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1
、
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2010
年以来，
国际上与
Ovarian
cancer
、
Breast cancer
< br>、
Leukemia
相关的文献有多少篇？写出
3
篇研究性论文标题和摘要，
写出
5
篇综述性论文标题和摘要；
数据库
：科学引文索引数据库
(SCI
：
Sc
ience Citation Index)
与
Ovarian cancer
相关
的文献有
11,303
篇
与
Breast cancer
相关的
文献有
56,209
篇
与
Leukemia
相关的文献有
< br>32,912
篇
综述性论文标题和摘要
1.
Hemochromatosis and ovarian
cancer
摘要
:
Evaluation
of:
Gannon
PO,
Medelci
S,
Le
Page
C et
al.
Impact
of
hemochromatosis gene
(HFE)
mutations on epithelial ovarian cancer risk and
prognosis. Int. J. Cancer 128(10), 2326-2334
(2011).
The
frequency
of
two
mutations
(C282Y
and
D62H)
of
the
hemochromatosis
gene
were
investigated in women with ovarian
cancer. A single allele mutation of the C282Y but
not the H63D
gene product was detected
in 8-9% of women with benign ovarian tumors (n =
124) and ovarian
cancers (n = 360)
compared with 2.5% for controls (n = 80)
representing a 4.9-fold increase in risk.
With high-grade serous ovarian cancers
(n = 179), the survival rate of women with a
single allele
C282Y
mutation
was
reduced
from
39
to
19
months.
These
results
implicate
mutations
of
the
hemochromatosis
gene
in
the
generation
and
severity
of
ovarian
cancers,
which
may
have
prognostic value.
2.
Differences
between women who pursued genetic testing for
hereditary breast
and ovarian cancer
and their at-risk relatives who did
not.
摘要
:
Purpose/Objectives: To (a) examine differences in
appraisals of hereditary breast and ovarian
cancer (HBOC), psychological distress,
family environment, and decisional conflict
between women
who pursued genetic
testing and their at-risk relatives who did not,
and (b) examine correlations
among
appraisals
of
HBOC,
psychological
distress,
family
environment,
and
decisional
conflict
regarding genetic testing in these two
cohorts of : Descriptive, cross-sectional cohort
g:
Two
clinics
affiliated
with
a
major
research
university
in
the
midwestern
United
: 372 women aged 18 years and older.
200 pursued genetic testing for BRCA1 and
BRCA2 mutations (probands) and 172 of
their female relatives who had a greater than 10%
prior
probability of being a mutation
carrier but had not pursued s: After providing
informed
consent,
probands
and
relatives
were
mailed
self-
administered
Research
Variables:
Perceived
risk,
knowledge
of
HBOC
risk
factors
and
modes
of
gene
inheritance,
perceived
severity,
perceived
controllability,
psychological
distress,
family
relationships,
family
communication,
and
decisional
conflict
about
genetic
gs:
T
tests
revealed
that
probands perceived
higher risk and had more psychological distress
associated with breast cancer.
Probands
had more knowledge regarding risk factors and gene
inheritance, and greater decisional
conflict
regarding
genetic testing.
Relatives
reported higher perceived
severity
and
controllability.
No
differences were observed in family relationships
and family communication between probands
and
relatives.
Pearson
correlations
revealed
different
patterns
in
knowledge,
perceived
controllability,
family
relationships,
and
decisional
conflict
between
probands
and
sions: Significant
differences exist between women who pursue genetic
testing and
those
who
do
not.
The
family
environment
influences
adjustment
to
HBOC
and
decisions
about
genetic ations for Nursing: Enhancing
the family communication process about HBOC
can provide informational and emotional
support to high-risk women and promote decision
making
about genetic testing.
3.
Incidence
and
mortality
in
epithelial
ovarian
cancer
by
family
history
of
any
cancer
摘要
:
Practically
all data on familial risk in ovarian and other
cancers are based on incident cancer,
whereas
familiality
in
cancer
mortality
is
largely
unknown.
If
fatal
forms
of
cancer
are
a
highly
familial
subtype, then familial risk for mortality may
exceed that of incidence, which is relevant for
clinical decision making and
counseling. Ovarian cancer patients in the
nationwide Swedish Family
Cancer
Database were classified according to fatal and
nonfatal (incident) family history. Familial
risks for incident and fatal ovarian
cancer were calculated for offspring based on
their parental or
sibling
family
history
of
any
cancer
using
standardized
incidence
ratios
(SIRs)
for
incidence
and
standardized mortality ratios (SMRs)
for mortality. Offspring without family history
were referents.
The database included
24,757 mothers and 8138 daughters with
ovarian cancer. When a mother
had ovarian cancer, the SIR for
incident ovarian cancer in daughters was 2.69, and
when a sister
had ovarian cancer it was
3.49. The SMRs for fatal cancer by fatal cancer in
probands were 3.39
and 5.80,
respectively. For fatal serous cancers among
siblings, the SMR was 6.16, compared with
10.01 for the endometrioid type.
Ovarian cancer was associated with
maternal (SIR, 1.22; SMR,
1.56) and
sororal breast cancer (SIR, 1.27). Another
discordant association was between ovarian
and paternal prostate cancer (SIR,
1.12; SMR, 1.66). Fatal familial risks were higher
for concordant
ovarian, ovarian-breast,
and ovarian-prostate cancers than the
corresponding incident risks. This
may
suggest that highly fatal subtypes exist for these
cancers, calling for genetic dissection. Cancer
2011. 2011 American Cancer Society.
Copyright 2011 American Cancer Society.
4.
Knock-down
of
amphiregulin
inhibits
cellular
invasion
in
inflammatory
breast
cancer.
摘要
:
We have
previously shown that SUM-149 human breast cancer
cells require an amphiregulin
(AREG)
autocrine
loop
for
cell
proliferation.
We
also
demonstrated
that
AREG
can
increase
epidermal
growth
factor
receptor
(EGFR)
stability
and
promote
EGFR
localization
to
the
plasma
membrane. In the present studies we
successfully knocked-down AREG expression in
SUM-149
cells
by
lentiviral
infection
of
AREG
shRNA.
In
the
absence
of
AREG
expression,
SUM-149
cell
growth
was
slowed,
but
not
completely
inhibited.
Furthermore,
cells
infected
with
AREG
shRNA
constructs showed an increase in EGFR
protein expression by Western blot.
Immunofluorescence
and confocal
microscopy showed that following AREG knock-down,
EGFR continued to localize to
the
cell
surface.
Soft
agar
assays
demonstrated
that
AREG
knock-down
cells
retain
anchorage-independent growth capacity.
Additionally mammosphere forming assays and
Adefluor
staining
analysis
showed
that
knock-down
of
AREG
expression
did
not
affect
the
expression
of
stem
cell
phenotypes.
However,
following
AREG
knock-down,
SUM-149
cells
demonstrated
a
dramatic
decrease
in
their
ability
to
invade
a
Matrigel
matrix.
Consistent
with
this
observation,
microarray
analysis comparing cells infected with a non-
silencing vector to the AREG knock-down
cells,
identified
genes
associated
with
the
invasive
phenotype
such
as
RHOB
and
DKK1,
and
networks associated with
cell motility such as integrin-linked kinase
signaling, and focal adhesion
kinase
signaling. AREG was also found to modulate WNT and
Notch signaling in these cells. Thus,
AREG functions in regulating the
invasive phenotype, and we propose that this
regulation may be
through altered
signaling that occurs when AREG activates plasma
membrane localized EGFR. J.
Cell.
Physiol. 226: 2691-2701, 2011. 2011 Wiley-Liss,
Inc. Copyright 2011 Wiley-Liss, Inc.
5.
Prognostic
impact
of
c-KIT
mutations
in
core
binding
factor
acute
myeloid
leukemia.
摘要
:
This study
sought to define the prognostic impact of c-KIT
mutations in core binding factor
acute
myeloid leukemia (CBF AML) patients. A total of
116 patients diagnosed as CBF AML in Asan
Medical
Center
from
January 1999
to
May
2010
were
enrolled
in
this study. We
applied
melting
curve analyses and direct
sequencing methods to confirm c-KIT mutations in
exon 17 (mutKIT17)
and exon 8
(mutKIT8). Of the total 116 patients, mutKIT17
were found in 36 (31%) and mutKIT8
were
found
in
7
(6%).
In
patients
with
t(8;21),
prognosis
was
significantly
poorer
in
those
with
mutKIT17 compared to those without the
mutation. This difference was limited to adults.
In patients
with inv(16), there was no
prognostic impact of c-KIT mutations. Therefore,
an analysis of mutKIT17
in adult CBF
AML patients with t(8;21) is recommended as a
means to predict prognosis. Copyright
2011 Elsevier Ltd. All rights
reserved.
研究性论文标题和摘要
1.
Prolactin
increases
survival
and
migration
of
ovarian
cancer
cells:
Importance
of
prolactin
receptor
type
and
therapeutic
potential
of
S179D
and
G129R
receptor
antagonists.
摘要
:
Variably-
spliced prolactin receptors (PRLRs) and PRL are
expressed by the ovarian cancer cell
lines, TOV-112D, OV-90 and TOV-21G.
Incubation in the PRLR antagonists, G129R- or
S179D-PRL, or
anti-PRL reduced cell
number, indicating a functional autocrine PRL
growth loop. Added PRL promoted,
and
the
antagonists
decreased,
cell
migration.
When
cells
were
stressed,
added
PRL
decreased
apoptosis and increased survival, and
the antagonists had the opposite effect. Cells
expressing higher
long:short
PRLR
ratios
had
increased
growth,
survival
and
migration
in
response
to
PRL.
Results
suggest
that
PRLR
antagonists
may
be
therapeutically
beneficial
in
ovarian cancer.
Copyright
2011
Elsevier Ireland Ltd.
All rights reserved
2.
(R)-FTY720
methyl
ether
is
a
specific
sphingosine
kinase
2
inhibitor:
Effect
on
sphingosine
kinase
2
expression
in
HEK
293
cells
and
actin
rearrangement
and
survival of MCF-7 breast
cancer cells
摘要
:
Sphingosine
kinase
2
(SK2)
catalyses
the
conversion
of
sphingosine
to
the
bioactive
lipid
sphingosine
1-phosphate
(Si
P).
We
report
here,
the
stereospecific
synthesis
of
an
analogue
of
FTY720 called
(R)-FTY720-OMe, which we show is a competitive
inhibitor of SK2. (R)-FTY720-OMe
failed
to
inhibit
sphingosine
kinase
1
activity,
thereby
demonstrating
specificity
for
SK2.
Prolonged
treatment
of
HEK
293
cells
with
(R)-FTY720-OMe
also
induced
a
reduction
in
SK2
expression.
In
addition. (R)-FTY720-OMe inhibited DNA
synthesis and prevented S1P-stimulated
rearrangement of
actin in MCF-7 breast
cancer cells. These findings demonstrate that SK2
functions as a pro-survival
protein
and
is
involved
in
promoting
actin
rearrangement
into
membrane
ruffles/lamellipodia
in
response to SIP in MCF-7 breast cancer
cells. (C) 2011 Elsevier Inc. All rights reserved
3.
The BH3-only protein Noxa is stimulated
during apoptosis of chronic lymphocytic
leukemia cells triggered by M2YN, a new
plant-derived extract.
摘要
:
Deficiency
of
apoptosis
is
a
hallmark
of
chronic
lymphocytic
leukemia
(CLL) cells.
M2Yn
is
a
natural extract from plants of central
Asia, identified for its antiangiogenic properties
and its ability to
block the migration
of malignant cells. Here, we report that in vitro
treatment of cells derived from CLL
patients with M2Yn results in
internucleosomal DNA fragmentation,
phosphatidylserine externalization,
mitochondrial membrane depolarization,
caspase-3 activation and cleavage of the caspase
substrate
PARP-1. The extents of these
effects depend on the patients and are mostly
comparable to those of
flavopiridol
or
hyperforin,
two
known
plant-
derived
apoptosis
inducers
of
CLL
cells.
M2Yn
does
not
modulate Mcl-1 expression, while
downregulation of this antiapoptotic protein is
involved in the action
of flavopiridol.
By contrast, M2Yn, like hyperforin, upregulates
the Noxa protein, possibly by inhibiting
proteasomal
activity.
This
BH3-only
protein
is
known
to
trigger
the
activation
of
the
pro-apoptotic
protein
Bak
through
displacement
of
the
Mcl-1/Bak
complex
at
the
mitochondrial
membrane,
as
actually
observed
here
in
M2Yn-treated
cells.
Our
data,
therefore,
show
that
M2Yn
can
induce
the
caspase-dependent mitochondrial pathway
of apoptosis in CLL cells via a mechanism
resembling that
of hyperforin. Our data
also confirm that the BH3-only protein Noxa is a
relevant target for CLL therapy.
2
、
请
以
”
P53
”
、
”
BRCA1
”
、
”
BRCA2
”
、
”
RAD51D
”
、
”
MSH6
”<
/p>
、
”
MLH1
”
为关键词，在
NCBI
的网站上搜索人
的序列，要
求列出下列信息：
物种的拉丁文、
< br>序列的
ACCNUM
和碱基序列，
并
找出这些基因在酵母、
果蝇和小鼠中的同源基因，
列出物种的拉丁文，
序列的
ACCNUM
；
（
Saccharomyces
ce
revisiae
，
Drosophila
melanogaster
，
Mus
Musculus
）
P53
：
Homo sapiens
NC_000017.10
Chromosome: 17; NC_000017.10
(7571720..7590863, complement)
与
Saccharomyces
cerevisiae
同源基因为
BK006938.2
与
Drosophila melanogaster
同源基因为
BT021431.1
与
Mus
Musculus
同源基因为
AK156276.1
BRCA1
：
Homo sapiens
NC_000017.10
Chromosome: 17; NC_000017.10
(41196312..41277500, complement)
与
Saccharomyces
cerevisiae
同源基因为
BK006949.2
与
Drosophila
melanogaster
同源基因为
AE014134.5
与
Mus
Musculus
同源基因为
AL590996.12
BRCA2
：
Homo sapiens
NC_000013.10
Chromosome: 13; NC_000013.10
(32889617..32973809)
与
Saccharomyces
cerevisiae
同源基因为
BK006939
与
Drosophila
melanogaster
同源基因为
AE014134
与
Mus
Musculus
同源基因为
AC154885
RAD51D
：
Homo sapiens
NC_000017.10
Chromosome: 17; NC_000017.10
(33426811..33446888, complement)
与
Saccharomyces
cerevisiae
同源基因为
S66120
与
Drosophila
melanogaster
同源基因为
AE014298
与
Mus
Musculus
同源基因为
AK011387
MSH6
：
Homo sapiens
NC_000002.11
Chromosome: 2; NC_000002.11
(48010221..48034092)
与
Saccharomyces
cerevisiae
同源基因为
BK006942
与
Drosophila
melanogaster
同源基因为
BT050543
与
Mus
Musculus
同源基因为
AC087233
MLH1
：
Homo sapiens
NC_000003.11
Chromosome: 3; NC_000003.11
(37034841..37092337)
与
Saccharomyces
cerevisiae
同源基因为
BK006940
与
Drosophila
melanogaster
同源基因为
AE013599
与
Mus
Musculus
同源基因为
AK171052
3
、请分别用核酸
< br>-
核酸、核酸
-
蛋白质的
blast
方法，分析以下这个序
列可能是一
个什么样的序列，要求列出：
blast
程序、比对的数据库、
相似性最高的序列的
ACCNUM
、<
/p>
相似性最高序列所在的物种和相似