemias
implicated
occur
childhood,
indicating
inherited
intergenerational
genotoxicity.
Cannabis
is
important
carcinogen
alcohol
fulfills
qualitative
quantitative
criteria
causality
25/41
cancers.
transgenerational
effects
are
prominent.
These
confirm
clinical
salience
as
major
multigenerational
community
carcinogen.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: May 21, 2024
Abstract
Hematopoietic
stem
cell
(HSC)
mutations
can
result
in
clonal
hematopoiesis
(CH)
with
heterogeneous
clinical
outcomes.
Here,
we
investigate
how
the
state
preceding
Tet2
mutation
impacts
pre-malignant
phenotype.
Using
an
inducible
system
for
analysis
of
myeloid
progenitors,
find
that
epigenetic
features
clones
at
similar
differentiation
status
are
highly
and
functionally
respond
differently
to
mutation.
Cell
stage
also
influences
response
indicating
origin’s
epigenome
modulates
clone-specific
behaviors
CH.
Molecular
associated
higher
risk
outcomes
include
Sox4
sensitizes
cells
inactivation,
inducing
dedifferentiation,
altered
metabolism
increasing
vivo
output
mutant
cells,
as
confirmed
primary
GMP
HSC
models.
Our
findings
validate
hypothesis
predispose
specific
dominance,
explaining
why
identical
genetic
different
phenotypes.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 18, 2025
Abstract
Immune
escape
is
a
critical
hallmark
of
cancer
progression
and
underlies
resistance
to
multiple
immunotherapies.
However,
it
remains
unclear
when
the
genetic
events
associated
with
immune
occur
during
development.
Here,
we
integrate
functional
genomics
studies
immunomodulatory
genes
tumor
evolution
reconstruction
approach
infer
across
38
types
from
Pan-Cancer
Analysis
Whole
Genomes
dataset.
Different
cancers
favor
mutations
in
different
pathways.
For
example,
antigen
presentation
machinery
highly
mutated
colorectal
adenocarcinoma,
lung
squamous
cell
carcinoma,
chromophobe
renal
protein
methylation
pathway
bladder
transitional
carcinoma
adenocarcinoma.
We
also
observe
timing
patterns
instance,
impacting
involved
cellular
amino
acid
metabolism
were
more
likely
happen
late
pancreatic
Mutations
glucocorticoid
receptor
regulatory
network
tended
early,
while
TNF
pathways
B-cell
non-Hodgkin
lymphoma.
NOD1/2
signaling
DNA
binding
transcription
factor
activity
breast
adenocarcinoma
ovarian
Together,
these
results
delineate
evolutionary
trajectories
highlight
opportunities
for
improved
immunotherapy
cancer.
Significance
Despite
its
role
progression,
poorly
understood.
types.
Our
have
important
implications
developing
biomarkers
immunoprevention
treatment
strategies
