Are submicroscopic chromosomal inversions predisposing factors for the t(9;22)(q34;q11.2) translocation in chronic myeloid leukemia?

Juan Ramón González García, Martín Daniel Domínguez Cruz, César Borjas Gutiérrez

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Article in Molecular cytogenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

0.2field-weighted citation impact, top 43% 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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 2 citations in OpenAlex.

Masked inv dup(22)(q11.23), tetrasomy 8 and trisomy 19 in a blast crisis-chronic myeloid leukemia after interrupted Imatinib-treatment.Molecular cytogenetics · 2015
Article

4 · The record

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5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Juan Ramón González GarcíaDivisión de Genética, CIBO-Instituto Mexicano del Seguro Social, Sierra Mojada # 800, Colonia Independencia, CP 44340 Guadalajara, Jalisco México.

Martín Daniel Domínguez CruzDivisión de Genética, CIBO-Instituto Mexicano del Seguro Social, Sierra Mojada # 800, Colonia Independencia, CP 44340 Guadalajara, Jalisco México ; Doctorado en Genetica Humana, CUCS-Universidad de Guadalajara, Guadalajara, Jalisco México.

César Borjas GutiérrezDivisión de Genética, CIBO-Instituto Mexicano del Seguro Social, Sierra Mojada # 800, Colonia Independencia, CP 44340 Guadalajara, Jalisco México ; Doctorado en Genetica Humana, CUCS-Universidad de Guadalajara, Guadalajara, Jalisco México.

Mexican Social Security Institute · MXUniversidad de Guadalajara · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A complex chromosomal rearrangement observed in a patient with chronic myeloid leukemia was explained as the consequence of a multistep process. The explanation involved an initial t(9;22) translocation with breakpoints distant from the BCR and ABL1 genes followed by genomic deletions that produced the BCR-ABL1 hybrid gene. We present an alternative model that fits the origin of the patient's rearrangement better. The present model links submicroscopic inversions with the occurrence of the t(9;22) translocation and opens a new approach on the research on the disease.

Indexed as

Chronic myeloid leukemiaDupliconsNon-allelic homologous recombinationSubmicroscopic inversiont(9;22) translocation

Identifiers

PMID25741382

DOI10.1186/s13039-015-0116-9

PMCPMC4348163

OpenAlexW2104648567

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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.