Evidence map›Paper›PMID 17989712›Full record

ArticleLeukemia2008

Amplification at 7q22 targets cyclin-dependent kinase 6 in T-cell lymphoma.

S Nagel, E Leich, H Quentmeier, C Meyer, M Kaufmann, H G Drexler, A Zettl, A Rosenwald, R A F MacLeod

Abstract read
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In one paragraph

Article in Leukemia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. CDK4/6 and MAPK-Crosstalk as Opportunity for Cancer Treatment.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  11. Article
  12. CDK6 Inhibition: A Novel Approach in AML Management.International journal of molecular sciences · 2020
    Review
  13. CDK6 coordinatesBlood · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Elevated nuclear CDK6 is associated with an unfavorable prognosis in lung adenocarcinoma patients.International journal of clinical and experimental pathology · 2017
    Article
  19. Article
  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

9 authors at 2 institutions in 1 country.

S NagelDepartment of Human and Animal Cell Cultures, DSMZ, Braunschweig, Germany. sna@dsmz.de
E Leich
H Quentmeier
C Meyer
M Kaufmann
H G Drexler
A Zettl
A Rosenwald
R A F MacLeod
Leibniz Institute DSMZ – German Collection of Microorganisms and Cell Cultures · DEUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recurrent chromosomal aberrations in hematopoietic tumors target genes involved in pathogenesis. Their identification and functional characterization are therefore important for the establishment of rational therapies. Here, we investigated genomic amplification at 7q22 in the T-cell lymphoma cell line SU-DHL-1 belonging to the subtype of anaplastic large-cell lymphoma (ALCL). Cytogenetic analysis mapped this amplicon to 86-95 Mb. Copy-number determination quantified the amplification level at 5- to 6-fold. Expression analysis of genes located within this region identified cyclin-dependent kinase 6 (CDK6) as a potential amplification target. In comparison with control cell lines, SU-DHL-1 expressed considerably higher levels of CDK6. Functionally, SU-DHL-1 cells exhibited reduced sensitivity to rapamycin treatment, as indicated by cell growth and cell cycle analysis. Rapamycin reportedly inhibits degradation of the CDK inhibitor p27 with concomitant downregulation of cyclin D3, implying a proliferative advantage for CDK6 overexpression. Amplification of the CDK6 locus was analyzed in primary T-cell lymphoma samples and, while detected infrequently in those classified as ALCL (1%), was detected in 23% of peripheral T-cell lymphomas not otherwise specified. Taken together, analysis of the 7q22 amplicon identified CDK6 as an important cell cycle regulator in T-cell lymphomas, representing a novel potential target for rational therapy.

Indexed as

Chromosomes, Human, Pair 7Gene DosageCell Line, TumorChromosome AberrationsCyclin-Dependent Kinase 6Cytogenetic AnalysisDrug ResistanceGene Expression Regulation, NeoplasticHumansLymphoma, Large-Cell, AnaplasticLymphoma, T-CellLymphoma, T-Cell, PeripheralSirolimusTumor Cells, CulturedCyclin-Dependent Kinase 6Sirolimus

Identifiers

PMID17989712
OpenAlexW1964262847

What OpenQuestion holds

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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.