Evidence map›Paper›PMID 30909668›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2019

Hypoxia-Inducible Factor1-Α (HIF1α) and Vascular Endothelial Growth Factor-A (VEGF-A) Expression in De Novo AML Patients

Mohammad Jabari, Mehdi Allahbakhshian Farsani, Sina Salari, Mohsen Hamidpour, Vahid Amiri, Mohammad Hossein Mohammadi

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  9. Expression Changes of SIRT1 and FOXO3a Significantly Correlate with Oxidative Stress Resistance Genes in AML Patients.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
    Article
  10. Article
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  12. Targeting hypoxia in solid and haematological malignancies.Journal of experimental & clinical cancer research : CR · 2022
    Review
  13. Article
  14. Article
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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

6 authors at 1 institution in 1 country.

Mohammad JabariHSCT Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Email: Drmohammadi@sbmu.ac.ir
Mehdi Allahbakhshian FarsaniHSCT Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Email: Drmohammadi@sbmu.ac.ir
Sina SalariLaboratory Hematology and Blood Banking Department, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Mohsen HamidpourHSCT Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Email: Drmohammadi@sbmu.ac.ir
Vahid AmiriHSCT Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Email: Drmohammadi@sbmu.ac.ir
Mohammad Hossein MohammadiHSCT Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Email: Drmohammadi@sbmu.ac.ir
Shahid Beheshti University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Bone marrow hypoxia can promote leukemia progression in human cases of acute myeloid leukemia (AML). In addition, low oxygen tension is able to regulate the expression of different genes involved in malignancy. In this study, we hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF-A) genes were assessed as principal regulators of hypoxia in do novo AML patients. Methods: Peripheral blood and bone marrow samples were collected from 57 AML patients and 17 normal control subjects with informed consent. Expression of HIF1α and VEGF-A was then evaluated using quantitative real-time PCR (Q-Real time PCR) and data were analyzed with SPSS 16. Result: HIF1α and VEGF-A showed overexpression in AML patients compared to normal controls (P <0.0001 and P<0.005, respectively). The expression level of HIF1α was significantly higher in AML-M3 cases versus AML-non M3 cases. Furthermore, there was a positive correlation between HIF1α and VEGF-A ( P <0.0001 and r = 0.497). Conclusion: Adding to the many studies on the role of hypoxia in solid tumors, our data indicate that HIF1a and VEGF-A overexpression also occurs in AML patients. We consider that this is possibly involved in leukemic cell growth and therefore could be a promising target for clinical control.

Indexed as

AdolescentAdultAgedAged, 80 and overBiomarkers, TumorCase-Control StudiesChildChild, PreschoolFemaleFollow-Up StudiesHumansHypoxia-Inducible Factor 1, alpha SubunitInfantLeukemia, Myeloid, AcuteMaleMiddle AgedBiomarkers, TumorHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor AVEGFA protein, humanAcute myeloid leukemiaHIF1αhypoxiaVEGF

Identifiers

PMID30909668
PMCPMC6825791
OpenAlexW2923084788

What OpenQuestion holds

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Registered trials

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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.