Evidence map›Paper›PMID 24832791›Full record

ArticleGenes, chromosomes & cancer2014

Amplification of 2p as a genomic marker for transformation in lymphoma.

Anna Kwiecinska, Koichi Ichimura, Mattias Berglund, Andrii Dinets, Luqman Sulaiman, V Peter Collins, Catharina Larsson, Anna Porwit, Svetlana Bajalica Lagercrantz

Open access · bronzeAbstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2014. 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
2.7field-weighted citation impact, top 10% 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, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. ConcurrentCancers · 2020
    Article
  10. Review
  11. Article
  12. Article
  13. Expression of exportin-1 in diffuse large B-cell lymphoma: immunohistochemistry and TCGA analyses.International journal of clinical and experimental pathology · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

9 authors at 5 institutions in 3 countries.

Anna KwiecinskaDepartment of Oncology-Pathology, Karolinska Institutet, CCK Karolinska University Hospital, Solna, Sweden.
Koichi Ichimura
Mattias Berglund
Andrii Dinets
Luqman Sulaiman
V Peter Collins
Catharina Larsson
Anna Porwit
Svetlana Bajalica Lagercrantz
Karolinska Institutet · SEAddenbrooke's Hospital · GBKarolinska University Hospital · SEUniversity of Toronto · CAUppsala University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To outline further genetic mechanisms of transformation from follicular lymphoma (FL) to diffuse large B-cell lymphoma (DLBCL), we have performed whole genome array-CGH in 81 tumors from 60 patients [29 de novo DLBCL (dnDLBCL), 31 transformed DLBCL (tDLBCL), and 21 antecedent FL]. In 15 patients, paired tumor samples (primary FL and a subsequent tDLBCL) were available, among which three possessed more than two subsequent tumors, allowing us to follow specific genetic alterations acquired before, during, and after the transformation. Gain of 2p15-16.1 encompassing, among others, the REL, BCL11A, USP34, COMMD1, and OTX1 genes was found to be more common in the tDLBCL compared with dnDLBCL (P < 0.001). Furthermore, a high-level amplification of 2p15-16.1 was also detected in the FL stage prior to transformation, indicating its importance during the transformation event. Quantitative real-time PCR showed a higher level of amplification of REL, USP34, and COMMD1 (all involved in the NFκΒ-pathway) compared with BCL11A, which indicates that the altered genes disrupting the NFκΒ pathway may be the driver genes of transformation rather than the previously suggested BCL11A. Moreover, a 17q21.33 amplification was exclusively found in tDLBCL, never in FL (P < 0.04) or dnDLBCL, indicating an upregulation of genes of importance during the later phase of transformation. Taken together, our study demonstrates potential genomic markers for disease progression to clinically more aggressive forms. We also confirm the importance of the TP53-, CDKN2A-, and NFκΒ-pathways for the transformation from FL to DLBCL.

Indexed as

Chromosome AberrationsAdolescentAdultAgedAged, 80 and overChild, PreschoolChromosomes, Human, Pair 17Chromosomes, Human, Pair 2Disease ProgressionFemaleGenetic MarkersHumansLymphoma, FollicularLymphoma, Large B-Cell, DiffuseMaleMiddle AgedGenetic MarkersNF-kappa B

Identifiers

PMID24832791
PMCPMC4369132
OpenAlexW2141843344

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.