Evidence map›Paper›PMID 23257783›Full record

ArticleLeukemia2013

MCL1 is deregulated in subgroups of diffuse large B-cell lymphoma.

S-S Wenzel, M Grau, C Mavis, S Hailfinger, A Wolf, H Madle, G Deeb, B Dörken, M Thome, P Lenz and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Novel eIF4A1 inhibitors with anti-tumor activity in lymphoma.Molecular medicine (Cambridge, Mass.) · 2022
    Article
  11. The Pt(International journal of molecular sciences · 2022
    Article
  12. Review
  13. Article
  14. BH3 Mimetics in Hematologic Malignancies.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Review
  17. Targeting MCL-1 in cancer: current status and perspectives.Journal of hematology & oncology · 2021
    Review
  18. Article
  19. Review
  20. Review
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

14 authors at 5 institutions in 3 countries.

S-S WenzelDepartment of Hematology, Oncology and Tumor Immunology, Molecular Cancer Research Center, Charité-Universitätsmedizin Berlin, Germany.
M Grau
C Mavis
S Hailfinger
A Wolf
H Madle
G Deeb
B Dörken
M Thome
P Lenz
S Dirnhofer
F J Hernandez-Ilizaliturri
A Tzankov
G Lenz
Charité - Universitätsmedizin Berlin · DERoswell Park Comprehensive Cancer Center · USPhilipps University of Marburg · DEUniversity Hospital of Basel · CHUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid cell leukemia-1 (MCL1) is an anti-apoptotic member of the BCL2 family that is deregulated in various solid and hematological malignancies. However, its role in the molecular pathogenesis of diffuse large B-cell lymphoma (DLBCL) is unclear. We analyzed gene expression profiling data from 350 DLBCL patient samples and detected that activated B-cell-like (ABC) DLBCLs express MCL1 at significantly higher levels compared with germinal center B-cell-like DLBCL patient samples (P=2.7 × 10(-10)). Immunohistochemistry confirmed high MCL1 protein expression predominantly in ABC DLBCL in an independent patient cohort (n=249; P=0.001). To elucidate molecular mechanisms leading to aberrant MCL1 expression, we analyzed array comparative genomic hybridization data of 203 DLBCL samples and identified recurrent chromosomal gains/amplifications of the MCL1 locus that occurred in 26% of ABC DLBCLs. In addition, aberrant STAT3 signaling contributed to high MCL1 expression in this subtype. Knockdown of MCL1 as well as treatment with the BH3-mimetic obatoclax induced apoptotic cell death in MCL1-positive DLBCL cell lines. In summary, MCL1 is deregulated in a significant fraction of ABC DLBCLs and contributes to therapy resistance. These data suggest that specific inhibition of MCL1 might be utilized therapeutically in a subset of DLBCLs.

Indexed as

Gene Expression ProfilingAntineoplastic AgentsComparative Genomic HybridizationHumansImmunohistochemistryLymphoma, Large B-Cell, DiffuseMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2Real-Time Polymerase Chain ReactionAntineoplastic AgentsMyeloid Cell Leukemia Sequence 1 ProteinProto-Oncogene Proteins c-bcl-2

Identifiers

PMID23257783
OpenAlexW2093663447

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.