Evidence map›Paper›PMID 35114947›Full record

ArticleBMC cancer2022

Evolution of TP53 abnormalities during CLL disease course is associated with telomere length changes.

Helena Olbertova, Karla Plevova, Sarka Pavlova, Jitka Malcikova, Jana Kotaskova, Kamila Stranska, Michaela Spunarova, Martin Trbusek, Veronika Navrkalova, Barbara Dvorackova and 7 more

Abstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
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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

17 authors.

Helena OlbertovaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Karla PlevovaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Sarka PavlovaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Jitka MalcikovaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Jana KotaskovaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Kamila StranskaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Michaela SpunarovaDepartment of Internal Medicine Hematology and Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Martin TrbusekDepartment of Internal Medicine Hematology and Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Veronika NavrkalovaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Barbara DvorackovaDepartment of Internal Medicine Hematology and Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Nikola TomCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Karol PalCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Marie JarosovaDepartment of Internal Medicine Hematology and Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Yvona BrychtovaDepartment of Internal Medicine Hematology and Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Anna PanovskaDepartment of Internal Medicine Hematology and Oncology, University Hospital Brno and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
Michael DoubekCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic.
Sarka PospisilovaCentral European Institute of Technology, Masaryk University, 625 00, Brno, Czech Republic. sarka.pospisilova@ceitec.muni.cz.ORCID http://orcid.org/0000-0001-7136-2680

Funding

Grantová Agentura České Republiky GACR 19-11299SGrantová Agentura České Republiky GACR 19-15737SMinisterstvo Školství, Mládeže a Tělovýchovy CZ.02.1.01/0.0/0.0/18_046/0015515Ministerstvo Zdravotnictví Ceské Republiky AZV NU21-08-00237Ministerstvo Zdravotnictví Ceské Republiky AZV NV19-03-00091Ministerstvo Zdravotnictví Ceské Republiky MH-CZ RVO 65269705Technologická Agentura České Republiky LM2018132Technologická Agentura České Republiky LM2018133
6 · The paper itself

Abstract

backgroundTelomeres are protective structures at chromosome ends which shorten gradually with increasing age. In chronic lymphocytic leukemia (CLL), short telomeres have been associated with unfavorable disease outcome, but the link between clonal evolution and telomere shortening remains unresolved.

methodsWe investigated relative telomere length (RTL) in a well-characterized cohort of 198 CLL patients by qPCR and focused in detail on a subgroup 26 patients who underwent clonal evolution of TP53 mutations (evolTP53). In the evolTP53 subgroup we explored factors influencing clonal evolution and corresponding changes in telomere length through measurements of telomerase expression, lymphocyte doubling time, and BCR signaling activity.

resultsAt baseline, RTL of the evolTP53 patients was scattered across the entire RTL spectrum observed in our CLL cohort. RTL changed in the follow-up samples of 16/26 (62%) evolTP53 cases, inclining to reach intermediate RTL values, i.e., longer telomeres shortened compared to baseline while shorter ones prolonged. For the first time we show that TP53 clonal shifts are linked to RTL change, including unexpected RTL prolongation. We further investigated parameters associated with RTL changes. Unstable telomeres were significantly more frequent among younger patients (P = 0.032). Shorter telomeres were associated with decreased activity of the B-cell receptor signaling components p-ERK1/2, p-ZAP-70/SYK, and p-NFκB (P = 0.04, P = 0.01, and P = 0.02, respectively).

conclusionsOur study revealed that changes of telomere length reflect evolution in leukemic subclone proportion, and are associated with specific clinico-biological features of the explored cohort.

Indexed as

Clonal EvolutionFemaleHumansLeukemia, Lymphocytic, Chronic, B-CellMaleMiddle AgedMutationProto-Oncogene Proteins c-bcrSignal TransductionTelomeraseTelomereTumor Suppressor Protein p53Proto-Oncogene Proteins c-bcrTelomeraseTP53 protein, humanTumor Suppressor Protein p53BCR signalingChronic Lymphocytic LeukemiaClonal evolutionTelomereTP53

Identifiers

PMID35114947
PMCPMC8812042

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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.