Valeria Latorre

Publications (3)39.66 Total impact

• Source

  Available from: Mario Capasso

  Dataset: Diskin et al Nat Gen 2012

  Sharon J Diskin, Mario Capasso, Robert W Schnepp, Kristina A Cole, Edward F Attiyeh, Cuiping Hou, Maura Diamond, Erica L Carpenter, Cynthia Winter, Hanna Lee, Jayanti Jagannathan, Valeria Latorre, Achille Iolascon, Hakon Hakonarson, Marcella Devoto, John M Maris
• Source

  Available from: Mario Capasso

  Article: Common variation at 6q16 within HACE1 and LIN28B influences susceptibility to neuroblastoma.

  Sharon J Diskin, Mario Capasso, Robert W Schnepp, Kristina A Cole, Edward F Attiyeh, Cuiping Hou, Maura Diamond, Erica L Carpenter, Cynthia Winter, Hanna Lee, Jayanti Jagannathan, Valeria Latorre, Achille Iolascon, Hakon Hakonarson, Marcella Devoto, John M Maris
  [show abstract] [hide abstract]
  ABSTRACT: Neuroblastoma is a cancer of the sympathetic nervous system that accounts for approximately 10% of all pediatric oncology deaths. Here, we report a genome-wide association study of 2,817 neuroblastoma cases and 7,473 controls. We identified two new associations at 6q16, the first within HACE1 (rs4336470; combined P = 2.7 × 10(-11); odds ratio 1.26, 95% confidence interval (CI) 1.18-1.35) and the second within LIN28B (rs17065417; combined P = 1.2 × 10(-8); odds ratio 1.38, 95% CI 1.23-1.54). Expression of LIN28B and let-7 miRNA correlated with rs17065417 genotype in neuroblastoma cell lines, and we observed significant growth inhibition upon depletion of LIN28B, specifically in neuroblastoma cells that were homozygous for the risk allele. Low HACE1 and high LIN28B expression in diagnostic primary neuroblastomas were associated with worse overall survival (P = 0.008 and 0.014, respectively). Taken together, these data show that common variants in HACE1 and LIN28B influence neuroblastoma susceptibility and indicate that both genes likely have a role in disease progression.
  Nature Genetics 09/2012; 44(10):1126-30. · 35.53 Impact Factor
• Source

  Available from: Sharon J Diskin

  Article: Replication of neuroblastoma SNP association at the BARD1 locus in African-Americans.

  Valeria Latorre, Sharon J Diskin, Maura A Diamond, Haitao Zhang, Hakon Hakonarson, John M Maris, Marcella Devoto
  [show abstract] [hide abstract]
  ABSTRACT: Neuroblastoma is an often fatal pediatric cancer more frequent in European-American than African-American children. African-American children, however, are at higher risk for the more severe form of neuroblastoma and have worse overall survival than European-American children. Genome-wide association studies (GWAS) have identified several single-nucleotide polymorphisms (SNP) associated to neuroblastoma in children of European descent. Knowledge of their association to neuroblastoma in African-American children is still lacking. We genotyped and imputed SNPs located in three gene regions reported to be associated to neuroblastoma in children of European descent, and tested them for association in 390 African-American patients with neuroblastoma compared with 2,500 healthy, ethnically matched controls. SNPs in the BARD1 gene region show a similar pattern of association to neuroblastoma in African-American and European-American children. The more restricted extent of linkage disequilibrium in the African-American population suggests a smaller candidate region for the putative causal variants than previously reported. Limited association was observed at the other two gene regions tested, including LMO1 in 11p15 and FLJ22536 in 6p22. Common BARD1 SNPs affect risk of neuroblastoma in African-Americans. The role of other SNPs associated to neuroblastoma in children of European descent could not be confirmed, possibly due to different patterns of linkage disequilibrium or limited statistical power to detect association to variants with small effect on disease risk. Extension of GWAS to populations of African descent is important to confirm their results and validity beyond the European populations and can help to refine the location of the putative causal variants.
  Cancer Epidemiology Biomarkers &amp Prevention 02/2012; 21(4):658-63. · 4.12 Impact Factor