Evidence map›Paper›PMID 26526573›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

Deregulation of miR-1, miR486, and let-7a in cytogenetically normal acute myeloid leukemia: association with NPM1 and FLT3 mutation and clinical characteristics.

Samaneh Sadat Seyyedi, Masoud Soleimani, Marjan Yaghmaie, Monireh Ajami, Mansoureh Ajami, Shahram Pourbeyranvand, Kamran Alimoghaddam, Seyed Mohammad Akrami

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

8 authors at 2 institutions in 1 country.

Samaneh Sadat SeyyediDepartment of Medical Genetics, Tehran University of Medical Sciences, International Campus (TUMS-IC), Tehran, Iran.
Masoud SoleimaniDepartment of Hematology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Marjan YaghmaieHematology-Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Monireh AjamiDepartment of Hematology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Mansoureh AjamiDepartment of Hematology, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Shahram PourbeyranvandDepartment of Anatomy, School of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
Kamran AlimoghaddamHematology-Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Seyed Mohammad AkramiDepartment of Medical Genetics, Tehran University of Medical Sciences, Tehran, Iran. akramism@tums.ac.ir.
Tarbiat Modares University · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytogenetically normal acute myeloid leukemia (CN-AML) constitutes the largest subgroup of AML patients that is associated with molecular alteration. MiRNAs have been shown to be aberrantly expressed in CN-AML. In addition, specific miRNA (miR) expression patterns were found to be associated with certain genetic alterations in these patients. This study investigated the expression level of miR-1, miR-486, and let-7a in 45 CN-AML patients well characterized for FLT3 and/or NPM1 mutations using real-time quantitative RT-PCR and evaluated the association between candidate miRs expression and clinical features. Our data revealed that miR-1 was significantly overexpressed in CN-AML patients, and increasing expression of miR-1 correlated with NPM1 mutation (P < 0.05) and lower hemoglobin level was also observed in patients with miR-1 overexpression (P < 0.05). The expression of miR-1 was much higher in AML-M2 compared with other subtypes. Further, we found significantly increasing miR-486 expression in 40 of 45 (89 %) CN-AML patients. There was no significant association of upregulation of miR-486 with clinical parameters. The expression level of miR-486 was increased in AML-M2 subtype. The levels of let-7a were significantly increased in CN-AML patients compared to the healthy control and significantly higher in the NPM1 ± CN-AML patients. There was no correlation detected between the level of let-7a and FLT3+. An increasing expression level of let-7a was demonstrated in M2 subtype. In addition, our data showed no significant association between increasing let-7a and clinical characteristic. Comparison of peripheral blood and bone marrow results in 30 CN-AML patients showed that there is a considerable concordance between PB and BM in the results of candidate miR levels (P < 0.001). In conclusion, further studies should also be performed to detect functional mechanism of these miRs.

Indexed as

AdultAgedBone MarrowFemalefms-Like Tyrosine Kinase 3Gene Expression Regulation, LeukemicHumansLeukemia, Myeloid, AcuteMaleMicroRNAsMiddle AgedMutationNuclear ProteinsNucleophosminPrognosisFLT3 protein, humanfms-Like Tyrosine Kinase 3MicroRNAsMIRN1 microRNA, humanMIRN486 microRNA, humanmirnlet7 microRNA, humanNPM1 protein, humanNuclear ProteinsNucleophosminCytogenetically normal AMLlet-7amiR-1miR-486

Identifiers

PMID26526573
OpenAlexW1916500361

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.