Evidence map›Paper›PMID 22110895›Full record

ArticleMediterranean journal of hematology and infectious diseases2011

Molecular pathogenesis of secondary acute promyelocytic leukemia.

M Joannides, A N Mays, A R Mistry, S K Hasan, A Reiter, J L Wiemels, C A Felix, F Lo Coco, N Osheroff, E Solomon and 1 more

Open access · goldAbstract read
In one paragraph

Article in Mediterranean journal of hematology and infectious diseases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Therapy-related acute promyelocytic leukemia: a systematic review.Medical oncology (Northwood, London, England) · 2013
    Pooled it
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  17. Phytochemicals as Anticancer and Chemopreventive Topoisomerase II Poisons.Phytochemistry reviews : proceedings of the Phytochemical Society of Europe · 2014
    Article
  18. Topoisomerase II and leukemia.Annals of the New York Academy of Sciences · 2014
    Review
  19. DNA damage and repair in human cancer: molecular mechanisms and contribution to therapy-related leukemias.International journal of environmental research and public health · 2012
    Review
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

11 authors at 7 institutions in 4 countries.

M JoannidesDepartment of Medical & Molecular Genetics, King's College London School of Medicine, UK.
A N Mays
A R Mistry
S K Hasan
A Reiter
J L Wiemels
C A Felix
F Lo Coco
N Osheroff
E Solomon
D Grimwade
King's College London · GBFondazione Santa Lucia · ITChildren's Hospital of Philadelphia · USHeidelberg University · DEKing's College School · GBUniversity of California, San Francisco · USVanderbilt University · US

Funding

FUNCTION AND BIOLOGY OF EUKARYOTIC DNA TOPOISOMERASESR01GM033944 · NIGMS · VANDERBILT UNIVERSITY · PI OSHEROFF, NEIL · 1985 to 2015
$5.5M
NIGMS NIH HHS R01 GM033944
6 · The paper itself

Abstract

Balanced chromosomal translocations that generate chimeric oncoproteins are considered to be initiating lesions in the pathogenesis of acute myeloid leukemia. The most frequent is the t(15;17)(q22;q21), which fuses the PML and RARA genes, giving rise to acute promyelocytic leukemia (APL). An increasing proportion of APL cases are therapy-related (t-APL), which develop following exposure to radiotherapy and/or chemotherapeutic agents that target DNA topoisomerase II (topoII), particularly mitoxantrone and epirubicin. To gain insights into molecular mechanisms underlying the formation of the t(15;17) we mapped the translocation breakpoints in a series of t-APLs, which revealed significant clustering according to the nature of the drug exposure. Remarkably, in approximately half of t-APL cases arising following mitoxantrone treatment for breast cancer or multiple sclerosis, the chromosome 15 breakpoint fell within an 8-bp "hotspot" region in PML intron 6, which was confirmed to be a preferential site of topoII-mediated DNA cleavage induced by mitoxantrone. Chromosome 15 breakpoints falling outside the "hotspot", and the corresponding RARA breakpoints were also shown to be functional topoII cleavage sites. The observation that particular regions of the PML and RARA loci are susceptible to topoII-mediated DNA damage induced by epirubicin and mitoxantrone may underlie the propensity of these agents to cause APL.

Identifiers

PMID22110895
PMCPMC3219647
OpenAlexW2069657839

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.