Invasive Fungal Disease After Chimeric Antigen Receptor-T Immunotherapy in Adult and Pediatric Patients
Paschalis Evangelidis,
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Konstantinos Tragiannidis,
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Athanasios Vyzantiadis
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et al.
Pathogens,
Journal Year:
2025,
Volume and Issue:
14(2), P. 170 - 170
Published: Feb. 8, 2025
Invasive
fungal
diseases
(IFDs)
have
been
documented
among
the
causes
of
post-chimeric
antigen
receptor-T
(CAR-T)
cell
immunotherapy
complications,
with
incidence
IFDs
in
CAR-T
therapy
recipients
being
measured
between
0%
and
10%,
globally.
are
notorious
for
their
potentially
life-threatening
nature
challenging
diagnosis
treatment.
In
this
review,
we
searched
recent
literature
aiming
to
examine
risk
factors
epidemiology
post-CAR-T
infusion.
Moreover,
role
antifungal
prophylaxis
is
investigated.
especially
vulnerable
due
several
that
contribute
patient’s
immunosuppression.
Those
include
underlying
hematological
malignancies,
lymphodepleting
chemotherapy
administered
before
treatment,
existing
leukopenia
hypogammaglobinemia,
use
high-dose
corticosteroids
interleukin-6
blockers
as
countermeasures
immune
effector
cell-associated
neurotoxicity
syndrome
cytokine
release
syndrome,
respectively.
mostly
occur
within
first
60
days
following
infusion
T
cells,
but
cases
even
a
year
after
described.
Aspergillus
spp.,
Candida
Pneumocystis
jirovecii
main
cause
these
infections
therapy.
More
real-world
data
regarding
population
essential.
Language: Английский
Cancer-related cognitive impairment in patients with hematologic malignancies after CAR T cell therapy: a systematic review and meta-analysis of prevalence
Supportive Care in Cancer,
Journal Year:
2025,
Volume and Issue:
33(4)
Published: March 22, 2025
Abstract
Purpose
Cancer-related
cognitive
impairment
is
one
of
the
symptoms
neurotoxicity
among
patients
receiving
chimeric
antigen
receptor
(CAR)
T
cell
therapy.
Evidence
overall
estimated
prevalence
cancer-related
following
CAR
T-cell
therapy
with
hematologic
malignancies
at
short-term
and
long-term
follow-ups
lacking.
This
review
aimed
to
summarize
functioning
status
estimate
follow-up
within
1
month,
12
months,
>
months
after
Methods
PubMed,
Cochrane
Library,
EMBASE,
CINAHL
Plus,
Web
Science,
PsycINFO
via
ProQuest
from
inception
through
August
2024.
Studies
that
reported
on
valid
measures
were
included.
Data
pooled
using
a
random-effects
model.
Results
In
total,
16
studies
involving
1407
The
rates
assessed
neuropsychological
tests
timepoints
(<
1–12
months)
24%
[95%
prediction
interval
(PI)
16–33%],
33%
(95%,
PI
9–64%),
35%
23–48%),
respectively.
estimates
other
ranging
4
38%
across
different
timepoints.
leave-one-out
meta-analyses
quantified
impact
these
potential
outliers
estimation
prevalence.
Conclusions
findings
stress
importance
developing
targeted
interventions
prevent
or
manage
in
cancer
during
both
periods.
also
highlights
need
for
further
research
this
area
improve
our
understanding
disease
mechanisms
implement
preventive
strategies
managing
impairment.
Language: Английский
Genetic Susceptibility in Endothelial Injury Syndromes after Hematopoietic Cell Transplantation and Other Cellular Therapies: Climbing a Steep Hill
Current Issues in Molecular Biology,
Journal Year:
2024,
Volume and Issue:
46(5), P. 4787 - 4802
Published: May 15, 2024
Hematopoietic
stem
cell
transplantation
(HSCT)
remains
a
cornerstone
in
the
management
of
patients
with
hematological
malignancies.
Endothelial
injury
syndromes,
such
as
HSCT-associated
thrombotic
microangiopathy
(HSCT-TMA),
veno-occlusive
disease/sinusoidal
obstruction
syndrome
(SOS/VOD),
and
capillary
leak
(CLS),
constitute
complications
after
HSCT.
Moreover,
endothelial
damage
is
prevalent
immunotherapy
chimeric
antigen
receptor-T
(CAR-T)
can
be
manifested
cytokine
release
(CRS)
or
immune
effector
cell-associated
neurotoxicity
(ICANS).
Our
literature
review
aims
to
investigate
genetic
susceptibility
syndromes
HSCT
CAR-T
therapy.
Variations
complement
pathway-
function-related
genes
have
been
associated
development
HSCT-TMA.
In
these
genes,
CFHR5,
CFHR1,
CFHR3,
CFI,
ADAMTS13,
CFB,
C3,
C4,
C5,
MASP1
are
included.
Thus,
variations
might
predisposition
activation,
which
also
exaggerated
by
other
factors
(such
acute
graft-versus-host
disease,
infections,
calcineurin
inhibitors).
Few
studies
examined
SOS/VOD
syndrome,
implicated
include
CFH,
methylenetetrahydrofolate
reductase,
heparinase.
Finally,
specific
mutations
onset
CRS
(PFKFB4,
CX3CR1)
ICANS
(PPM1D,
DNMT3A,
TE2,
ASXL1).
More
research
essential
this
field
achieve
better
outcomes
for
our
patients.
Language: Английский