Evidence map›Paper›PMID 33247697›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2020

TP53, SPOP and PIK3CA Genes Status in Prostate Cancer.

Mazhar Salim Al Zoubi, Raed Otoum, Mohammed S Alorjani, Samir Al Bashir, Bahaa Al Trad, Manal Issam Abualrja, Sohaib M Al-Khatib, Khalid Al-Batayneh

Open access · goldAbstract read
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
    Article
  2. Article
  3. Review
  4. Novel Mutations inCurrent issues in molecular biology · 2024
    Article
  5. Article
  6. MicroRNA Dysregulation in Prostate Cancer.Pharmacogenomics and personalized medicine · 2022
    Article
  7. 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 1 institution in 1 country.

Mazhar Salim Al ZoubiDepartment of Basic Medical Sciences, Faculty of Medicine, Yarmouk University, Irbid 211-63, Jordan.ORCID 0000-0003-0248-4777
Raed OtoumDepartment of Biological Sciences, Faculty of Science, Yarmouk University, Irbid 211-63, Jordan.
Mohammed S AlorjaniDepartments of Pathology and Microbiology, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan.
Samir Al BashirDepartments of Pathology and Microbiology, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan.
Bahaa Al TradDepartment of Biological Sciences, Faculty of Science, Yarmouk University, Irbid 211-63, Jordan.
Manal Issam AbualrjaDepartment of Basic Medical Sciences, Faculty of Medicine, Yarmouk University, Irbid 211-63, Jordan.
Sohaib M Al-KhatibDepartments of Pathology and Microbiology, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan.ORCID 0000-0003-1754-6993
Khalid Al-BataynehDepartment of Biological Sciences, Faculty of Science, Yarmouk University, Irbid 211-63, Jordan.
Yarmouk University · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances in molecular biology make the identification of prostate cancer (PC) subsets a priority for more understanding of the molecular pathogenesis and treatment options. Genetic alterations in many genes such as TP53, SPOP and PIK3CA genes have been reported in PC with variable frequencies worldwide. We aimed to investigate genetic alterations in the hotspot lesions of TP53, SPOP and PIK3CA genes by direct sequencing and the expression of TP53 and PIK3CA by RT-PCR in prostate cancer, and to explore the correlation between TP53, SPOP and PIK3CA alterations and tumorigenesis of prostate cancer. Seventy-nine FFPE prostate samples from patients who underwent radical prostatectomy were obtained, subjected to genomic DNA extraction and sequenced for mutations in exons 5, 6, 7 and 8 of TP53 gene, exons 4 and 5 of SPOP gene and exons 9 and 20 of PIK3CA gene. RT-PCR was performed for the expression evaluation of the PIK3CA gene. Our results showed a high frequency of TP53 mutations (11/79, 13.9 %) in the selected population. On the other hand, SPOP and PIK3CA genes did not show any genetic alteration in the sequenced exons. PIK3CA gene overexpression was detected in 6% of the cohort by RT-PCR. TP53 mutation is the most frequent genetic alteration and likely has a major role in the pathogenesis of PC in the Jordanian population.<br />.

Indexed as

AgedAged, 80 and overBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesExonsFollow-Up StudiesGenomicsHumansMaleMiddle AgedNuclear ProteinsPrognosisProstatectomyProstatic NeoplasmsRepressor ProteinsTumor Suppressor Protein p53Biomarkers, TumorClass I Phosphatidylinositol 3-KinasesNuclear ProteinsPIK3CA protein, humanRepressor ProteinsSPOP protein, humanTP53 protein, humanTumor Suppressor Protein p53p53PIK3CAProstate CancerSPOPTp53

Identifiers

PMID33247697
PMCPMC8033120
OpenAlexW3110147008

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.