JNCI Journal of the National Cancer Institute,
Journal Year:
2021,
Volume and Issue:
113(10), P. 1285 - 1298
Published: March 31, 2021
Cellular
senescence
is
an
essential
tumor
suppressive
mechanism
that
prevents
the
propagation
of
oncogenically
activated,
genetically
unstable,
and/or
damaged
cells.
Induction
cell
also
one
underlying
mechanisms
by
which
cancer
therapies
exert
antitumor
activity.
However,
increasing
body
evidence
from
preclinical
studies
demonstrates
radiation
and
chemotherapy
cause
accumulation
senescent
cells
(SnCs)
both
in
normal
tissue.
SnCs
tumors
can,
paradoxically,
promote
relapse,
metastasis,
resistance
to
therapy,
part,
through
expression
senescence-associated
secretory
phenotype.
In
addition,
tissue
can
contribute
certain
radiation-
chemotherapy-induced
side
effects.
Because
its
multiple
roles,
cellular
could
serve
as
important
target
fight
against
cancer.
This
commentary
provides
a
summary
discussion
at
National
Cancer
Institute
Workshop
on
Radiation,
Senescence,
(August
10-11,
2020,
Institute,
Bethesda,
MD)
regarding
current
status
research,
heterogeneity
therapy-induced
senescence,
senotherapeutics
molecular
biomarkers,
concept
"one-two
punch"
therapy
(consisting
therapeutics
induce
followed
selective
clearance
SnCs),
integration
with
personalized
adaptive
therapy.
It
identifies
key
knowledge
gaps
outlines
future
directions
this
emerging
field
improve
treatment
outcomes
for
patients.
Cancer Discovery,
Journal Year:
2022,
Volume and Issue:
12(1), P. 31 - 46
Published: Jan. 1, 2022
The
hallmarks
of
cancer
conceptualization
is
a
heuristic
tool
for
distilling
the
vast
complexity
phenotypes
and
genotypes
into
provisional
set
underlying
principles.
As
knowledge
mechanisms
has
progressed,
other
facets
disease
have
emerged
as
potential
refinements.
Herein,
prospect
raised
that
phenotypic
plasticity
disrupted
differentiation
discrete
hallmark
capability,
nonmutational
epigenetic
reprogramming
polymorphic
microbiomes
both
constitute
distinctive
enabling
characteristics
facilitate
acquisition
capabilities.
Additionally,
senescent
cells,
varying
origins,
may
be
added
to
roster
functionally
important
cell
types
in
tumor
microenvironment.
SIGNIFICANCE:
Cancer
daunting
breadth
scope
its
diversity,
spanning
genetics,
tissue
biology,
pathology,
response
therapy.
Ever
more
powerful
experimental
computational
tools
technologies
are
providing
an
avalanche
"big
data"
about
myriad
manifestations
diseases
encompasses.
integrative
concept
embodied
helping
distill
this
increasingly
logical
science,
new
dimensions
presented
perspective
add
value
endeavor,
fully
understand
development
malignant
progression,
apply
medicine.
Genes & Development,
Journal Year:
2020,
Volume and Issue:
34(23-24), P. 1565 - 1576
Published: Dec. 1, 2020
Cellular
senescence
is
a
stress
response
that
elicits
permanent
cell
cycle
arrest
and
triggers
profound
phenotypic
changes
such
as
the
production
of
bioactive
secretome,
referred
to
senescence-associated
secretory
phenotype
(SASP).
Acute
induction
protects
against
cancer
limits
fibrosis,
but
lingering
senescent
cells
drive
age-related
disorders.
Thus,
targeting
delay
aging
limit
dysfunction,
known
“senotherapy,”
gaining
momentum.
While
drugs
selectively
kill
cells,
termed
“senolytics”
are
major
focus,
SASP-centered
approaches
emerging
alternatives
target
diseases.
Here,
we
summarize
regulation
functions
SASP
highlight
therapeutic
potential
modulation
complimentary
or
an
alternative
current
senolytic
approaches.
Cell,
Journal Year:
2022,
Volume and Issue:
185(10), P. 1630 - 1645
Published: May 1, 2022
Atherosclerosis
is
an
inflammatory
disease
of
the
large
arteries
that
major
cause
cardiovascular
(CVD)
and
stroke.
Here,
we
review
current
understanding
molecular,
cellular,
genetic,
environmental
contributions
to
atherosclerosis,
from
both
individual
pathway
systems
perspectives.
We
place
emphasis
on
recent
developments,
some
which
have
yielded
unexpected
biology,
including
previously
unknown
heterogeneity
smooth
muscle
cells
in
atherosclerotic
lesions,
roles
for
senescence
clonal
hematopoiesis,
links
gut
microbiome.
