Evidence map›Paper›PMID 17278262›Full record

ArticleBritish journal of haematology2007

Transformation of follicular lymphoma to diffuse large B-cell lymphoma proceeds by distinct oncogenic mechanisms.

Andrew J Davies, Andreas Rosenwald, George Wright, Abigail Lee, Kim W Last, Dennis D Weisenburger, Wing C Chan, Jan Delabie, Rita M Braziel, Elias Campo and 10 more

Abstract read
In one paragraph

Article in British journal of haematology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
–field-weighted citation impact
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

53 citing papers in PubMed.

  1. Trial
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  4. Article
  5. Review
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  9. Article
  10. Article
  11. Article
  12. Histologic transformation of follicular lymphoma: pathologists' viewpoint.Journal of clinical and experimental hematopathology : JCEH · 2023
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. TheInternational journal of molecular sciences · 2019
    Article
  18. Review
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  20. 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

20 authors.

Andrew J DaviesCancer Research UK Medical Oncology Unit, St Bartholomew's Hospital, London, UK. andrew.davies@cancer.org.uk
Andreas Rosenwald
George Wright
Abigail Lee
Kim W Last
Dennis D Weisenburger
Wing C Chan
Jan Delabie
Rita M Braziel
Elias Campo
Randy D Gascoyne
Elaine S Jaffe
Konrad Muller-Hermelink
German Ott
Maria Calaminici
Andrew J Norton
Lindsey K Goff
Jude Fitzgibbon
Louis M Staudt
T Andrew Lister

Funding

Molecular Signatures to Improve Diagnosis and Outcome PrU01CA114778 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CHAN, WING C. · 2005 to 2009
$8.7M
REGULATION OF GENE EXPRESSION IN NORMAL AND MALIGNANT HUMAN LYMPHOCYTESZ01SC004024 · SC · CLINICAL SCIENCES · PI STAUDT, LOUIS · 1996 to 2007
$4.4M
Lymphoma Disease Discovery and DefintionZ01SC000550 · SC · DIVISION OF CLINICAL SCIENCES - NCI · PI JAFFE, ELAINE · 1996 to 2008
$2.3M
Intramural NIH HHSNCI NIH HHS U01 CA114778
6 · The paper itself

Abstract

This study was undertaken to further elucidate the biological mechanisms underlying the frequent event of transformation of follicular lymphoma (FL) to diffuse large B-cell lymphoma (t-FL). The gene expression profiles of 20 paired lymph node biopsies, derived from the same patient pre- and post-transformation, were analysed using the Lymphochip cDNA microarray. TP53 mutation analysis was performed and copy number alterations at the c-REL and CDNK2A examined. Immunohistochemistry was performed on an independent panel of paired transformation paraffin-embedded samples. Transformed follicular lymphoma was predominantly of the germinal centre B-like phenotype both at the mRNA and protein level. Despite this homogeneity, transformation proceeded by at least two pathways. One mechanism was characterised by high proliferation, as assessed by the co-ordinately expressed genes of the proliferation signature. This group was associated with the presence of recurrent oncogenic abnormalities. In the remaining cases, proliferation was not increased and transformation proceeded by alternative routes as yet undetermined. Genes involved in cellular proliferation prevailed amongst those that were significantly increased upon transformation and T cell and follicular dendritic-associated genes predominated amongst those that decreased. t-FL is a germinal centre B (GCB)-like malignancy that evolves by two pathways, one that is similar in proliferation rate to the antecedent FL and the other that has a higher proliferation rate and is characterised by the presence of recognised oncogenic abnormalities.

Indexed as

Cell Transformation, NeoplasticGene Expression ProfilingOligonucleotide Array Sequence AnalysisCell ProliferationDisease ProgressionGenes, mycHumansLymphoma, FollicularLymphoma, Large B-Cell, DiffuseTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID17278262
PMCPMC2532951

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.