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
Molecular Oncology,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 28, 2025
Colorectal
cancer
(CRC)
patients
with
microsatellite‐stable
(MSS)
tumors
are
mostly
treated
chemotherapy.
Clinical
benefits
of
targeted
therapies
depend
on
mutational
states
and
tumor
location.
Many
carry
mutations
in
KRAS
proto‐oncogene,
GTPase
(
)
or
B‐Raf
serine/threonine
kinase
BRAF
),
rendering
them
more
resistant
to
therapies.
We
performed
whole‐exome
sequencing
RNA‐Sequencing
28
the
Athens
Comprehensive
Cancer
Center
CRC
cohort,
molecularly
characterized
based
their
microsatellite
instability
(MSI)
status,
single‐nucleotide
variations
(SNVs)/copy
number
alterations
(CNAs),
pathway/transcription
factor
activities
at
individual
patient
level.
Variants
were
classified
using
a
computational
score
for
integrative
variant
annotation
prioritization.
Complementing
this
public
multi‐omics
datasets,
we
identified
activation
transforming
growth
beta
(TGFβ)
signaling
be
strongly
activated
MSS
patients,
whereas
Janus
(JAK)–signal
transducer
activator
transcription
(STAT)
mitogen‐activated
protein
(MAPK)
molecular
cascades
specifically
MSI
tumors.
unraveled
mechanisms
consistently
perturbed
transcriptional
circuits
Runt‐related
factors
(RUNX
factors)
as
putative
biomarkers
CRC,
given
role
regulation
pathways
involved
progression
immune
evasion.
Assessing
immunogenicity
context
RAS/RAF
MSI/MSS
status
revealed
critical
impact
that
have
immunogenicity,
particularly
subgroup,
implications
diagnosis
treatment.
Frontiers in Genetics,
Journal Year:
2023,
Volume and Issue:
14
Published: Sept. 29, 2023
Background:
The
pathogenic
genes
of
colorectal
cancer
(CRC)
have
not
yet
been
fully
elucidated,
and
there
is
currently
a
lack
effective
therapeutic
targets.
This
study
used
bioinformatics
methods
to
explore
experimentally
validate
the
most
valuable
biomarkers
for
further
investigate
their
potential
as
Methods:
We
analyzed
differentially
expressed
(DEGs)
based
on
Gene
Expression
Omnibus
(GEO)
dataset
screened
out
hub
genes.
ROC
curve
univariate
Cox
analysis
Cancer
Genome
Atlas
(TCGA)
revealed
diagnostically
prognostically
Immunohistochemistry
(IHC)
experiments
were
then
conducted
expression
level
these
selected
in
cancer.
set
enrichment
(GSEA)
was
performed
evaluate
enriched
signaling
pathways
associated
with
gene.
Using
CIBERSORT
algorithm
R
software,
we
immune
infiltrating
cell
abundance
both
high
low
gene
groups
examined
gene's
correlation
cells
checkpoints.
Additionally,
drug
sensitivity
utilizing
DepMap
database,
explored
between
levels
ferroptosis
dataset.
Results:
identified
total
159
DEGs,
including
7
genes:
SPP1,
MMP1,
CXCL8,
CXCL1,
TIMP1,
MMP3,
CXCL10.
Further
TIMP1
diagnostic
prognostic
biomarker
cancer,
IHC
verifying
its
expression.
GSEA
results
showed
that
group
involved
many
pathways.
Analysis
TCGA
database
positive
infiltration
macrophages
(M0,
M1,
M2)
neutrophils,
well
checkpoint
genes,
CTLA-4
HAVCR2.
Drug
analysis,
using
lines
exhibiting
elevated
more
responsive
certain
drugs,
such
CC-90003,
Pitavastatin,
Atuveciclib,
CT7001,
compared
those
TIMP1.
Furthermore,
positively
correlated
ferroptosis-related
GPX4
HSPA5.
Conclusion:
can
be
immunological
microenvironment,
sensitivity,
inhibition
this
disease.
Clinical and Translational Medicine,
Journal Year:
2023,
Volume and Issue:
13(11)
Published: Nov. 1, 2023
Colorectal
cancer
(CRC)
has
become
one
of
the
most
common
tumours
with
high
morbidity,
mortality
and
distinctive
evolution
mechanism.
The
neoantigens
arising
from
somatic
mutations
have
considerable
treatment
targets
in
management
CRC.
As
cancer-specific
aberrant
peptides,
can
trigger
robust
host
immune
response
exert
anti-tumour
effects
while
minimising
emergence
adverse
events
commonly
associated
alternative
therapeutic
regimens.
In
this
review,
we
summarised
mechanism,
generation,
identification
prognostic
significance
neoantigens,
as
well
strategies
challenges
neoantigen-based
therapy
evidence
suggests
that
establishment
personalised
holds
great
promise
an
effective
approach
for
patients
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
