Evidence map›Paper›PMID 20703256›Full record

Trial reportLeukemia2010

Analysis of genomic breakpoints in p190 and p210 BCR-ABL indicate distinct mechanisms of formation.

J Score, M J Calasanz, O Ottman, F Pane, R F Yeh, M A Sobrinho-Simões, S Kreil, D Ward, C Hidalgo-Curtis, J V Melo and 4 more

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Leukemia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. In Ph+BCR-ABL1Leukemia · 2020
    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

14 authors.

J ScoreWessex Regional Genetics Laboratory, Salisbury and Human Genetics Division, University of Southampton School of Medicine, Southampton, UK.
M J Calasanz
O Ottman
F Pane
R F Yeh
M A Sobrinho-Simões
S Kreil
D Ward
C Hidalgo-Curtis
J V Melo
J Wiemels
B Nadel
N C P Cross
F H Grand

Funding

BACKTRACKING TRANSLOCATIONS IN CHILDHOOD LEUKEMIAR01CA089032 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WIEMELS, JOSEPH LEO · 2001 to 2006
$1.6M
NCI NIH HHS R01 CA089032
6 · The paper itself

Abstract

We sought to understand the genesis of the t(9;22) by characterizing genomic breakpoints in chronic myeloid leukemia (CML) and BCR-ABL-positive acute lymphoblastic leukemia (ALL). BCR-ABL breakpoints were identified in p190 ALL (n=25), p210 ALL (n=25) and p210 CML (n=32); reciprocal breakpoints were identified in 54 cases. No evidence for significant clustering and no association with sequence motifs was found except for a breakpoint deficit in repeat regions within BCR for p210 cases. Comparison of reciprocal breakpoints, however, showed differences in the patterns of deletion/insertions between p190 and p210. To explore the possibility that recombinase-activating gene (RAG) activity might be involved in ALL, we performed extra-chromosomal recombination assays for cases with breakpoints close to potential cryptic recombination signal sequence (cRSS) sites. Of 13 ALL cases tested, 1/10 with p190 and 1/3 with p210 precisely recapitulated the forward BCR-ABL breakpoint and 1/10 with p190 precisely recapitulated the reciprocal breakpoint. In contrast, neither of the p210 CMLs tested showed functional cRSSs. Thus, although the t(9;22) does not arise from aberrant variable (V), joining (J) and diversity (D) (V(D)J) recombination, our data suggest that in a subset of ALL cases RAG might create one of the initiating double-strand breaks.

Indexed as

Chromosome BreakpointsBase SequenceChromosomes, Human, Pair 22Chromosomes, Human, Pair 9Fusion Proteins, bcr-ablGenome, HumanHomeodomain ProteinsHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMolecular Sequence DataPrecursor Cell Lymphoblastic Leukemia-LymphomaPrognosisSequence Homology, Nucleic AcidTranslocation, GeneticFusion Proteins, bcr-ablHomeodomain ProteinsRAG-1 protein

Identifiers

PMID20703256

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.