Evidence map›Paper›PMID 22562027›Full record

ArticleIranian biomedical journal2012

Cytogenetic and FMS-like tyrosine kinase 3 mutation analyses in acute promyelocytic leukemia patients.

Marjan Yaghmaie, Kamran Alimoghaddam, Hossein Mozdarani, Ardeshir Ghavamzadeh, Marjan Hajhashemi, Mozaffar Aznab, Seyed H Ghaffari

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Iranian biomedical journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact, top 88% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Marjan YaghmaieDept. of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modarres University, P. O. Box 14115-111, Tehran.
Kamran AlimoghaddamHaematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Hossein MozdaraniDept. of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modarres University, P. O. Box 14115-111, Tehran.
Ardeshir GhavamzadehHaematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Marjan HajhashemiHaematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Mozaffar AznabHematology, Oncology Ward of Imam Reza Hospital, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Seyed H GhaffariHaematology, Oncology and Stem Cell Transplantation Research Center, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Shariati Hospital · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe secondary genetic changes other than the promyelocytic leukemia-retinoic acid receptor (PML-RARA) fusion gene may contribute to the acute promyelocytic leukemogenesis. Chromosomal alterations and mutation of FLT3 (FMS-like tyrosine kinase 3) tyrosine kinase receptor are the frequent genetic alterations in acute myeloid leukemia. However, the prognostic significance of FLT3 mutations in acute promyelocytic leukemia (APL) is not firmly established.

methodsIn this study, the chromosomal abnormalities were analyzed by bone marrow cytogenetic in 45 APL patients and FLT3 internal tandem duplications (ITD) screening by fragment length analysis and FLT3 D835 mutation by melting curve analysis were screened in 23 APL samples.

resultsCytogenetic study showed 14.3% trisomy 8 and 17.1% chromosomal abnormalities other than t(15;17). About 13% of the patients had FLT3 ITD, and 26% had D835 point mutation. FLT3 ITD mutation was associated with higher white blood cell count at presentation and poor prognosis.

conclusionThe PML-RARA translocation alone may not be sufficient to induce leukemia. Therefore, we assume that FLT3 mutations and the other genetic and chromosomal alterations may cooperate with PML-RARA in the development of APL disease.

Indexed as

AdolescentAdultBiomarkers, TumorChromosome AberrationsChromosome DuplicationDNA Mutational AnalysisFemalefms-Like Tyrosine Kinase 3HumansLeukemia, Promyelocytic, AcuteLeukocyte CountMaleMiddle AgedMutationOncogene Proteins, FusionPrognosisBiomarkers, Tumorfms-Like Tyrosine Kinase 3Oncogene Proteins, Fusionpromyelocytic leukemia-retinoic acid receptor alpha fusion oncoproteinAcute promyelocytic leukemiaChromosome aberrationsFMS-like tyrosine kinase 3

Identifiers

PMID22562027
PMCPMC3614257
OpenAlexW2107360358

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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.