Evidence map›Paper›PMID 23023714›Full record

ReviewThe Journal of clinical investigation2012

Molecular pathogenesis of chronic lymphocytic leukemia.

Gianluca Gaidano, Robin Foà, Riccardo Dalla-Favera

Abstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
–field-weighted citation impact
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

77 citing papers in PubMed.

  1. Article
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  3. ComplexInternational journal of molecular sciences · 2026
    Review
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17 more citing papers are in PubMed but not listed here.

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

3 authors.

Gianluca GaidanoDivision of Hematology, Department of Translational Medicine, Amedeo Avogadro University of Eastern Piedmont, Novara, Italy.
Robin Foà
Riccardo Dalla-Favera

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) is the most common leukemia in adults. Here, we highlight important genetic alterations that contribute to tumorigenesis, clinical progression, and chemorefractoriness of CLL. All CLLs share a common gene expression profile that suggests derivation from antigen-experienced B cells, a model supported by frequent B cell receptor repertoire skewing and stereotypy. Many CLL patients carry mutated immuno-globulin heavy-chain variable genes, while approximately 35% harbor unmutated IgV genes, which are associated with an inferior outcome. Deletion of chromosome 13q14, which is the most common genetic mutation at diagnosis, is considered an initiating lesion that frequently results in disruption of the tumor suppressor locus DLEU2/MIR15A/MIR16A. Next-generation sequencing has revealed additional recurrent genetic lesions that are implicated in CLL pathogenesis. These advancements in the molecular genetics of CLL have important implications for stratifying treatment based on molecular prognosticators and for targeted therapy.

Indexed as

AnimalsAntigensB-LymphocytesCell LineageCell Transformation, NeoplasticChromosome AberrationsDisease ProgressionGene Expression ProfilingGenes, ImmunoglobulinGenes, Tumor SuppressorHumansImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionLeukemia, ExperimentalLeukemia, Lymphocytic, Chronic, B-CellMiceAntigensDLEU2 lncRNA, humanImmunoglobulin Heavy ChainsImmunoglobulin Variable RegionNeoplasm ProteinsRNA, Long NoncodingTransferasesTumor Suppressor Proteins

Identifiers

PMID23023714
PMCPMC3461921

What OpenQuestion holds

Textmetadata
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.