Journal of the Egyptian National Cancer Institute,
Journal Year:
2025,
Volume and Issue:
37(1)
Published: April 11, 2025
Abstract
Background
With
the
third
incident
rate
and
a
second
mortality
rate,
colorectal
cancer
(CRC)
continues
to
be
one
of
most
prevalent
deadly
malignancies
worldwide.
Adenomas
usually
develop
into
adenocarcinomas
in
(CRC),
process
that
can
halted
by
early
detection
prevention
care.
Main
body
Faecal
immunochemical
testing
(FIT)
endoscopies
are
examples
current
screening
tools
dramatically
lower
incidence
death
cancer.
Current
development
centre
on
non-invasive
methods
provide
better
accuracy
dangers,
such
as
blood-based
liquid
biopsies
imaging
modalities
like
CT
MR
colonography.
For
detection,
biopsies—especially
those
using
methylated
DNA
tests
SEPT9—offer
encouraging
outcomes.
Circulating
tumour
(ctDNA)
has
emerged
crucial
biomarker,
increasing
identification
therapy
monitoring.
Proteomic
metabolic
indicators
further
improve
figuring
out
who
is
at
high
risk
keeping
an
eye
for
recurrence.
The
rates
polyps
have
increased
due
advancements
technologies
artificial
intelligence
(AI),
narrow-band
(NBI),
high-definition
colonoscopy.
emphasis
been
preventive
measures,
chemoprevention
lifestyle
modifications,
dietary
fibre,
regular
exercise,
chemoprotective
drugs
aspirin
demonstrated
potential
lowering
There
still
issues
with
global
implementation
screening,
including
differences
access
between
socioeconomic
racial
groups.
Hope
more
individualized
efficient
CRC
provided
new
research
biomarkers
technological
polygenic
classification.
Conclusion
variety
invasive
techniques
available
identify
early.
To
enhance
prognosis
mortality,
undergone
tremendous
advancement.
Although
colonoscopy
faecal
assays
good
standards
detecting
advances
biopsy,
proteomics,
transformed
field
offered
less
invasive,
precise
choices,
surveillance,
circulating
other
show
potential.
ACS Pharmacology & Translational Science,
Journal Year:
2024,
Volume and Issue:
7(4), P. 967 - 990
Published: March 19, 2024
Precision
medicine
is
transforming
colorectal
cancer
treatment
through
the
integration
of
advanced
technologies
and
biomarkers,
enhancing
personalized
effective
disease
management.
Identification
key
driver
mutations
molecular
profiling
have
deepened
our
comprehension
genetic
alterations
in
cancer,
facilitating
targeted
therapy
immunotherapy
selection.
Biomarkers
such
as
microsatellite
instability
(MSI)
DNA
mismatch
repair
deficiency
(dMMR)
guide
decisions,
opening
avenues
for
immunotherapy.
Emerging
liquid
biopsies,
artificial
intelligence,
machine
learning
promise
to
revolutionize
early
detection,
monitoring,
selection
precision
medicine.
Despite
these
advancements,
ethical
regulatory
challenges,
including
equitable
access
data
privacy,
emphasize
importance
responsible
implementation.
The
dynamic
nature
with
its
tumor
heterogeneity
clonal
evolution,
underscores
necessity
adaptive
strategies.
future
lies
potential
enhance
patient
care,
clinical
outcomes,
understanding
this
intricate
disease,
marked
by
ongoing
evolution
field.
current
reviews
focus
on
providing
in-depth
knowledge
various
diverse
approaches
utilized
against
at
both
biochemical
levels.
Journal of Translational Medicine,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: April 30, 2024
Ischemic
heart
disease
is
one
of
the
leading
causes
mortality
worldwide,
and
thus
calls
for
development
more
effective
therapeutic
strategies.
This
study
aimed
to
identify
potential
targets
coronary
(CHD)
myocardial
infarction
(MI)
by
investigating
causal
relationship
between
plasma
proteins
these
conditions.
Medicine,
Journal Year:
2025,
Volume and Issue:
104(4), P. e41331 - e41331
Published: Jan. 24, 2025
Colorectal
cancer
(CRC)
is
one
of
the
most
common
cancers
worldwide
and
inflammation
believed
to
play
an
important
role
in
CRC.
In
this
study,
we
comprehensively
analyzed
causal
association
between
91
circulating
inflammatory
cytokines
risk
CRC
using
Mendelian
randomization
(MR).
Based
on
genome-wide
study
summary
statistics,
examined
effects
A
series
MR
methods,
including
bidirectional
MR,
replication
sample
multivariable
were
employed
provide
more
robust
estimates.
After
validation
with
3
methods
a
sensitivity
analyses,
2
factors
found
be
significantly
associated
at
genetic
level.
Specifically,
genetically
predicted
levels
glial
cell
line-derived
neurotrophic
factor
(GDNF)
(OR
=
1.12;
95%
CI:
1.05–1.19;
P
2.72
×
10
-4
)
tumor
necrosis
factor-related
apoptosis-inducing
ligand
(TRAIL)
0.93;
0.91–0.99;
1.00
-2
exerted
risk.
conclusion,
suggests
that
increased
GDNF
TRAIL
are
higher
lower
CRC,
respectively.
may
potential
therapeutic
targets
deserve
future
investigation.
Computational and Structural Biotechnology Journal,
Journal Year:
2024,
Volume and Issue:
23, P. 954 - 971
Published: Feb. 3, 2024
The
field
of
cancer
genomics
and
transcriptomics
has
evolved
from
targeted
profiling
to
swift
sequencing
individual
tumor
genome
transcriptome.
steady
growth
in
genome,
epigenome,
transcriptome
datasets
on
a
genome-wide
scale
significantly
increased
our
capability
capturing
signatures
that
represent
both
the
intrinsic
extrinsic
biological
features
tumors.
These
differences
can
help
precise
molecular
subtyping
cancer,
predicting
progression,
metastatic
potential,
resistance
therapeutic
agents.
In
this
review,
we
summarized
current
development
genomic,
methylomic,
transcriptomic,
proteomic
metabolic
research
highlighted
their
potentials
clinical
applications
improve
diagnosis,
prognosis,
treatment
decision
patients.
Journal of the American Society of Nephrology,
Journal Year:
2024,
Volume and Issue:
35(8), P. 1045 - 1057
Published: April 30, 2024
Key
Points
A
multiancestry
proteome-wide
Mendelian
randomization
analysis
was
conducted
for
IgA
nephropathy.
The
findings
from
the
study
would
help
prioritize
new
drug
targets
and
drug-repurposing
opportunities.
Background
therapeutic
options
nephropathy
are
rapidly
evolving,
but
early
diagnosis
targeted
treatment
remain
challenging.
We
aimed
to
identify
circulating
plasma
proteins
associated
with
by
studies
across
multiple
ancestry
populations.
Methods
In
this
study,
we
applied
colocalization
analyses
estimate
putative
causal
effects
of
2615
on
in
Europeans
235
East
Asians.
Following
two-stage
network
randomization,
multitrait
protein-altering
variant
annotation
were
performed
strengthen
reliability
results.
protein–protein
interaction
constructed
investigate
interactions
between
identified
existing
medications.
Results
Putative
184
13
protein–disease
pairs
European
Asian
ancestries
identified,
respectively.
Two
showed
shared
them
(CFHR1
FCRL2).
Supported
evidence
analysis,
potential
prioritized
four
opportunities
suggested.
further
provided
strong
medications
pathways
that
known
be
therapeutically
important.
Conclusions
Our
a
number
several
require
investigation.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Sept. 12, 2024
There
is
already
substantial
evidence
indicating
that
neutrophil
extracellular
trap
(NET)
formation
contributes
to
the
inflammatory
cascade
in
ulcerative
colitis
(UC).
However,
precise
regulatory
mechanisms
governing
this
process
remain
elusive.
This
study
aimed
determine
role
of
NET-related
genes
UC
and
reveal
possible
mechanisms.
Frontiers in Molecular Biosciences,
Journal Year:
2024,
Volume and Issue:
10
Published: Jan. 18, 2024
Objectives:
This
study
aimed
to
identify
plasma
proteins
that
are
associated
with
and
causative
of
breast
cancer
through
Proteome
Transcriptome-wide
association
studies
combining
Mendelian
Randomization.
Methods:
Utilizing
high-throughput
datasets,
we
designed
a
two-phase
analytical
framework
at
identifying
novel
both
cancer.
Initially,
conducted
Proteome/Transcriptome-wide
(P/TWAS)
significant
associations.
Subsequently,
Randomization
was
employed
ascertain
the
causation.
The
validity
robustness
our
findings
were
further
reinforced
external
validation
various
sensitivity
analyses,
including
Bayesian
colocalization,
Steiger
filtering,
heterogeneity
pleiotropy.
Additionally,
performed
functional
enrichment
analysis
identified
better
understand
their
roles
in
assess
potential
as
druggable
targets.
Results:
We
5
demonstrating
strong
associations
links
Specifically,
PEX14
(OR
=
1.201,
p
0.016)
CTSF
1.114,
<
0.001)
displayed
positive
causal
In
contrast,
SNUPN
0.905,
0.001),
CSK
0.962,
0.038),
PARK7
0.954,
negatively
disease.
For
ER-positive
subtype,
3
identified,
exhibiting
consistent
trends,
while
GDI2
0.920,
distinct
this
subtype.
ER-negative
1.645,
stood
out
sole
protein,
even
showing
stronger
effect
compared
These
robustly
supported
by
colocalization
analyses.
Conclusion:
Integrating
multiple
data
dimensions,
successfully
pinpointed
significantly
cancer,
offering
valuable
insights
for
future
research
new
biomarkers
therapeutic
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Oct. 15, 2024
This
study
aims
to
identify
colorectal
cancer
(CRC)-related
proteomic
profiles
and
develop
a
prediction
model
for
CRC
onset
by
integrating
with
genetic
non-genetic
factors
(QCancer-15)
improve
the
risk
stratification
estimate
of
personalized
initial
screening
age.
Here,
using
two-stage
strategy,
we
prioritize
15
protein
biomarkers
as
predictors
construct
score
(ProS).
The
polygenic
(PRS)
QCancer-15
(QCancer-S)
shows
improved
performance
(C-statistic:
0.79
vs.
0.71,
P
=
4.94E-03
in
training
cohort;
0.75
vs
0.69,
5.49E-04
validation
cohort)
net
benefit
than
QCancer-S
alone.
combined
markedly
stratifies
onset.
Participants
high
ProS,
PRS,
or
are
proposed
start
at
age
46,
41,
before
40
years
old.
In
this
work,
integration
blood
proteomics
PRS
demonstrates
clinical
implication
derivation
risk-adapted
starting
ages
screening,
which
may
contribute
decision-making
process
screening.
Discover Oncology,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 3, 2025
Abstract
Background
Chronic
lymphocytic
leukemia
(CLL)
is
a
common
hematologic
malignancy.
Although
previous
research
has
explored
associations
between
plasma
proteins
and
CLL,
the
causal
relationships
remain
unclear.
This
study
used
Mendelian
randomization
(MR)
to
investigate
relationship
7156
CLL
risk.
Methods
A
two-sample
MR
analysis
assessed
impact
of
specific
on
risk,
using
data
from
Finngen
Proteomics
project
(analyzing
828
participants)
UK
Biobank.
Additional
analyses
included
colocalization,
phenomenon-wide
MR,
protein–protein
interaction
networks.
Results
The
identified
nine
significantly
associated
with
Increased
levels
Peptidyl-prolyl
cis-trans
isomerase
E
(PPIE)
(OR
=
1.66,
95%
CI
1.22–2.27,
P
0.001)
were
an
increased
risk
developing
whereas
Protein
O-Mannosyltransferase
2
(POMGNT2)
0.62,
0.41–0.91,
0.017)
C–C
Motif
Chemokine
Ligand
14(CCL14)
0.80,
0.67–0.94,
0.010)
reduced
CLL.
Colocalization
suggested
that
PPIE
may
share
pathogenic
variants
(PP.H4
0.758).
Phenomenon-wide
also
indicated
other
clinical
features,
including
rheumatic
diseases
type
diabetes.
Protein–protein
drug-gene
highlighted
CDC5L
SNW1
as
potential
therapeutic
targets.
Conclusion
identifies
linked
offering
new
insights
into
disease's
pathogenesis.
Further
needed
validate
these
findings
explore
their
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Jan. 17, 2025
Vitiligo
is
a
complex
autoimmune
disease
characterized
by
the
loss
of
melanocytes,
leading
to
skin
depigmentation.
Despite
advances
in
understanding
its
genetic
and
molecular
basis,
precise
mechanisms
driving
vitiligo
remain
elusive.
Integrating
multiple
layers
omics
data
can
provide
comprehensive
view
pathogenesis
identify
potential
therapeutic
targets.
The
study
aims
delineate
using
an
integrative
multiomics
strategy.
We
focus
on
exploring
regulatory
influence
JAK/STAT
pathway
Cathepsin
S,
target
vitiligo.
Our
GWAS-meta
analysis
pinpointed
five
druggable
genes:
ERBB3,
RHOH,
CDK10,
MC1R,
NDUFAF3,
underwent
drug
exploration
docking.
SMR
linked
CTSS,
CTSH,
STX8,
KIR2DL3,
GRHPR
through
pQTL
eQTL
associations.
Microarray
single-cell
RNA-seq
showed
differential
expression
CTSS
STAT1/3
patients'
blood
lesions.
offers
novel
perspectives
vitiligo's
highlighting
pathway's
role
regulating
for
antigen
processing
melanocytes.
Further
research
needed
confirm
these
results
assess
related
genes.