Evidence map›Paper›PMID 24704113›Full record

ArticleCancer genetics2014

Copy neutral loss of heterozygosity in 20q in chronic lymphocytic leukemia/small lymphocytic lymphoma.

Jianming Pei, Valentin Robu, Madelyn Feder, Mitchell Cheung, Erin Neumann-Domer, Jacqueline Talarchek, Essel Dulaimi, Michael M Millenson, Joseph R Testa

Abstract read
In one paragraph

Article in Cancer genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

2 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Del(20q) in patients with chronic lymphocytic leukemia: a therapy-related abnormality involving lymphoid or myeloid cells.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2015
    Article
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

9 authors at 1 institution in 1 country.

Jianming PeiCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, USA; Clinical Cytogenomics Laboratory, Fox Chase Cancer Center, Philadelphia, PA, USA.
Valentin RobuDepartment of Pathology, Fox Chase Cancer Center, Philadelphia, PA, USA.
Madelyn FederClinical Cytogenomics Laboratory, Fox Chase Cancer Center, Philadelphia, PA, USA.
Mitchell CheungCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, USA.
Erin Neumann-DomerClinical Cytogenomics Laboratory, Fox Chase Cancer Center, Philadelphia, PA, USA.
Jacqueline TalarchekCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, USA.
Essel DulaimiDepartment of Pathology, Fox Chase Cancer Center, Philadelphia, PA, USA.
Michael M MillensonDepartment of Medical Oncology, Fox Chase Cancer Center, Philadelphia, PA, USA.
Joseph R TestaCancer Biology Program, Fox Chase Cancer Center, Philadelphia, PA, USA; Clinical Cytogenomics Laboratory, Fox Chase Cancer Center, Philadelphia, PA, USA. Electronic address: Joseph.Testa@fccc.edu.
Fox Chase Cancer Center · US

Funding

WORD PROCESSING CENTER--COREP30CA006927 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI Margaret von Mehren · 1985 to 2026
$138.8M
NCI NIH HHS CA-06927NCI NIH HHS P30 CA006927
6 · The paper itself

Abstract

Single nucleotide polymorphism (SNP)-based chromosome microarray analysis was used to uncover copy neutral loss of heterozygosity (LOH) in the long arm of chromosome 20 in blood or bone marrow specimens from three patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL). All three patients presented with lymph node enlargement. Whereas one of the patients has had a complicated clinical course, the other two have a more indolent disease. Sequence analysis of the tumor suppressor gene ASXL1, which is located in 20q and is commonly mutated in malignant myeloid diseases and occasionally in CLL/SLL specimens, revealed no mutations in our three patients with copy neutral LOH in 20q. The possible contribution of other imprinted microRNAs and antisense genes residing in 20q to the pathogenesis of a subset of CLL/SLL patients is discussed. These findings illustrate the value of SNP arrays for the detection of novel recurrent genomic alterations that may contribute to CLL/SLL onset or progression.

Indexed as

Chromosomes, Human, Pair 20HeterozygoteHumansLeukemia, Lymphocytic, Chronic, B-CellPolymorphism, Single Nucleotidechromosome 20chromosome microarray analysisChronic lymphocytic leukemiacopy neutral loss of heterozygosityimprinting

Identifiers

PMID24704113
PMCPMC4010307
OpenAlexW2167215508

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.