Evidence map›Paper›PMID 20812997›Full record

ArticleBritish journal of haematology2010

Comparison of familial and sporadic chronic lymphocytic leukaemia using high resolution array comparative genomic hybridization.

Sunita R Setlur, Chunhwa Ihm, Joelle Tchinda, Soheil Shams, Lillian Werner, Eun Kyung Cho, Christina Thompson, Kimberly Phillips, Laura Z Rassenti, Thomas J Kipps and 4 more

Open access · greenAbstract readComparative StudyMulticenter Study
In one paragraph

Article in British journal of haematology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Familial leukemias.Current treatment options in oncology · 2015
    Review
  3. Article
  4. Genomic approaches to chronic lymphocytic leukemia.Hematology/oncology clinics of North America · 2013
    Review
  5. Review
  6. Integrative genomic analysis implicates gain of PIK3CA at 3q26 and MYC at 8q24 in chronic lymphocytic leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Article
  7. Article
  8. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 1 country.

Sunita R SetlurDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Chunhwa Ihm
Joelle Tchinda
Soheil Shams
Lillian Werner
Eun Kyung Cho
Christina Thompson
Kimberly Phillips
Laura Z Rassenti
Thomas J Kipps
Donna Neuberg
Arnold S Freedman
Charles Lee
Jennifer R Brown
Dana-Farber Cancer Institute · USBrigham and Women's Hospital · USHarvard University · USMoores Cancer CenterBroad Institute · USSunny BioDiscovery (United States) · US

Funding

Tissue CoreP01CA081534 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KIPPS, THOMAS J · 2000 to 2016
$59.5M
The Role of BCL-6 in Berminal Center FormationP01CA092625 · NCI · DANA-FARBER CANCER INSTITUTE · PI SHIPP, MARGARET A · 2001 to 2011
$32.9M
Molecular Cytogenetic Tools for the ZebrafishR01CA111560 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI LEE, CHARLES · 2004 to 2008
$1.6M
Genetic Alterations in Families with Multiple LymphomasK23CA115682 · NCI · DANA-FARBER CANCER INSTITUTE · PI BROWN, JENNIFER R · 2005 to 2009
$754k
CpG Plus Rituximab Therapy in Follicular LymphomaR21CA103244 · NCI · DANA-FARBER CANCER INSTITUTE · PI FREEDMAN, ARNOLD S. · 2004 to 2005
$567k
NCI NIH HHS 2P01CA092625NCI NIH HHS CA-103244NCI NIH HHS CA111560NCI NIH HHS K23 CA115682NCI NIH HHS P01 CA081534NCI NIH HHS P01-CA081534NCI NIH HHS P01 CA092625NCI NIH HHS R01 CA111560NCI NIH HHS R21 CA103244
6 · The paper itself

Abstract

Approximately 10% of patients with chronic lymphocytic leukaemia (CLL) have a family history of the disease or a related lymphoproliferative disorder, yet the relationship of familial CLL to genomic abnormalities has not been characterized in detail. We therefore studied 75 CLL patients, half familial and half sporadic, using high-resolution array comparative genomic hybridization (CGH), in order to better define the relationship of genomic abnormalities to familial disease and other biological prognostic factors. Our results showed that the most common high-risk deletion in CLL, deletion 11q, was significantly associated with sporadic disease. Comparison of familial to sporadic disease additionally identified a copy number variant region near the centromere on 14q, proximal to IGH@, in which gains were associated both with familial CLL, and with mutated IGHV and homozygous deletion of 13q. Homozygous deletion of 13q was also found to be associated with mutated IGHV and low expression of ZAP-70, and a significantly longer time to first treatment compared to heterozygous deletion or lack of alteration. This study is the first high resolution effort to investigate and report somatic genetic differences between familial and sporadic CLL.

Indexed as

Chromosome AberrationsAdultAgedChromosome DeletionChromosomes, Human, Pair 11Chromosomes, Human, Pair 13Chromosomes, Human, Pair 14Comparative Genomic HybridizationFemaleGenetic Predisposition to DiseaseHumansIn Situ Hybridization, FluorescenceLeukemia, Lymphocytic, Chronic, B-CellMaleMiddle Aged

Identifiers

PMID20812997
PMCPMC3584328
OpenAlexW1503002026

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.