Evidence map›Paper›PMID 34092056›Full record

ArticleHaematologica2022

The complex karyotype landscape in chronic lymphocytic leukemia allows the refinement of the risk of Richter syndrome transformation.

Andrea Visentin, Laura Bonaldi, Gian Matteo Rigolin, Francesca Romana Mauro, Annalisa Martines, Federica Frezzato, Stefano Pravato, Leila Romano Gargarella, Maria Antonella Bardi, Maurizio Cavallari and 10 more

Open access · goldAbstract readMulticenter Study
In one paragraph

Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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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

20 authors at 7 institutions in 2 countries.

Andrea VisentinHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua.
Laura BonaldiImmunology and Molecular Oncology Unit, Veneto Institute of Oncology IOV-IRCSS, Padua.
Gian Matteo RigolinHematology section, Department of Medical Sciences, Azienda Ospedaliera- Universitaria, Arcispedale S. Anna, University of Ferrara.
Francesca Romana MauroHematology division, Department of Precision and Translational Medicine, "Sapienza" University, Rome.
Annalisa MartinesImmunology and Molecular Oncology Unit, Veneto Institute of Oncology IOV-IRCSS, Padua.
Federica FrezzatoHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua.
Stefano PravatoHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua.
Leila Romano GargarellaHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua.
Maria Antonella BardiHematology section, Department of Medical Sciences, Azienda Ospedaliera- Universitaria, Arcispedale S. Anna, University of Ferrara.
Maurizio CavallariHematology section, Department of Medical Sciences, Azienda Ospedaliera- Universitaria, Arcispedale S. Anna, University of Ferrara.
Eleonora VoltaHematology section, Department of Medical Sciences, Azienda Ospedaliera- Universitaria, Arcispedale S. Anna, University of Ferrara.
Francesco CavazziniHematology section, Department of Medical Sciences, Azienda Ospedaliera- Universitaria, Arcispedale S. Anna, University of Ferrara.
Mauro NanniHematology division, Department of Precision and Translational Medicine, "Sapienza" University, Rome.
Monica FaccoHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua.
Francesco PiazzaHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua.
Anna GuariniHematology division, Department of Precision and Translational Medicine, "Sapienza" University, Rome.
Robin FoàHematology division, Department of Precision and Translational Medicine, "Sapienza" University, Rome.
Gianpietro SemenzatoHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua.
Antonio CuneoHematology section, Department of Medical Sciences, Azienda Ospedaliera- Universitaria, Arcispedale S. Anna, University of Ferrara.
Livio TrentinHematology and Clinical Immunology Unit, Department of Medicine, University of Padua, Padua, Italy; Veneto Institute of Molecular Medicine, Padua. livio.trentin@unipd.it.
Veneto Institute of Molecular Medicine · ITArcispedale Sant'Anna · ITSapienza University of Rome · ITUniversity of Ferrara · ITUniversity of Padua · ITIstituto Oncologico Veneto · ITMolecular Oncology (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complex karyotype (CK) at chronic lymphocytic leukemia (CLL) diagnosis is a negative biomarker of adverse outcome. Since the impact of CK and its subtypes, namely type-2 CK (CK with major structural abnormalities) or high-CK (CK with ≥5 chromosome abnormalities), on the risk of developing Richter syndrome (RS) is unknown, we carried out a multicenter real-life retrospective study to test its prognostic impact. Among 540 CLL patients, 107 harbored a CK at CLL diagnosis, 78 were classified as CK2 and 52 as high-CK. Twenty-eight patients developed RS during a median follow-up of 6.7 years. At the time of CLL diagnosis, CK2 and high-CK were more common and predicted the highest risk of RS transformation, together with advanced Binet stage, unmutated (U)-IGHV, 11q-, and TP53 abnormalities. We integrated these variables into a hierarchical model: high-CK and/or CK2 patients showed a 10-year time to RS (TTRS) of 31%; U-IGHV/11q- /TP53 abnormalities/Binet stage B-C patients had a 10-year TTRS of 12%; mutated (M)-IGHV without CK and TP53 disruption a 10-year TTRS of 3% (P<0.0001). We herein demonstrate that CK landscape at CLL diagnosis allows the risk of RS transformation to be refined and we recapitulated clinico-biological variables into a prognostic model.

Indexed as

Leukemia, Lymphocytic, Chronic, B-CellLymphoma, Large B-Cell, DiffuseHumansKaryotypeMutationRetrospective Studies

Identifiers

PMID34092056
PMCPMC8968897
OpenAlexW3170307255

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.