British Journal of Cancer,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Aug. 31, 2024
Abstract
Lung
cancer
has
a
significant
incidence
among
the
population
and,
unfortunately,
an
unfavourable
prognosis
in
most
cases.
The
World
Health
Organization
(WHO)
classifies
lung
tumours
into
two
subtypes
based
on
their
phenotype:
Non-Small
Cell
Cancer
(NSCLC)
and
Small
(SCLC).
SCLC
treatment,
despite
advances
chemotherapy
radiotherapy,
is
often
unsuccessful
for
recurrence
highlighting
need
to
develop
novel
therapeutic
strategies.
In
this
review,
we
describe
genetic
landscape
tumour
microenvironment
that
characterize
pathological
processes
of
how
they
are
responsible
immune
evasion.
immunosuppressive
mechanisms
engaged
critical
factors
understand
failure
immunotherapy
conversely,
suggest
new
signalling
pathways,
such
as
cGAS/STING,
should
be
investigated
possible
targets
stimulate
innate
response
subtype
cancer.
full
comprehension
immunity
cells
thus
crucial
open
challenges
successful
treating
improving
patient
outcomes.
Translational Oncology,
Journal Year:
2024,
Volume and Issue:
47, P. 102027 - 102027
Published: July 1, 2024
Small
cell
lung
cancer
(SCLC)
is
a
high-grade
neuroendocrine
tumor
characterized
by
initial
sensitivity
to
chemotherapy,
followed
the
development
of
drug
resistance.
The
underlying
mechanisms
resistance
in
SCLC
have
not
been
fully
elucidated.
Aldo-keto
reductase
family
1
member
C3
(AKR1C3),
known
be
associated
with
chemoradiotherapy
diverse
tumors.
We
aim
evaluate
prognostic
significance
and
immune
characteristics
AKR1C3
investigate
its
potential
role
promoting
SCLC.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Aug. 1, 2024
Cancer
cell
proliferation
requires
precise
control
of
E2F1
activity;
excess
activity
promotes
apoptosis.
Here,
we
developed
cell-permeable
and
bioavailable
macrocycles
that
selectively
kill
small
lung
cancer
(SCLC)
cells
with
inherent
high
by
blocking
RxL-mediated
interactions
cyclin
A
B
select
substrates.
Genome-wide
CRISPR/Cas9
knockout
random
mutagenesis
screens
found
A/B
RxL
macrocyclic
inhibitors
(cyclin
A/Bi)
induced
apoptosis
paradoxically
B-
Cdk2-dependent
spindle
assembly
checkpoint
activation
(SAC).
Mechanistically,
A/Bi
hyperactivate
their
RxL-interactions
Myt1,
respectively,
ultimately
leading
to
SAC
mitotic
death.
Base
editor
identified
variants
confer
resistance
including
several
disrupted
B:Cdk
interactions.
Unexpectedly
but
consistent
our
base
screens,
the
formation
neo-morphic
Cdk2-cyclin
complexes
promote
Finally,
orally-bioavailable
robustly
inhibited
tumor
growth
in
chemotherapy-resistant
patient-derived
xenograft
models
SCLC.
This
work
uncovers
gain-of-function
mechanisms
which
induce
cancers
E2F
activity,
suggests
as
a
therapeutic
strategy
for
SCLC
other
driven
activity.
Experimental Hematology and Oncology,
Journal Year:
2024,
Volume and Issue:
13(1)
Published: Aug. 5, 2024
Abstract
Small
cell
lung
cancer
(SCLC)
is
a
recalcitrant
characterized
by
early
metastasis,
rapid
tumor
growth
and
poor
prognosis.
In
recent
decades,
the
epidemiology,
initiation
mutation
characteristics
of
SCLC,
as
well
abnormal
signaling
pathways
contributing
to
its
progression,
have
been
widely
studied.
Despite
extensive
investigation,
fewer
drugs
approved
for
SCLC.
Recent
advancements
in
multi-omics
studies
revealed
diverse
classifications
SCLC
that
are
featured
distinct
therapeutic
vulnerabilities.
With
accumulation
samples,
different
subtypes
specific
treatments
these
were
further
explored.
The
identification
molecular
has
opened
up
novel
avenues
treatment
SCLC;
however,
inconsistent
uncertain
classification
hindered
translation
from
basic
research
clinical
applications.
Therefore,
comprehensives
review
essential
conclude
emerging
related
targeting
vulnerabilities
within
pathways.
this
current
review,
we
summarized
risk
factors,
classification,
We
hope
will
facilitate
subtyping
theory
application.
Clinical Cancer Research,
Journal Year:
2024,
Volume and Issue:
30(20), P. 4729 - 4742
Published: Aug. 16, 2024
Histologic
transformation
from
EGFR-mutant
non-small
cell
lung
cancer
(NSCLC)
to
small-cell
(SCLC)
is
a
key
mechanism
of
resistance
EGFR
tyrosine
kinase
inhibitors
(TKI).
However,
transcriptomic
changes
between
NSCLC
and
transformed
SCLC
(t-SCLC)
remain
unexplored.
British Journal of Cancer,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Aug. 31, 2024
Abstract
Lung
cancer
has
a
significant
incidence
among
the
population
and,
unfortunately,
an
unfavourable
prognosis
in
most
cases.
The
World
Health
Organization
(WHO)
classifies
lung
tumours
into
two
subtypes
based
on
their
phenotype:
Non-Small
Cell
Cancer
(NSCLC)
and
Small
(SCLC).
SCLC
treatment,
despite
advances
chemotherapy
radiotherapy,
is
often
unsuccessful
for
recurrence
highlighting
need
to
develop
novel
therapeutic
strategies.
In
this
review,
we
describe
genetic
landscape
tumour
microenvironment
that
characterize
pathological
processes
of
how
they
are
responsible
immune
evasion.
immunosuppressive
mechanisms
engaged
critical
factors
understand
failure
immunotherapy
conversely,
suggest
new
signalling
pathways,
such
as
cGAS/STING,
should
be
investigated
possible
targets
stimulate
innate
response
subtype
cancer.
full
comprehension
immunity
cells
thus
crucial
open
challenges
successful
treating
improving
patient
outcomes.
