Evidence map›Paper›PMID 12048236›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Chromosome translocations and covert leukemic clones are generated during normal fetal development.

Hiroshi Mori, Susan M Colman, Zhijian Xiao, Anthony M Ford, Lyn E Healy, Craig Donaldson, Jill M Hows, Cristina Navarrete, Mel Greaves

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 220 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
220citing papers in PubMed, 2 pooled it
33.1field-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

220 citing papers in PubMed, 2 syntheses or guidelines pooled it, 610 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Modulation of theInternational journal of molecular sciences · 2025
    Trial
  4. The risks of delay?Haematologica · 2026
    Article
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160 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

9 authors at 2 institutions in 1 country.

Hiroshi MoriLeukaemia Research Fund Centre for Cell and Molecular Biology, Institute of Cancer Research, Chester Beatty Laboratories, London SW3 6JB, UK.
Susan M Colman
Zhijian Xiao
Anthony M Ford
Lyn E Healy
Craig Donaldson
Jill M Hows
Cristina Navarrete
Mel Greaves
Institute of Cancer Research · GBBlood Cancer UK · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies on monozygotic twins with concordant leukemia and retrospective scrutiny of neonatal blood spots of patients with leukemia indicate that chromosomal translocations characteristic of pediatric leukemia often arise prenatally, probably as initiating events. The modest concordance rate for leukemia in identical twins ( approximately 5%), protracted latency, and transgenic modeling all suggest that additional postnatal exposure and/or genetic events are required for clinically overt leukemia development. This notion leads to the prediction that chromosome translocations, functional fusion genes, and preleukemic clones should be present in the blood of healthy newborns at a rate that is significantly greater than the cumulative risk of the corresponding leukemia. Using parallel reverse transcriptase-PCR and real-time PCR (Taqman) screening, we find that the common leukemia fusion genes, TEL-AML1 or AML1-ETO, are present in cord bloods at a frequency that is 100-fold greater than the risk of the corresponding leukemia. Single-cell analysis by cell enrichment and immunophenotype/fluorescence in situ hybridization multicolor staining confirmed the presence of translocations in restricted cell types corresponding to the B lymphoid or myeloid lineage of the leukemias that normally harbor these fusion genes. The frequency of positive cells (10(-4) to 10(-3)) indicates substantial clonal expansion of a progenitor population. These data have significant implications for the pathogenesis, natural history, and etiology of childhood leukemia.

Indexed as

Embryonic and Fetal DevelopmentTranslocation, GeneticBase SequenceCore Binding Factor Alpha 2 SubunitDNADNA PrimersETS Translocation Variant 6 ProteinFetal BloodHumansInfant, NewbornIn Situ Hybridization, FluorescenceLeukemiaMolecular Sequence DataOncogene Proteins, FusionPolymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionAML1-ETO fusion protein, humanCore Binding Factor Alpha 2 SubunitDNADNA PrimersETS Translocation Variant 6 ProteinOncogene Proteins, FusionRNA, MessengerRUNX1 Translocation Partner 1 ProteinTEL-AML1 fusion proteinTranscription Factors

Identifiers

PMID12048236
PMCPMC123052
OpenAlexW2120723555

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.