Evidence map›Paper›PMID 24967369›Full record

ReviewBioMed research international2014

Genetic abnormalities in chronic lymphocytic leukemia: where we are and where we go.

Anna Puiggros, Gonzalo Blanco, Blanca Espinet

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 148 citations in OpenAlex.

  1. Article
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  4. Review
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  8. Leukemic Stem Cells and Hematological Malignancies.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
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  12. Review
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  15. Article
  16. Prognostic Value of the miR-17~92 Cluster in Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2023
    Article
  17. Article
  18. Review
  19. Article
  20. Article

3 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 at 2 institutions in 1 country.

Anna PuiggrosLaboratori de Citogenètica Molecular, Servei de Patologia, Hospital del Mar, Passeig Marítim 25-29, 08003 Barcelona, Spain ; GRETNHE, Programa de Recerca en Càncer, Institut Hospital del Mar d'Investigacions Mèdiques, Doctor Aiguader 88, 08003 Barcelona, Spain.ORCID 0000-0001-9627-4978
Gonzalo BlancoLaboratori de Citogenètica Molecular, Servei de Patologia, Hospital del Mar, Passeig Marítim 25-29, 08003 Barcelona, Spain ; GRETNHE, Programa de Recerca en Càncer, Institut Hospital del Mar d'Investigacions Mèdiques, Doctor Aiguader 88, 08003 Barcelona, Spain ; Department of Experimental and Health Sciences, Universitat Pompeu Fabra, Doctor Aiguader 88, 08003 Barcelona, Spain.ORCID 0000-0001-6557-3764
Blanca EspinetLaboratori de Citogenètica Molecular, Servei de Patologia, Hospital del Mar, Passeig Marítim 25-29, 08003 Barcelona, Spain ; GRETNHE, Programa de Recerca en Càncer, Institut Hospital del Mar d'Investigacions Mèdiques, Doctor Aiguader 88, 08003 Barcelona, Spain.ORCID 0000-0002-4294-8145
Hospital Del Mar · ESUniversitat Pompeu Fabra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal abnormalities in chronic lymphocytic leukemia (CLL) are detected in up to 80% of patients. Among them, deletions of 11q, 13q, 17p, and trisomy 12 have a known prognostic value and play an important role in CLL pathogenesis and evolution, determining patients outcome and therapeutic strategies. Standard methods used to identify these genomic aberrations include both conventional G-banding cytogenetics (CGC) and fluorescence in situ hybridization (FISH). Although FISH analyses have been implemented as the gold standard, CGC allows the identification of chromosomal translocations and complex karyotypes, the latest associated with poor outcome. Genomic arrays have a higher resolution that allows the detection of cryptic abnormalities, although these have not been fully implemented in routine laboratories. In the last years, next generation sequencing (NGS) methods have identified a wide range of gene mutations (e.g., TP53, NOTCH1, SF3B1, and BIRC3) which have improved our knowledge about CLL development, allowing us to refine both the prognostic subgroups and better therapeutic strategies. Clonal evolution has also recently arisen as a key point in CLL, integrating cytogenetic alterations and mutations in a dynamic model that improve our understanding about its clinical course and relapse.

Indexed as

Chromosome DeletionChromosomes, Human, Pair 12High-Throughput Nucleotide SequencingHumansIn Situ Hybridization, FluorescenceLeukemia, Lymphocytic, Chronic, B-CellNeoplasm ProteinsOligonucleotide Array Sequence AnalysisTrisomyNeoplasm Proteins

Identifiers

PMID24967369
PMCPMC4054680
OpenAlexW1980088271

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.