A program using loss-of-constitutional-heterozygosity data to ascertain the location of predisposing genes in cancer families.

2.50
Hdl Handle:
http://hdl.handle.net/10541/97438
Title:
A program using loss-of-constitutional-heterozygosity data to ascertain the location of predisposing genes in cancer families.
Authors:
Rohde, K; Teare, M Dawn; Scherneck, S; Santibanez-Koref, Mauro F
Abstract:
We present a modification of the MLINK program, which enables the formal incorporation of data on loss of constitutional heterozygosity (LOCH) into likelihood calculations. This is an implementation of a previously described approach to localise tumour suppressor genes involved in inherited cancer predisposition. LOCH data are treated as additional observations on disease phenotype. The main effect of including extra data is to enhance the power to detect linkage. In this way, the method facilitates the use of small families, in particular parent-offspring pairs, which would otherwise be uninformative. The technique also has an advantage in view of the increasing use of archival material, which is often derived from specimens taken for histopathological analysis, and may contain tumour tissue which can also be used to obtain additional information. We describe the use of the program, the interpretation of the results and the advantages and limitations of this approach.
Affiliation:
Department of Bioinformatics, Max Delbrück Centre for Molecular Medicine, Berlin Buch, Germany.
Citation:
A program using loss-of-constitutional-heterozygosity data to ascertain the location of predisposing genes in cancer families., 45 (6):337-45 Hum. Hered.
Journal:
Human Heredity
Issue Date:
27-Apr-2010
URI:
http://hdl.handle.net/10541/97438
DOI:
10.1159/000154302
PubMed ID:
8537081
Type:
Article
Language:
en
ISSN:
0001-5652
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorRohde, Ken
dc.contributor.authorTeare, M Dawnen
dc.contributor.authorScherneck, Sen
dc.contributor.authorSantibanez-Koref, Mauro Fen
dc.date.accessioned2010-04-27T11:11:15Z-
dc.date.available2010-04-27T11:11:15Z-
dc.date.issued2010-04-27T11:11:15Z-
dc.identifier.citationA program using loss-of-constitutional-heterozygosity data to ascertain the location of predisposing genes in cancer families., 45 (6):337-45 Hum. Hered.en
dc.identifier.issn0001-5652-
dc.identifier.pmid8537081-
dc.identifier.doi10.1159/000154302-
dc.identifier.urihttp://hdl.handle.net/10541/97438-
dc.description.abstractWe present a modification of the MLINK program, which enables the formal incorporation of data on loss of constitutional heterozygosity (LOCH) into likelihood calculations. This is an implementation of a previously described approach to localise tumour suppressor genes involved in inherited cancer predisposition. LOCH data are treated as additional observations on disease phenotype. The main effect of including extra data is to enhance the power to detect linkage. In this way, the method facilitates the use of small families, in particular parent-offspring pairs, which would otherwise be uninformative. The technique also has an advantage in view of the increasing use of archival material, which is often derived from specimens taken for histopathological analysis, and may contain tumour tissue which can also be used to obtain additional information. We describe the use of the program, the interpretation of the results and the advantages and limitations of this approach.en
dc.language.isoenen
dc.subjectCanceren
dc.subject.meshFemale-
dc.subject.meshHeterozygote-
dc.subject.meshHumans-
dc.subject.meshLinkage (Genetics)-
dc.subject.meshLod Score-
dc.subject.meshModels, Genetic-
dc.subject.meshNeoplasms-
dc.subject.meshPedigree-
dc.titleA program using loss-of-constitutional-heterozygosity data to ascertain the location of predisposing genes in cancer families.en
dc.typeArticleen
dc.contributor.departmentDepartment of Bioinformatics, Max Delbrück Centre for Molecular Medicine, Berlin Buch, Germany.en
dc.identifier.journalHuman Heredityen

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