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Abramson Cancer CenterNCI CANCERLIT® Search: BRCA1 Gene - March 2002
National Cancer Institute®
Last Modified: March 1, 2002
Table of Contents
1
UI - 11748305
AU - Eng C; Brody LC; Wagner TM; Devilee P; Vijg J; Szabo C; Tavtigian SV;
TI -
Nathanson KL; Ostrander E; Frank TS; Steering Committee of the Breast
Cancer Information Core (BIC) Consortium
Interpreting epidemiological research: blinded comparison of methods
used to estimate the prevalence of inherited mutations in BRCA1.
SO - J Med Genet 2001 Dec;38(12):824-33
AD - Clinical Cancer Genetics and Human Cancer Genetics Programs,
Comprehensive Cancer Center, and Division of Human Genetics, Department
of Internal Medicine, The Ohio State University, Columbus, OH 43210,
USA. eng-1@medctr.osu.edu
While sequence analysis is considered by many to be the most sensitive
method of detecting unknown mutations in large genes such as BRCA1, most
published estimates of the prevalence of mutations in this gene have
been derived from studies that have used other methods of gene analysis.
In order to determine the relative sensitivity of techniques that are
widely used in research on BRCA1, a set of blinded samples containing 58
distinct mutations were analysed by four separate laboratories. Each
used one of the following methods: single strand conformational
polymorphism analysis (SSCP), conformation sensitive gel electrophoresis
(CSGE), two dimensional gene scanning (TDGS), and denaturing high
performance liquid chromatography (DHPLC). Only the laboratory using
DHPLC correctly identified each of the mutations. The laboratory using
TDGS correctly identified 91% of the mutations but produced three
apparent false positive results. The laboratories using SSCP and CSGE
detected abnormal migration for 72% and 76% of the mutations,
respectively, but subsequently confirmed and reported only 65% and 60%
of mutations, respectively. False negatives therefore resulted not only
from failure of the techniques to distinguish wild type from mutant, but
also from failure to confirm the mutation by sequence analysis as well
as from human errors leading to misreporting of results. These findings
characterise sources of error in commonly used methods of mutation
detection that should be addressed by laboratories using these methods.
Based upon sources of error identified in this comparison, it is likely
that mutations in BRCA1 and BRCA2 are more prevalent than some studies
have previously reported. The findings of this comparison provide a
basis for interpreting studies of mutations in susceptibility genes
across many inherited cancer syndromes.
2
UI - 11750836
AU - Petit JY; Greco M; EUSOMA
TI -
Quality control in prophylactic mastectomy for women at high risk of
breast cancer.
SO - Eur J Cancer 2002 Jan;38(1):23-6
AD - Division of Plastic Surgery, European Institute of Oncology, via
Ripamonti 435, Milan, Italy. jean.petit@ieo.it
3
UI - 11773283
AU - Geisler JP; Hatterman-Zogg MA; Rathe JA; Buller RE
TI -
Frequency of BRCA1 dysfunction in ovarian cancer.
SO - J Natl Cancer Inst 2002 Jan 2;94(1):61-7
AD - Division of Gynecologic Oncology, Department of Obstetrics and
Gynecology, Holden Comprehensive Cancer Center, University of Iowa, Iowa
City 52242, USA.
BACKGROUND: Ovarian cancer is one of the most common hereditary cancers
in women. Mutations in the BRCA1 gene increase a woman's risk of ovarian
cancer. Testing for BRCA1 mutations is cumbersome and impractical for
large populations. Therefore, we developed an efficient strategy to
detect various types of BRCA1 dysfunction and also determined the
relative frequency of BRCA1 dysfunction in ovarian cancer. METHODS:
Tumors from 221 patients with epithelial ovarian cancer were screened
for loss of heterozygosity (LOH) at the BRCA1 locus. BRCA1 complementary
DNA (cDNA) and genomic DNA from all cancers with BRCA1 LOH (106 tumors)
or noninformative status (15 tumors) were polymerase chain reaction
(PCR) amplified and analyzed for protein truncation in a coupled
transcription/translation test. When truncated BRCA1 protein was
detected, the BRCA1 gene from both the tumor and a paired blood sample
was sequenced. When BRCA1 expression in tumor cDNA was not detected with
a protein truncation test, a methylation-specific PCR was used to
determine whether the promoter region of BRCA1 was methylated and thus
inactivated. All statistical tests were two-sided. RESULTS: Fifty-one
(23.1%) of 221 tumors had BRCA1 dysfunction, including 18 with germline
mutations, 15 with somatic mutations, and 18 with monoallelic or
biallelic hypermethylated promoters. By the consideration of only tumors
with LOH or that were noninformative, the efficiency for detecting BRCA1
dysfunction improved to 45 (37.2%) of 121 tumors. Therefore,
LOH/noninformative was a strong predictor of mutation status (Fisher's
exact test, P<.001). However, this subset of tumors did not include
those with BRCA1 missense mutations (estimated at six [2.7%] of 221 not
detected by our method) or biallelic promoter methylation (estimated at
six [2.7%] of 221). CONCLUSIONS: BRCA1 dysfunction in ovarian cancer is
common and occurs via multiple mechanisms. The use of LOH, rather than a
family history of ovarian cancer, as a first step in a screening
strategy, followed by protein truncation testing, appears to increase
the chance of identifying tumors with BRCA1 dysfunction.
4
UI - 11832208
AU - Venkitaraman AR
TI -
Cancer susceptibility and the functions of BRCA1 and BRCA2.
SO - Cell 2002 Jan 25;108(2):171-82
AD - University of Cambridge, CRC Department of Oncology, Hutchison/MRC
Research Centre, Hills Road, Cambridge CB2 2XZ, United Kingdom.
arv22@cam.ac.uk
Inherited mutations in BRCA1 or BRCA2 predispose to breast, ovarian, and
other cancers. Their ubiquitously expressed protein products are
implicated in processes fundamental to all cells, including DNA repair
and recombination, checkpoint control of cell cycle, and transcription.
Here, I examine what is known about the biological functions of the BRCA
proteins and ask how their disruption can induce susceptibility to
specific types of cancer.
5
UI - 11850376
AU - Morrow M; Gradishar W
TI -
Breast cancer.
SO - BMJ 2002 Feb 16;324(7334):410-4
AD - Department of Surgery, Northwestern University, Chicago, IL 60611, USA.
mmorrow@nmh.org
6
UI - 11857083
AU - Baldeyron C; Jacquemin E; Smith J; Jacquemont C; De Oliveira I; Gad S;
TI -
Feunteun J; Stoppa-Lyonnet D; Papadopoulo D
A single mutated BRCA1 allele leads to impaired fidelity of double
strand break end-joining.
SO - Oncogene 2002 Feb 21;21(9):1401-10
AD - UMR 218 du CNRS, Institut Curie, Section de Recherche, Paris 75248,
cedex05, France.
Heterozygosity for mutations in the BRCA1 gene in humans confers high
risk for developing breast cancer, but a biochemical basis for this
phenotype has not yet been determined. Evidence has accumulated
implicating BRCA1, in the maintenance of genomic integrity and the
protection of cells against DNA double strand breaks (DSB). Here we
present evidence that human cells heterozygous for BRCA1 mutations
exhibit impaired DNA end-joining, which is the major DSB repair pathway
in mammalian somatic cells. Using an in vivo host cell end-joining
assay, we observed that the fidelity of DNA end-joining is strongly
reduced in three BRCA1(+/-) cell lines in comparison to two control cell
lines. Moreover, cell-free BRCA1(+/-) extracts are unable to promote
accurate DNA end-joining in an in vitro reaction. The steady-state level
of the wild type BRCA1 protein was significantly lower than the 50%
expected in BRCA1(+/-) cells and thus may underlie the observed
end-joining defect. Together, these data strongly suggest that BRCA1 is
necessary for faithful rejoining of broken DNA ends and that a single
mutated BRCA1 allele is sufficient to impair this process. This defect
will compromise genomic stability in BRCA1 germ-line mutation carriers,
triggering the genetic changes necessary for the initiation of
neoplastic transformation.
7
UI - 11709053
AU - Mullan PB; McWilliams S; Quinn J; Andrews H; Gilmore P; McCabe N;
TI -
McKenna S; Harkin DP
Uncovering BRCA1-regulated signalling pathways by microarray-based
expression profiling.
SO - Biochem Soc Trans 2001 Nov;29(Pt 6):678-83
AD - Cancer Research Centre, Department of Oncology, Queen's University
Belfast, University Floor, Belfast City Hospital, Lisburn Road, Belfast
BT9 7AB, N. Ireland, UK.
The introduction of microarray technology to the scientific and medical
communities has dramatically changed the way in which we now address
basic biomedical questions. Expression profiling using microarrays
facilitates an experimental approach where alterations in the transcript
level of entire transcriptomes can be simultaneously assayed in response
to defined stimuli. We have used microarray analysis to identify
downstream transcriptional targets of the BRCA1 (Breast Cancer 1)
tumour-suppressor gene as a means of defining its function. BRCA1 has
been implicated in the predisposition to early onset breast and ovarian
cancer and while its exact function remains to be defined, roles in DNA
repair, cell-cycle control and transcriptional regulation have been
implied. In the current study we have generated cell lines with
tetracycline-regulated, inducible expression of BRCA1 as a tool to
identify genes, which might represent important effectors of BRCA1
function. Oligonucleotide array-based expression profiling identified a
number of genes that were upregulated at various times following
inducible expression of BRCA1 including the DNA damage-responsive gene
GADD45 (Growth Arrest after DNA Damage). Identified targets were
confirmed by Northern blot analysis and their functional significance as
BRCA1 targets examined.
8
UI - 11792738
AU - Benowitz S
TI -
French challenge to BRCA1 patent underlies European discontent.
SO - J Natl Cancer Inst 2002 Jan 16;94(2):80-1
9
UI - 11816590
AU - Wang J; Xu D; Kawde AN; Polsky R
TI -
Metal nanoparticle-based electrochemical stripping potentiometric
detection of DNA hybridization.
SO - Anal Chem 2001 Nov 15;73(22):5576-81
AD - Department of Chemistry and Biochemistry, New Mexico State University,
Las Cruces 88003, USA.
A new nanoparticle-based electrical detection of DNA hybridization,
based on electrochemical stripping detection of the colloidal gold tag,
is described. In this protocol, the hybridization of a target
oligonucleotide to magnetic bead-linked oligonucleotide probes is
followed by binding of the streptavidin-coated metal nanoparticles to
the captured DNA, dissolution of the nanometer-sized gold tag, and
potentiometric stripping measurements of the dissolved metal tag at
single-use thick-film carbon electrodes. An advanced magnetic processing
technique is used to isolate the DNA duplex and to provide low-volume
mixing. The influence of relevant experimental variables, including the
amounts of the gold nanoparticles and the magnetic beads, the duration
of the hybridization and gold dissolution steps, and the parameters of
the potentiometric stripping operation upon the hybridization signal, is
examined and optimized. Transmission electron microscopy micrographs
indicate that the hybridization event leads to the bridging of the gold
nanoparticles to the magnetic beads. Further signal amplification, and
lowering of the detection limits to the nanomolar and picomolar domains,
are achieved by precipitating gold or silver, respectively, onto the
colloidal gold label. The new electrochemical stripping
metallogenomagnetic protocol couples the inherent signal amplification
of stripping metal analysis with discrimination against nonhybridized
DNA, the use of microliter sample volumes, and disposable transducers
and, hence, offers great promise for decentralized genetic testing.
10
UI - 11786575
AU - Ben David Y; Chetrit A; Hirsh-Yechezkel G; Friedman E; Beck BD; Beller
TI -
U; Ben-Baruch G; Fishman A; Levavi H; Lubin F; Menczer J; Piura B;
Struewing JP; Modan B; National Israeli Study of Ovarian Cancer
Effect of BRCA mutations on the length of survival in epithelial ovarian
tumors.
SO - J Clin Oncol 2002 Jan 15;20(2):463-6
AD - Department of Gynecology, Haemek Medical Center, Afula.
PURPOSE: To study the role of BRCA mutations in ovarian cancer survival.
PATIENTS AND METHODS: Blood samples and specimens of ovarian tumors
(whenever blood samples were not available) at the time of the primary
surgery were obtained in the course of a nationwide case-control study
of women with ovarian cancer in Israel. The three common BRCA mutations
in Israel (185delAG, 5382insC, and 6174delT) were analyzed with a
multiplex polymerase chain reaction to amplify the exons containing the
three mutations using fluor-labeled primers in a single reaction.
Because each mutation is a small insertion or deletion, they can be
detected as length polymorphisms. Patients were followed for up to 5
years (range, 20 to 64 months). Statistical analysis was performed using
the Kaplan-Meier method and the log-rank test. Stepwise Cox regression
analysis was used for determination of independent prognostic factors.
RESULTS: This report is based on 896 blood or tumor specimens analyzed
for the presence of the BRCA mutations. Of these, 234 women (26.1%) were
found to be positive. A significant difference in survival pattern was
found between BRCA1/BRCA2 carriers and noncarriers among the women with
invasive ovarian cancer (median survival, 53.4 months v. 37.8 months;
3-year survival, 65.8% v. 51.9%, respectively). These differences were
independent of age at diagnosis or stage of the disease. CONCLUSION: Our
data indicate that the survival of patients with ovarian cancer is
affected by BRCA germline mutation, at least in the early years after
diagnosis.
11
UI - 11786581
AU - Schwartz MD; Peshkin BN; Hughes C; Main D; Isaacs C; Lerman C
TI -
Impact of BRCA1/BRCA2 mutation testing on psychologic distress in a
clinic-based sample.
SO - J Clin Oncol 2002 Jan 15;20(2):514-20
AD - Department of Oncology, Georgetown University, and Lombardi Cancer
Center, Washington, DC 20007, USA. schwartm@georgetown.edu
PURPOSE: Despite the increasingly widespread availability of BRCA1 and
BRCA2 genetic testing, little is known about the psychologic impact of
such testing in the clinical setting. The objective of this study was to
examine the long-term psychologic impact of receiving BRCA1/2 test
results within a clinic-based testing program. PATIENTS AND METHODS: The
participants were 279 high-risk women who underwent genetic counseling
and testing for alterations in the BRCA1/2 genes. At baseline (before
genetic testing) and at 6 months after the disclosure of mutation
status, we measured perceived risk for breast and ovarian cancer,
cancer-specific distress, and general distress. We examined the impact
of the test result on each of these outcomes at the 6-month follow-up.
Analyses were conducted separately for probands and their relatives who
were unaffected with cancer. RESULTS: We found no effect of test result
among affected probands. Among unaffected relatives, we found that
participants who received definitive negative test results exhibited
significant reductions in perceived risk and distress compared with
participants who received positive test results. Importantly, relatives
who received positive test results did not exhibit increased distress or
perceived risk. CONCLUSION: These results suggest that clinic-based
BRCA1/2 testing can lead to psychologic benefits for individuals who
receive negative test results. At 6 months after disclosure, those who
receive positive or uninformative test results do not exhibit increased
psychologic distress or perceived risk.
12
UI - 11846806
AU - Hegardt C; Johannsson OT; Oredsson SM
TI -
Rapid caspase-dependent cell death in cultured human breast cancer cells
induced by the polyamine analogue N(1),N(11)-diethylnorspermine.
SO - Eur J Biochem 2002 Feb;269(3):1033-9
AD - Department of Animal Physiology, Lund University, Sweden.
Cecilia.Hegardt@zoofys.lu.se
The spermine analogue N(1),N(11)-diethylnorspermine (DENSPM) efficiently
depletes the cellular pools of putrescine, spermidine and spermine by
down-regulating the activity of the polyamine biosynthetic enzymes and
up-regulating the activity of the catabolic enzyme spermidine/ spermine
N(1)-acetyltransferase (SSAT). In the breast cancer cell line L56Br-C1,
treatment with 10 microm DENSPM induced SSAT activity 60 and 240-fold at
24 and 48 h after seeding, respectively, which resulted in polyamine
depletion. Cell proliferation appeared to be totally inhibited and
within 48 h of treatment, there was an extensive apoptotic response.
Fifty percent of the cells were found in the sub-G(1) region, as
determined by flow cytometry, and the presence of apoptotic nuclei was
morphologically assessed by fluorescence microscopy. Caspase-3 and
caspase-9 activities were significantly elevated 24 h after seeding. At
48 h after seeding, caspase-3 and caspase-9 activities were further
elevated and at this time point a significant activation of caspase-8
was also found. The DENSPM-induced cell death was dependent on the
activation of the caspases as it was inhibited by the general caspase
inhibitor Z-Val-Ala-Asp fluoromethyl ketone. The results are discussed
in the light of the L56Br-C1 cells containing mutated BRCA1 and p53, two
genes involved in DNA repair.
13
UI - 11855879
AU - Leitao M; Boyd J
TI -
Preoperative CA-125 levels in patients with hereditary compared to
sporadic epithelial ovarian carcinoma.
SO - Gynecol Oncol 2002 Mar;84(3):413-5
AD - Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York,
New York 10021, USA.
OBJECTIVE: The aim of this study was to determine whether a significant
difference in preoperative CA-125 levels exists between patients with
BRCA-associated hereditary ovarian carcinoma and those with sporadic
ovarian carcinoma and whether the CA-125 level predicts the probability
of optimal cytoreductive surgery. METHODS: From a retrospective cohort
of 189 consecutive ovarian cancer patients genotyped for BRCA mutation
status, data on preoperative CA-125 levels were available for 49/88
(56%) hereditary cases and 43/101 (43%) sporadic cases. Data on the
extent of surgical cytoreduction were obtained for all 92 patients with
available CA-125 data. Comparison of preoperative CA-125 levels between
hereditary and sporadic groups was assessed using the Kruskal-Wallis
chi(2) test. Correlation of surgical cytoreduction with preoperative
CA-125 level was assessed using Fisher's exact test. RESULTS: Mean
preoperative CA-125 levels were not significantly different among BRCA1
(2289 U/ml), BRCA2 (2586 U/ml), and sporadic (3307 U/ml) cases (P =
0.5). For hereditary cases, optimal cytoreduction was achieved in 59% of
patients with preoperative CA-125 levels of <500 U/ml and in 52% of
patients with preoperative levels >500 U/ml. For sporadic cases, optimal
cytoreduction was achieved in 62% of patients with CA-125 levels of <500
U/ml and in 20% of patients with levels >500 U/ml (P = 0.01).
CONCLUSIONS: Preoperative CA-125 levels are not significantly different
for patients with hereditary compared to sporadic ovarian carcinoma. The
probability of optimal cytoreduction is independent of the preoperative
CA-125 level for hereditary cases, but optimal cytoreduction is
significantly less likely for sporadic cases with CA-125 levels of >500
U/ml.
14
UI - 11857748
AU - Llort G; Munoz CY; Tuser MP; Guillermo IB; Lluch JR; Bale AE; Franco MA
TI -
Low frequency of recurrent BRCA1 and BRCA2 mutations in Spain.
SO - Hum Mutat 2002 Mar;19(3):307
AD - Unidad de Consejo Genetico. Servicio de Prevencion y Control del Cancer,
Instituto Catalonian National Cancer Institute, Barcelona, Spain.
BRCA1 and BRCA2 mutations underlie a substantial proportion of all
hereditary breast cancer. The mutational spectrum in these genes is very
broad, with hundreds of different BRCA mutations reported worldwide.
However, high frequency founder mutations make up a substantial fraction
of all mutations in some ethnic groups. We directly sequenced BRCA1 and
BRCA2 in 35 Spanish breast/ovarian cancer families and found 13
mutations of which 3 had been reported previously in Spain. The ten
novel mutations are: IVS5+1 G>A, 1491delA, Leu1086Ter, and Gln895Ter in
BRCA1; Glu49Ter, 5373delGTAT, 5947delCTCT, 6672delTA, 8281insA, and
Pro3039Leu (which also involves a splice site) in BRCA2. Our data, in
combination with previous reports, indicate that 14 mutations have been
seen recurrently in Spanish families. Analyzing these 14 mutations in 42
previously untested breast/ovarian cancer families revealed only two
families testing positive, one for BRCA1 185delAG and one for BRCA2
9254delATCAT. While several mutations have been found recurrently in
Spain, none appear to be high frequency founder mutations based on
studies of breast and ovarian cancer families. Copyright 2002
Wiley-Liss, Inc.
15
UI - 11857749
AU - Khoo US; Chan KY; Cheung AN; Xue WC; Shen DH; Fung KY; Ngan HY; Choy KW;
TI -
Pang CP; Poon CS; Poon AY; Ozcelik H
Recurrent BRCA1 and BRCA2 germline mutations in ovarian cancer: a
founder mutation of BRCA1 identified in the Chinese population.
SO - Hum Mutat 2002 Mar;19(3):307-8
AD - Department of Pathology, Queen Mary Hospital, The University of Hong
Kong, Hong Kong.
Previous mutational analysis for BRCA gene mutations in sporadic ovarian
cancer occurring in Chinese patients in Hong Kong identified six
germline BRCA1 mutations and one germline BRCA2 mutation, six of which
were novel (Khoo et al., 2000). Knowledge of BRCA gene mutations in the
Chinese population is relatively scant. In this study, we focussed on
whether any of these mutations could be recurrent in our Chinese
population, making use of archival paraffin embedded tissue. A
consecutive series of 214 ovarian cancer cases, half of Southern Chinese
origin from Hong Kong whilst the other half of Northern Chinese origin
from Beijing were used for the study. We identified one further novel
mutation, 1081delG, in BRCA1. This was found to occur in two unrelated
individuals with shared haplotype as revealed by allelotype analysis,
thus demonstrating founder effect. Two other recurrent mutations were
also identified, the 2371-2372delTG mutation in BRCA1 and the 3337C>T
mutation in BRCA2 recurring in two and three unrelated individuals
respectively, giving an overall prevalence 4.7% of recurrent BRCA
mutations in ovarian cancer in the Southern Chinese population. Most
importantly, all our recurrent mutation carriers were identified from
Southern Chinese patients from Hong Kong whilst such mutations were
absent in samples from the Northern Chinese. Our findings indicate
possible heterogeneity in the BRCA genotype between Northern and
Southern Chinese. The identification of a founder mutation and two
recurrent mutations moreover, has important implications towards
screening strategies for breast and ovarian cancer among Chinese of
southern ancestral origin who are now dispersed throughout the world.
Copyright 2002 Wiley-Liss, Inc.
16
UI - 11870660
AU - Bilimoria MM
TI -
Prophylactic surgery in hereditary cancer syndromes: an ounce of
prevention may be the only cure.
SO - J Surg Oncol 2002 Mar;79(3):131-3
17
UI - 11898812
AU - Kunkler I
TI -
Radiotherapy for breast cancer.
SO - N Engl J Med 2002 Mar 14;346(11):862-4
18
UI - 11715007
AU - Kauff ND; Scheuer L; Robson ME; Glogowski E; Kelly B; Barakat R; Heerdt
TI -
A; Borgen PI; Davis JG; Offit K
Insurance reimbursement for risk-reducing mastectomy and oophorectomy in
women with BRCA1 or BRCA2 mutations.
SO - Genet Med 2001 Nov-Dec;3(6):422-5
AD - Clinical Genetics Service, Department of Medicine, Memorial
Sloan-Kettering Cancer Center, New York, NY 10021, USA.
PURPOSE: Risk-reducing surgery is an important option for women with
BRCA1 and BRCA2 mutations. There are reports in the literature that
insurance reimbursement for these procedures varies greatly. Because
health insurance coverage significantly affects medical decision-making,
current information regarding reimbursement practices of third-party
payers is needed. METHODS: Retrospective study of hospital billing
records of 38 women with documented BRCA1 or BRCA2 mutations who
underwent either a risk-reducing mastectomy or a risk-reducing
oophorectomy between March 1, 1997, and July 30, 2000. RESULTS: Complete
billing and reimbursement information was available for 35 women
undergoing a total of 39 risk-reducing surgeries. A total of 38 of 39
(97%) risk-reducing surgeries were covered in full, less applicable
coinsurance and deductibles. The rate of insurance reimbursement did not
vary with type of insurance, personal history of cancer, or type of
procedure. CONCLUSION: Insurance carriers reimbursed the vast majority
of BRCA mutation carriers undergoing risk-reducing surgery.
19
UI - 11905676
AU - Evans G; Eeles R
TI -
Hereditary cancer.
SO - Lancet Oncol 2000 Sep;1(1):12-3
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.
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