Evidence map›Paper›PMID 30975981›Full record

ArticleCell death & disease2019

IBTK contributes to B-cell lymphomagenesis in Eμ-myc transgenic mice conferring resistance to apoptosis.

Eleonora Vecchio, Gaetanina Golino, Antonio Pisano, Francesco Albano, Cristina Falcone, Simona Ceglia, Enrico Iaccino, Selena Mimmi, Giuseppe Fiume, Giorgio Giurato and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. IBtkα Activates the β-Catenin-Dependent Transcription ofInternational journal of molecular sciences · 2022
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. 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

13 authors at 2 institutions in 1 country.

Eleonora VecchioDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy. eleonoravecchio@unicz.it.
Gaetanina GolinoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Antonio PisanoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Francesco AlbanoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Cristina FalconeDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Simona CegliaDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Enrico IaccinoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Selena MimmiDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Giuseppe FiumeDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Giorgio GiuratoLaboratory of Molecular Medicine and Genomics, Department of Medicine, Surgery and Dentistry "Scuola Medica Salernitana", University of Salerno, Baronissi, SA, Italy.
Domenico BrittiDepartment of Health Science, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Giuseppe ScalaDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy.
Ileana QuintoDepartment of Experimental and Clinical Medicine, University Magna Græcia of Catanzaro, Catanzaro, 88100, Italy. quinto@unicz.it.
Magna Graecia University · ITUniversity of Salerno · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence supports the involvement of IBTK in cell survival and tumor growth. Previously, we have shown that IBTK RNA interference affects the wide genome expression and RNA splicing in cell-type specific manner. Further, the expression of IBTK gene progressively increases from indolent to aggressive stage of chronic lymphocytic leukemia and decreases in disease remission after therapy. However, the role of IBTK in tumorigenesis has not been elucidated. Here, we report that loss of the murine Ibtk gene raises survival and delays tumor onset in Eμ-myc transgenic mice, a preclinical model of Myc-driven lymphoma. In particular, we found that the number of pre-cancerous B cells of bone marrow and spleen is reduced in Ibtk

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisB-LymphocytesBone Marrow CellsCell Cycle CheckpointsCell ProliferationCell SurvivalHEK293 CellsHeLa CellsHumansLymphoma, B-CellMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicAdaptor Proteins, Signal TransducingIBtk protein, humanIBtk protein, mouseProto-Oncogene Proteins c-bcl-2Proto-Oncogene Proteins c-mycTumor Suppressor Protein p53

Identifiers

PMID30975981
PMCPMC6459904
OpenAlexW2939496493

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.