Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
163, P. 114846 - 114846
Published: May 9, 2023
The
emergence
of
drug
resistance
and
metastasis
has
long
been
a
difficult
problem
for
cancer
treatment.
Recent
studies
have
shown
that
stem
cell
populations
are
key
factors
in
the
regulation
aggressiveness,
relapse
resistance.
Cancer
(CSC)
highly
plastic
self-renewing,
giving
them
unique
metabolic,
metastatic,
chemotherapy
properties.
N6-methyladenosine
(m6A)
is
most
abundant
internal
modification
mRNA
involved
variety
growth
development
processes,
including
RNA
transcription,
alternative
splicing,
degradation,
translation.
It
also
linked
to
various
cancers.
At
present,
important
role
m6A
tumour
progression
gradually
attracting
attention,
especially
stemness
process.
Abnormal
modifications
regulate
metastasis,
recurrence
This
paper
aims
explore
regulatory
mechanism
CSCs
clinical
therapy,
clarify
its
network,
provide
theoretical
guidance
targets
improvement
therapeutic
effects.
Cell,
Journal Year:
2023,
Volume and Issue:
186(8), P. 1729 - 1754
Published: April 1, 2023
Pancreatic
ductal
adenocarcinoma
(PDAC)
remains
one
of
the
deadliest
cancers.
Significant
efforts
have
largely
defined
major
genetic
factors
driving
PDAC
pathogenesis
and
progression.
tumors
are
characterized
by
a
complex
microenvironment
that
orchestrates
metabolic
alterations
supports
milieu
interactions
among
various
cell
types
within
this
niche.
In
review,
we
highlight
foundational
studies
driven
our
understanding
these
processes.
We
further
discuss
recent
technological
advances
continue
to
expand
complexity.
posit
clinical
translation
research
endeavors
will
enhance
currently
dismal
survival
rate
recalcitrant
disease.
Nature Methods,
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 20, 2024
Abstract
Spatially
resolved
omics
technologies
are
transforming
our
understanding
of
biological
tissues.
However,
the
handling
uni-
and
multimodal
spatial
datasets
remains
a
challenge
owing
to
large
data
volumes,
heterogeneity
types
lack
flexible,
spatially
aware
structures.
Here
we
introduce
SpatialData,
framework
that
establishes
unified
extensible
multiplatform
file-format,
lazy
representation
larger-than-memory
data,
transformations
alignment
common
coordinate
systems.
SpatialData
facilitates
annotations
cross-modal
aggregation
analysis,
utility
which
is
illustrated
in
context
multiple
vignettes,
including
integrative
analysis
on
Xenium
Visium
breast
cancer
study.
Adaptive
therapy
is
a
dynamic
cancer
treatment
protocol
that
updates
(or
‘adapts’)
decisions
in
anticipation
of
evolving
tumor
dynamics.
This
broad
term
encompasses
many
possible
protocols
patient-specific
dose
modulation
or
timing.
maintains
high
levels
burden
to
benefit
from
the
competitive
suppression
treatment-sensitive
subpopulations
on
treatment-resistant
subpopulations.
evolution-based
approach
has
been
integrated
into
several
ongoing
planned
clinical
trials,
including
metastatic
castrate
resistant
prostate
cancer,
ovarian
and
BRAF-mutant
melanoma.
In
previous
few
decades,
experimental
investigation
adaptive
progressed
synergistically
with
mathematical
computational
modeling.
this
work,
we
discuss
11
open
questions
The
are
split
three
sections:
(1)
integrating
appropriate
components
models
(2)
design
validation
dosing
protocols,
(3)
challenges
opportunities
translation.
Advanced Science,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 22, 2025
Abstract
Intratumoral
heterogeneity,
including
epithelial–mesenchymal
transition
(EMT),
is
one
major
cause
of
therapeutic
resistance.
The
induction
ferroptosis,
an
iron‐dependent
death,
has
the
potential
in
overcoming
this
resistance
to
traditional
treatment
modalities.
However,
roles
distinct
EMT
phenotypes
ferroptosis
remain
enigma.
This
study
reports
that
3D
soft
fibrin
microenvironment
confers
colorectal
cancer
(CRC)
cells
hybrid
phenotype
and
high
level
ferroptosis.
activation
histone
acetylation
WNT/β‐catenin
signaling
drives
phenotypic
transition,
which
promotes
defense
CRCs
against
via
glutathione
peroxidases/ferritin
axis.
Unexpectedly,
E‐cadherin
knockout
but
not
2D
mediates
integrin
β
3
marked‐late
state
further
enhances
integrin‐mediated
tension
mitochondrial
reprogramming.
inhibition
α
v
‐mediated
WNT/β‐catenin‐mediated
sensitizes
with
without
deficiency
vivo,
respectively.
Further,
patient‐derived
tumoroids
associated
CRC
In
summary,
uncovers
previously
unappreciated
cell
membrane
only
predict
efficacy
also
potentiate
development
new
ferroptosis‐based
targeted
strategies.
