Evidence map›Paper›PMID 29370077›Full record

ArticleDiseases (Basel, Switzerland)2018

p53 Gene (NY-CO-13) Levels in Patients with Chronic Myeloid Leukemia: The Role of Imatinib and Nilotinib.

Hayder M Al-Kuraishy, Ali I Al-Gareeb, Ali K Al-Buhadilly

Open access · goldAbstract read
In one paragraph

Article in Diseases (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Gene Therapy Today and Tomorrow.Diseases (Basel, Switzerland) · 2019
    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

3 authors at 1 institution in 1 country.

Hayder M Al-KuraishyDepartment Of Pharmacology, Toxicology, and Medicine, College of Medicine Al-mustansiriyah University, P.O. Box 14132 Baghdad, Iraq. Hayderm36@yahoo.com.ORCID 0000-0003-3097-2962
Ali I Al-GareebDepartment Of Pharmacology, Toxicology, and Medicine, College of Medicine Al-mustansiriyah University, P.O. Box 14132 Baghdad, Iraq. dr.alialgareeb78@yahoo.com.ORCID 0000-0001-8284-8897
Ali K Al-BuhadillyDepartment Of Pharmacology, Toxicology, and Medicine, College of Medicine Al-mustansiriyah University, P.O. Box 14132 Baghdad, Iraq. alikadm1977@yahoo.com.
Mustansiriyah University · IQ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The p53 gene is also known as tumor suppressor p53. The main functions of the p53 gene are an anticancer effect and cellular genomic stability via various pathways including activation of DNA repair, induction of apoptosis, and arresting of cell growth at the G1/S phase. Normally, the p53 gene is inactivated by mouse double minute 2 proteins (mdm2), but it is activated in chronic myeloid leukemia (CML). Tyrosine kinase inhibitors are effective chemotherapeutic agents in the management of CML. The purpose of the present study was to evaluate the differential effect of imatinib and nilotinib on p53 gene serum levels in patients with CML. A total number of 60 patients with chronic myeloid leukemia with ages ranging from 47 to 59 years were recruited from the Iraqi Hematology Center. They started with tyrosine kinase inhibitors as first-line chemotherapy. They were divided into two groups-Group A, 29 patients treated with imatinib and Group B, 31 patients treated with nilotinib-and compared with 28 healthy subjects for evaluation p53 serum levels regarding the selective effect of either imatinib or nilotinib. There were significantly (

conclusionsNilotinib is more effective than imatinib in raising p53 serum levels in patients with chronic myeloid leukemia.

Indexed as

CMLimatinibnilotinibp53

Identifiers

PMID29370077
PMCPMC5871959
OpenAlexW2789673253

What OpenQuestion holds

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LicenceCC BY
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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.