Evidence map›Paper›PMID 16734728›Full record

ArticleCancer science2006

Characterization of target genes at the 2p15-16 amplicon in diffuse large B-cell lymphoma.

Noriko Fukuhara, Hiroyuki Tagawa, Yoshihiro Kameoka, Yumiko Kasugai, Sivasundaram Karnan, Junichi Kameoka, Takeshi Sasaki, Yasuo Morishima, Shigeo Nakamura, Masao Seto

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. SP1 and NFY Regulate the Expression ofInternational journal of molecular sciences · 2022
    Article
  5. Article
  6. Review
  7. Genetic lesions in diffuse large B-cell lymphomas.Annals of oncology : official journal of the European Society for Medical Oncology · 2015
    Review
  8. Article
  9. SWI/SNF chromatin remodeling complexes and cancer.American journal of medical genetics. Part C, Seminars in medical genetics · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. The role of the NFkappaB signalling pathway in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2008
    Review
  14. Review
  15. 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

10 authors at 3 institutions in 1 country.

Noriko FukuharaDivision of Molecular Medicine, Aichi Cancer Center Research Institute, Nagoya 464-8681, Japan.
Hiroyuki Tagawa
Yoshihiro Kameoka
Yumiko Kasugai
Sivasundaram Karnan
Junichi Kameoka
Takeshi Sasaki
Yasuo Morishima
Shigeo Nakamura
Masao Seto
Aichi Cancer Center · JPTohoku University · JPNagoya University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amplification of 2p has been observed as a recurrent alteration in diffuse large B-cell lymphoma (DLBCL). Whereas two candidate oncogenes, REL and BCL11A, have been investigated as targets for 2p amplification, the question remains as to whether the true target gene in the amplicon is REL, BCL11A or both. We previously identified frequent genomic gains of chromosomal 2p in 25 out of 99 DLBCL cases by means of genome-wide array comparative genomic hybridization (CGH). All of these 25 cases included recurrent copy number gain at 2p15-16. In the study presented here, cases were analyzed in greater detail by means of contig bacterial artificial chromosome (BAC) array CGH for the 4.5-Mb region at 2p15-16, which contained 33 BAC clones. We confined the minimal common region to 500-kb in length, where only the candidate oncogene REL, and not BCL11A, is located. Real-time quantitative PCR was carried out to investigate the correlation between genomic gain and expression. It showed a significant correlation for both genes, indicating that these two genes are common targets for the 2p15-16 amplicon. However, given the fact that REL is more frequently amplified than BCL11A, the REL gene may play a more important role than BCL11A in the pathogenesis of DLBCL.

Indexed as

Gene AmplificationChromosomes, Artificial, BacterialChromosomes, Human, Pair 2HumansLymphoma, B-CellLymphoma, Large B-Cell, DiffuseNucleic Acid HybridizationReverse Transcriptase Polymerase Chain Reaction

Identifiers

PMID16734728
PMCPMC11159140
OpenAlexW2090653520

What OpenQuestion holds

Textmetadata
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.