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The RNA editing enzyme APOBEC1 induces somatic mutations and a compatible mutational signature is present in esophageal adenocarcinomas.
[esophageal adenocarcinoma]
The
AID
/
APOBECs
are
deaminases
that
act
on
cytosines
in
a
diverse
set
of
pathways
and
some
of
them
have
been
linked
to
the
onset
of
genetic
alterations
in
cancer
.
Among
them
,
APOBEC
1
is
the
only
family
member
to
physiologically
target
RNA
,
as
the
catalytic
subunit
in
the
Apolipoprotein
B
mRNA
editing
complex
.
APOBEC
1
has
been
linked
to
cancer
development
in
mice
but
its
oncogenic
mechanisms
are
not
yet
well
understood
.
We
analyze
whether
expression
of
APOBEC
1
induces
a
mutator
phenotype
in
vertebrate
cells
,
likely
through
direct
targeting
of
genomic
DNA
.
We
show
its
ability
to
increase
the
inactivation
of
a
stably
inserted
reporter
gene
in
a
chicken
cell
line
that
lacks
any
other
AID
/
APOBEC
proteins
,
and
to
increase
the
number
of
imatinib-resistant
clones
in
a
human
cellular
model
for
chronic
myeloid
leukemia
through
induction
of
mutations
in
the
BCR
-
ABL
1
fusion
gene
.
Moreover
,
we
find
the
presence
of
an
AID
/
APOBEC
mutational
signature
in
esophageal
adenocarcinomas
,
a
type
of
tumor
where
APOBEC
1
is
expressed
,
that
mimics
the
one
preferred
by
APOBEC
1
in
vitro
.
Our
findings
suggest
that
the
ability
of
APOBEC
1
to
trigger
genetic
alterations
represents
a
major
layer
in
its
oncogenic
potential
.
Such
APOBEC
1
-
induced
mutator
phenotypes
could
play
a
role
in
the
onset
of
esophageal
adenocarcinomas
.
APOBEC
1
could
be
involved
in
cancer
promotion
at
the
very
early
stages
of
carcinogenesis
,
as
it
is
highly
expressed
in
Barrett
's
esophagus
,
a
condition
often
associated
with
esophageal
adenocarcinoma
.