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Mauro, Francesca R

0000-0003-2425-9474

Mayo Clinic

Hematology, Department of Cellular Biotechnologies and Hematology, 'Sapienza' University, Rome, Italy.

Citations 4

Immunoglobulin heavy chain variable region gene and prediction of time to first treatment in patients with chronic lymphocytic leukemia: Mutational load or mutational status? Analysis of 1003 cases

American Journal of Hematology | July 9, 2018 | Volume: 93 | Issue: 9 | Pages: No page available

10.1002/ajh.25206 | PMID 29984867

Comparison between the CLL‐IPI and the Barcelona‐Brno prognostic model: Analysis of 1299 newly diagnosed cases

American Journal of Hematology | November 3, 2017 | Volume: 93 | Issue: 2 | Pages: No page available

10.1002/ajh.24960 | PMID 29098721

Validation of the CLL-IPI and comparison with the MDACC prognostic index in newly diagnosed patients

Blood | August 22, 2016 | Volume: 128 | Issue: 16 | Pages: 2093-2095

10.1182/blood-2016-07-728261 | PMID 27549308

A high-density SNP genome-wide linkage search of 206 families identifies susceptibility loci for chronic lymphocytic leukemia

Blood | August 8, 2007 | Volume: 110 | Issue: 9 | Pages: 3326-3333

10.1182/blood-2007-05-091561 | PMID 17687107

Abstract Chronic lymphocytic leukemia (CLL) and other B-cell lymphoproliferative disorders display familial aggregation. To identify a susceptibility gene for CLL, we assembled families from the major European (ICLLC) and American (GEC) consortia to conduct a genome-wide linkage analysis of 101 new CLL pedigrees using a high-density single nucleotide polymorphism (SNP) array and combined the results with data from our previously reported analysis of 105 families. Here, we report on the combined analysis of the 206 families. Multipoint linkage analyses were undertaken using both nonparametric (model-free) and parametric (model-based) methods. After the removal of high linkage disequilibrium SNPs, we obtained a maximum nonparametric linkage (NPL) score of 3.02 (P = .001) on chromosome 2q21.2. The same genomic position also yielded the highest multipoint heterogeneity LOD (HLOD) score under a common recessive model of disease susceptibility (HLOD = 3.11; P = 7.7 × 10−5), which was significant at the genome-wide level. In addition, 2 other chromosomal positions, 6p22.1 (corresponding to the major histocompatibility locus) and 18q21.1, displayed HLOD scores higher than 2.1 (P < .002). None of the regions coincided with areas of common chromosomal abnormalities frequently observed in CLL. These findings provide direct evidence for Mendelian predisposition to CLL and evidence for the location of disease loci.