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  • Migliorini, Gabriele (author)

Variation at 10p12.2 and 10p14 influences risk of childhood B-cell acute lymphoblastic leukemia and phenotype

  • Article/chapterEnglish2013

Publisher, publication year, extent ...

  • American Society of Hematology,2013

Numbers

  • LIBRIS-ID:oai:lup.lub.lu.se:5458d725-9ff9-4662-855e-8cf2044ee1ca
  • https://lup.lub.lu.se/record/4274202URI
  • https://doi.org/10.1182/blood-2013-03-491316DOI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:art swepub-publicationtype
  • Subject category:ref swepub-contenttype

Notes

  • Acute lymphoblastic leukemia (ALL) is the major pediatric cancer diagnosed in economically developed countries with B-cell precursor (BCP)-ALL, accounting for approximately 70% of ALL. Recent genome-wide association studies (GWAS) have provided the first unambiguous evidence for common inherited susceptibility to BCP-ALL, identifying susceptibility loci at 7p12.2, 9p21.3, 10q21.2, and 14q11.2. To identify additional BCP-ALL susceptibility loci, we conducted a GWAS and performed a meta-analysis with a published GWAS totaling 1658 cases and 4723 controls, with validation in 1449 cases and 1488 controls. Combined analysis identified novel loci mapping to 10p12.2 (rs10828317, odds ratio [OR] = 1.23; P = 2.30 x 10(-9)) and 10p14marked by rs3824662(OR = 1.31; P = 8.62 x 10(-12)). The single nucleotide polymorphism rs10828317 is responsible for the N215S polymorphism in exon 7 of PIP4K2A, and rs3824662 localizes to intron 3 of the transcription factor and putative tumor suppressor gene GATA3. The rs10828317 association was shown to be specifically associated with hyperdiploid ALL, whereas the rs3824662-associated risk was confined to nonhyperdiploid non-TEL-AML1 + ALL. The risk allele of rs3824662 was correlated with older age at diagnosis (P < .001) and significantly worse event-free survivorship (P < .0001). These findings provide further insights into the genetic and biological basis of inherited genetic susceptibility to BCP-ALL and the influence of constitutional genotype on disease development.

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Added entries (persons, corporate bodies, meetings, titles ...)

  • Fiege, Bettina (author)
  • Hosking, Fay J. (author)
  • Ma, Yussanne (author)
  • Kumar, Rajiv (author)
  • Sherborne, Amy L. (author)
  • da Silva Filho, Miguel Inacio (author)
  • Vijayakrishnan, Jayaram (author)
  • Koehler, Rolf (author)
  • Thomsen, Hauke (author)
  • Irving, Julie A. (author)
  • Allan, James M. (author)
  • Lightfoot, Tracy (author)
  • Roman, Eve (author)
  • Kinsey, Sally E. (author)
  • Sheridan, Eamonn (author)
  • Thompson, Pamela (author)
  • Hoffmann, Per (author)
  • Noethen, Markus M. (author)
  • Muehleisen, Thomas W. (author)
  • Eisele, Lewin (author)
  • Zimmermann, Martin (author)
  • Bartram, Claus R. (author)
  • Schrappe, Martin (author)
  • Greaves, Mel (author)
  • Stanulla, Martin (author)
  • Hemminki, KariLund University,Lunds universitet,Allmänmedicin och klinisk epidemiologi,Forskargrupper vid Lunds universitet,Family Medicine and Clinical Epidemiology,Lund University Research Groups(Swepub:lu)med-khk (author)
  • Houlston, Richard S. (author)
  • Allmänmedicin och klinisk epidemiologiForskargrupper vid Lunds universitet (creator_code:org_t)

Related titles

  • In:Blood: American Society of Hematology122:19, s. 3298-33071528-00200006-4971

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