Cardiovascular Research,
Год журнала:
2022,
Номер
118(18), С. 3451 - 3466
Опубликована: Авг. 24, 2022
Heart
failure
(HF)
and
cancer
are
the
leading
causes
of
death
worldwide
accumulating
evidence
demonstrates
that
HF
affect
one
another
in
a
bidirectional
way.
Patients
with
at
increased
risk
for
developing
cancer,
is
associated
accelerated
tumour
growth.
The
presence
malignancy
may
induce
systemic
metabolic,
inflammatory,
microbial
alterations
resulting
impaired
cardiac
function.
In
addition
to
pathophysiologic
mechanisms
shared
between
HF,
overlaps
also
exist
pathways
required
normal
physiology
Therefore,
these
explain
cardiotoxicity
as
result
targeted
anti-cancer
therapies.
This
review
provides
an
overview
involved
connection
specifically
focusing
upon
current
'hot-topics'
mechanisms.
It
subsequently
describes
therapies
cardiotoxic
potential
overlap
their
targets
Abstract
Background
Fusobacterium
nucleatum
(
F.
)
is
a
microbial
risk
factor
whose
presence
increases
the
of
oral
squamous
cell
carcinoma
(OSCC)
progression.
However,
whether
it
can
promote
proliferation
OSCC
cells
remains
unknown.
Methods
In
this
study,
we
investigated
effect
on
using
in
vitro
and
vivo
experiments.
Results
Our
results
showed
that
promoted
proliferation,
doubling
count
after
72
h
(CCK-8
assay).
Cell
cycle
analysis
revealed
G2/M
phase
arrest.
interaction
with
CDH1
triggered
phosphorylation,
upregulating
downstream
protein
β-catenin
activating
cyclinD1
Myc.
Notably,
did
not
affect
noncancerous
cells,
unrelated
to
expression
levels
CAL27
cells.
Overexpression
phosphorylated
293T
upregulate
cycle-related
genes.
BALB/c
nude
experiments
increased
tumor
volume
Ki-67
index
intervention.
Conclusion
study
suggests
promotes
through
CDH1/β-catenin
pathway,
advancing
our
understanding
its
role
progression
highlighting
potential
as
therapeutic
target.
Periodontology 2000,
Год журнала:
2024,
Номер
96(1), С. 95 - 111
Опубликована: Март 19, 2024
Abstract
It
has
long
been
considered
that
the
oral
microbiome
is
tightly
connected
to
health
and
dysbiotic
changes
can
be
detrimental
occurrence
progression
of
dysplastic
mucosal
lesions
or
cancer.
Improved
understanding
concepts
microbial
dysbiosis
together
with
advances
in
high‐throughput
molecular
sequencing
these
pathologies
have
charted
greater
microbiological
detail
nature
their
clinical
state.
This
review
discusses
bacteriome
mycobiome
associated
lesions,
candidiasis,
squamous
cell
carcinoma,
aiming
delineate
information
available
date
pursuit
advancing
diagnostic
prognostic
utilities
for
medicine.
Cancers,
Год журнала:
2024,
Номер
16(17), С. 2997 - 2997
Опубликована: Авг. 28, 2024
Oral
squamous
cell
carcinoma
(OSCC)
is
the
most
common
head
and
neck
cancer.
Although
oral
cavity
an
easily
accessible
area
for
visual
examination,
OSCC
more
often
detected
at
advanced
stage.
The
global
prevalence
of
around
6%,
with
increasing
trends
posing
a
significant
health
problem
due
to
increase
in
morbidity
mortality.
microbiome
has
been
target
numerous
studies,
findings
highlighting
role
dysbiosis
developing
OSCC.
Dysbiosis
can
significantly
pathobionts
(bacteria,
viruses,
fungi,
parasites)
that
trigger
inflammation
through
their
virulence
pathogenicity
factors.
In
contrast,
chronic
bacterial
contributes
development
Pathobionts
also
have
other
effects,
such
as
impact
on
immune
system,
which
alter
responses
contribute
pro-inflammatory
environment.
Poor
hygiene
carbohydrate-rich
foods
risk
factors
mechanisms
are
not
yet
fully
understood
remain
frequent
research
topic.
For
this
reason,
narrative
review
concentrates
issue
potential
cause
OSCC,
well
underlying
involved.
Cardiovascular Research,
Год журнала:
2022,
Номер
118(18), С. 3451 - 3466
Опубликована: Авг. 24, 2022
Heart
failure
(HF)
and
cancer
are
the
leading
causes
of
death
worldwide
accumulating
evidence
demonstrates
that
HF
affect
one
another
in
a
bidirectional
way.
Patients
with
at
increased
risk
for
developing
cancer,
is
associated
accelerated
tumour
growth.
The
presence
malignancy
may
induce
systemic
metabolic,
inflammatory,
microbial
alterations
resulting
impaired
cardiac
function.
In
addition
to
pathophysiologic
mechanisms
shared
between
HF,
overlaps
also
exist
pathways
required
normal
physiology
Therefore,
these
explain
cardiotoxicity
as
result
targeted
anti-cancer
therapies.
This
review
provides
an
overview
involved
connection
specifically
focusing
upon
current
'hot-topics'
mechanisms.
It
subsequently
describes
therapies
cardiotoxic
potential
overlap
their
targets