Epigenomics,
Journal Year:
2024,
Volume and Issue:
16(23-24), P. 1453 - 1464
Published: Nov. 27, 2024
Neurofibromatosis
(NF)
is
identified
as
genetic
disorder
characterized
by
multiple
tumors
on
nerve
tissues.
NF1
the
most
prevalent
form,
neurofibromas
and
skin
changes.
neurofibromatosis
disorder,
distinct
from
rarer
NF2
schwannomatosis
(SWN)
conditions.
NF2,
including
NF2-related
SWN
(NF2-SWN),
predominantly
involves
schwannoma
formation
differs
Experimental Hematology and Oncology,
Journal Year:
2024,
Volume and Issue:
13(1)
Published: July 16, 2024
Abstract
Nuclear
factor-kappaB
(NF-ĸB)
plays
a
crucial
role
in
both
innate
and
adaptive
immune
systems,
significantly
influencing
various
physiological
processes
such
as
cell
proliferation,
migration,
differentiation,
survival,
stemness.
The
function
of
NF-ĸB
cancer
progression
response
to
chemotherapy
has
gained
increasing
attention.
This
review
highlights
the
inflammation
control,
biological
mechanisms,
therapeutic
implications
treatment.
is
instrumental
altering
release
inflammatory
factors
TNF-α,
IL-6,
IL-1β,
which
are
key
regulation
carcinogenesis.
Specifically,
conditions
including
colitis,
upregulation
can
intensify
inflammation,
potentially
leading
development
colorectal
cancer.
Its
pivotal
extends
regulating
tumor
microenvironment,
impacting
components
macrophages,
fibroblasts,
T
cells,
natural
killer
cells.
influences
tumorigenesis
dampen
anti-tumor
responses.
Additionally,
modulates
death
notably
by
inhibiting
apoptosis
ferroptosis.
It
also
dual
stimulating
or
suppressing
autophagy
cancers.
Beyond
these
functions,
controlling
stem
fostering
angiogenesis,
metastatic
potential
through
EMT
induction,
reducing
sensitivity
radiotherapy.
Given
its
oncogenic
capabilities,
research
focused
on
products
small
molecule
compounds
that
suppress
NF-ĸB,
offering
promising
avenues
for
therapy.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: July 2, 2024
Ferroptosis
induces
significant
changes
in
mitochondrial
morphology,
including
membrane
condensation,
volume
reduction,
cristae
alteration,
and
outer
rupture,
affecting
function
cellular
fate.
Recent
reports
have
described
the
intrinsic
iron
metabolism
its
intricate
connection
to
ferroptosis,
a
kind
of
cell
death
characterized
by
dependence
oxidative
stress
regulation.
Furthermore,
updated
molecular
insights
elucidated
significance
mitochondria
ferroptosis
implications
various
cancers.
In
context
cancer
therapy,
understanding
dual
role
anastasis
chemoresistance
is
crucial.
Targeting
pathways
involved
may
enhance
efficacy
inducers,
providing
synergistic
approach
overcome
chemoresistance.
Research
into
how
DNA
damage
response
(DDR)
proteins,
metabolic
changes,
redox
states
interact
during
can
offer
new
designing
combinatorial
therapeutic
regimens
against
several
cancers
associated
with
stemness.
These
treatments
could
potentially
inhibit
while
simultaneously
inducing
thereby
reducing
likelihood
cells
evading
developing
resistance
chemotherapy.
The
objective
this
study
explore
interplay
between
anastasis,
EMT
chemoresistance,
immunotherapeutics
better
understand
their
collective
impact
on
therapy
outcomes.
We
searched
public
research
databases
google
scholar,
PubMed,
relemed,
national
library
medicine
related
topic.
review,
we
discussed
tricarboxylic
acid
cycle
glycolysis
implicated
modulating
adding
complexity
regulatory
mechanisms.
Additionally,
reactive
oxygen
species
(ROS)
electron
transport
chain
(ETC)
has
garnered
attention.
Lipid
metabolism,
particularly
involving
GPX4
System
Xc-
plays
both
progression
cancer.
There
need
investigate
clinical
Integrating
strategies
targeting
exploring
potential
synergy
immunotherapy
represent
promising
avenues
for
advancing
chemoresistant
treatment.
Understanding
among
mitochondria,
ROS,
vital
oncology,
revolutionizing
personalized
treatment
drug
development.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Sept. 2, 2024
Hepatocellular
carcinoma
(HCC)
is
the
predominant
form
of
liver
cancer
and
ranks
as
third
leading
cause
cancer-related
mortality
globally.
The
performs
a
wide
range
tasks
primary
organ
responsible
for
metabolizing
harmful
substances
foreign
compounds.
Oxidative
stress
has
crucial
role
in
growth
improvement
hepatocellular
(HCC).
Nuclear
factor
erythroid
2
(
1
)-related
(Nrf2)
an
element
that
regulates
transcription
located
cytoplasm.
It
controls
balance
redox
reactions
by
stimulating
expression
many
genes
depend
on
antioxidant
response
elements.
Nrf2
contrasting
functions
normal,
healthy
HCC.
In
normal
liver,
provides
advantageous
benefits,
while
HCC
it
promotes
effects
support
survival
Continuous
activation
been
detected
its
advancement
aggressiveness.
addition,
Activation
may
lead
to
immune
evasion,
weakening
cells’
ability
attack
tumors
thereby
promoting
tumor
development.
Furthermore,
chemoresistance
HCC,
which
considered
chemotherapy
medications,
significantly
impedes
effectiveness
treatment.
Stress
management
typically
accomplished
activating
specific
signal
pathways
chemical
variables.
One
important
creation
nuclear
factor-E2-related
(Nrf2).
production
group
encode
proteins
protecting
cells
from
damage.
This
occurs
through
Nrf2/ARE
pathway,
mechanism
combating
oxidative
within
cells.