Evidence map›Paper›PMID 11607811›Full record

ReviewOncogene2001

Mechanisms of chromosomal translocations in B cell lymphomas.

R Küppers, R Dalla-Favera

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 258 papers.

0numbers the graph read from it
0cells of the map it votes in
258citing papers in PubMed
17.9field-weighted citation impact, top 1% 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

258 citing papers in PubMed, 653 citations in OpenAlex.

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198 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 2 countries.

R KüppersInstitute of Cancer Genetics, Columbia University, New York, NY 10032, USA. rkuppers@mac.genetik.uni-koeln.de
R Dalla-Favera
University of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reciprocal chromosomal translocations involving the immunoglobulin (Ig) loci are a hallmark of most mature B cell lymphomas and usually result in dysregulated expression of oncogenes brought under the control of the Ig enhancers. Although the precise mechanisms involved in the development of these translocations remains essentially unknown, a clear relationship has been established with the mechanisms that lead to Ig gene remodeling, including V(D)J recombination, isotype switching and somatic hypermutation. The common denominator of these three processes in the formation of Ig-associated translocations is probably represented by the fact that each of these processes intrinsically generates double-strand DNA breaks. Since isotype switching and somatic hypermutation occur in germinal center (GC) B cells, the origin of a large number of B cell lymphomas from GC B cells is likely closely related to aberrant hypermutation and isotype switching activity in these B cells.

Indexed as

Models, GeneticTranslocation, GeneticAllelesAnimalsDNA NucleotidyltransferasesHumansImmunoglobulinsLymphoma, B-CellLymphoma, Large B-Cell, DiffuseMiceMutationRecombination, GeneticVDJ RecombinasesDNA NucleotidyltransferasesImmunoglobulinsVDJ Recombinases

Identifiers

PMID11607811
OpenAlexW2011330486

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.