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Mapping of candidate region for chordoma development to 1p36.13 by LOH analysis
International journal of cancer, 2003-11, Vol.107 (3), p.493-497
Riva, Paola
Crosti, Francesca
Orzan, Francesca
Dalprà, Leda
Mortini, Pietro
Parafioriti, Antonina
Pollo, Bianca
Fuhrman Conti, Anna Maria
Miozzo, Monica
Larizza, Lidia
2003
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Riva, Paola
Crosti, Francesca
Orzan, Francesca
Dalprà, Leda
Mortini, Pietro
Parafioriti, Antonina
Pollo, Bianca
Fuhrman Conti, Anna Maria
Miozzo, Monica
Larizza, Lidia
Titel
Mapping of candidate region for chordoma development to 1p36.13 by LOH analysis
Ist Teil von
International journal of cancer, 2003-11, Vol.107 (3), p.493-497
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2003
Quelle
Free E-Journal (出版社公開部分のみ)
Beschreibungen/Notizen
Various cytogenetic and molecular findings indicate 1p36 loss as a consistent change in sporadic and inherited chordoma, a rare embryogenetic neoplasm arising from notochord remnants. We studied 27 sporadic chordomas by means of loss of heterozygosity (LOH) of 31 microsatellites localized to the 1p36.32–36.11 region, and restricted the minimal LOH interval shared by 85% of the tumours to 1p36.13. We also used RT‐PCR analysis to investigate the role of the candidate genes CASP9, EPH2A, PAX7, DAN and DVL1, which were selected on the basis of the physical mapping of the LOH region and their plausible oncosuppressor function. RT‐PCR analysis showed the presence of DAN and PAX7 transcript fragments of the expected size in all of 8 chordoma samples, whereas the CASP9‐specific fragment was observed in only 3 and EPH2A was absent in one. Smaller than expected DVL1 transcripts were found in 4 tumours as well as in their normal counterpart (nucleus pulposus), which also showed a typically sized transcript. Sequencing revealed the skipping of 3 exons in the smallest DVL1 fragment, thus leading to a frameshift and predicting a truncated DVL1 gene product. Our study of the largest cohort of chordoma patients recruited so far indicates a common molecular lesion at 1p36.13, and suggests that the CASP9, EPH2A and DVL1 genes may play an onco‐suppressing role and be involved in the development of chordoma. © 2003 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0020-7136
eISSN: 1097-0215
DOI: 10.1002/ijc.11421
Titel-ID: cdi_proquest_miscellaneous_75699607
Format
–
Schlagworte
1p36.13
,
Adult
,
Aged
,
Amino Acid Sequence
,
Base Sequence
,
Biological and medical sciences
,
candidate genes
,
chordoma
,
Chordoma - genetics
,
Chromosome Mapping
,
Chromosomes, Human, Pair 1
,
Diseases of the osteoarticular system
,
Female
,
Humans
,
LOH analysis
,
Loss of Heterozygosity
,
Male
,
Medical sciences
,
Middle Aged
,
Molecular Sequence Data
,
Reverse Transcriptase Polymerase Chain Reaction
,
RT‐PCR analysis
,
Tumors of striated muscle and skeleton
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