Evidence map›Paper›PMID 41677935›Full record

ArticleClinical and experimental medicine2026

Clinical and genetic insights into novel TP53 mutations in De Novo AML patients.

Afia Muhammad Akram, Sikandar Hayat, Hassan Yousaf, Noreen Sarwar, Asma Tahir, Sakina Ali, Fatima Yaqoob, Amjad Zafar, Hesham M Hassan, Mutwakel Dabiellil and 1 more

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Article in Clinical and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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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

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

11 authors.

Afia Muhammad AkramDepartment of Zoology, Division of Science and Technology, University of Education, Lahore, Pakistan. afiamakram@ue.edu.pk.
Sikandar HayatInstitute of Molecular Biology and Biotechnology, The University of Lahore, Lahore, Pakistan.
Hassan YousafDepartment of Chemistry and Biotechnology, Swinburne University of Technology, Melbourne, 3122, Australia.
Noreen SarwarDepartment of parasitology, University of veterinary and animal Sciences, Lahore, Pakistan.
Asma TahirDepartment of Zoology, Division of Science and Technology, University of Education, Lahore, Pakistan.
Sakina AliDepartment of Zoology, Division of Science and Technology, University of Education, Lahore, Pakistan.
Fatima YaqoobDepartment of Zoology, Division of Science and Technology, University of Education, Lahore, Pakistan.
Amjad ZafarDepartment of Oncology, Jinnah Hospital, Lahore, Pakistan.
Hesham M HassanDepartment of pathology, college of Medicine, King Khalid University, Abha, Saudi Arabia.
Mutwakel DabiellilUpper Nile University, PO Box 1660, Wau, Malakal Khartoum, South Sudan.
Malik Ihsan Ullah KhanInstitute of Molecular Biology and Biotechnology, The University of Lahore, Lahore, Pakistan. ihsan.ullah@imbb.uol.edu.pk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study intended to uncover any potential variations in TP53 gene particularly the exons 3–7 as this region is reported to have abundant oncogenic variations with adverse impacts on its structural stability and functional activities. The selected region of TP53 was amplified in ninety de novo AML patients and amplicons were Sanger sequenced to analyze possible nucleotide variations. Ten (10) mutations were found in the coding region of the TP53 exons 3–7 which are unique to the regional mutation data in AML patients. Further evaluation of identified variants by employing multiple bioinformatics techniques revealed likely hazardous impacts of majority of them due to their existence in the core DNA binding domain. Clinical features with the exception of platelet count did not differ significantly among the AML patients within TP53 wild type and TP53 mutant groups. Concurrently, no statistically considerable difference was observed in event free survival (EFS) (p = 0.67, HR = 1.222) or overall survival (OS) (p = 0.74, HR = 0.837) comparing two groups.

Indexed as

Leukemia, Myeloid, AcuteMutationTumor Suppressor Protein p53AdolescentAdultAgedAged, 80 and overComputational BiologyExonsFemaleHumansMaleMiddle AgedSequence Analysis, DNASurvival AnalysisYoung AdultTP53 protein, humanTumor Suppressor Protein p53Acute myeloid leukemiaCell cycleGenetic variationsIn Silico analysisTP53

Identifiers

PMID41677935
PMCPMC12909321

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