Evidence map›Paper›PMID 39350061›Full record

ArticleBMC cancer2024

Determination of the frequency and distribution of APC, PIK3CA, and SMAD4 gene mutations in Ugandan patients with colorectal cancer.

Richard Wismayer, Rosie Matthews, Celina Whalley, Julius Kiwanuka, Fredrick Elishama Kakembo, Steve Thorn, Henry Wabinga, Michael Odida, Ian Tomlinson

Abstract read
In one paragraph

Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

2 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
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

9 authors.

Richard WismayerDepartment of Surgery, Masaka Regional Referral Hospital, Masaka, Uganda. richardwismayer@rcsi.ie.
Rosie MatthewsInstitute of Genetics and Cancer, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, UK.
Celina WhalleyInstitute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
Julius KiwanukaDepartment of Epidemiology and Biostatistics, College of Health Sciences, Makerere University, Kampala, Uganda.
Fredrick Elishama KakemboDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Steve ThornInstitute of Genetics and Cancer, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, UK.
Henry WabingaDepartment of Pathology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Michael OdidaDepartment of Pathology, School of Biomedical Sciences, College of Health Sciences, Makerere University, Kampala, Uganda.
Ian TomlinsonInstitute of Genetics and Cancer, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uganda is a developing low-income country with a low incidence of colorectal cancer, which is steadily increasing. Ugandan colorectal cancer (CRC) patients are young and present with advanced-stage disease. In our population, there is a scarcity of genetic oncological studies, therefore, we investigated the mutational status of CRC tissues, focusing in particular on the adenomatous polyposis coli (APC), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), and SMAD4 genes. Our objective was to determine whether there were any differences between other populations and Ugandan patients. We performed next-generation sequencing on the extracted DNA from formalin-fixed paraffin-embedded adenocarcinoma samples from 127 patients (mean (SD) age: 54.9 (16.0) years; male:female sex ratio: 1.2:1). Most tumours were located in the rectum 56 (44.1%), 14 (11%) tumours were high grade, and 96 (75.6%) were moderate grade CRC. Stage III + IV CRC tumours were found in 109 (85.8%) patients. We identified 48 variants of APC, including 9 novel APC mutations that were all pathogenic or deleterious. For PIK3CA, we found 19 variants, of which 9 were deleterious or pathogenic. Four PIK3CA novel pathogenic or deleterious variants were included (c.1397C > G, c.2399_2400insA, c.2621G > C, c.2632C > G). Three SMAD4 variants were reported, including two pathogenic or deleterious variants (c.1268G > T, c.556dupC) and one tolerant (c.563A > C) variant. One novel SMAD4 deleterious mutation (c.1268G > T) was reported. In conclusion, we provide clinicopathological information and new genetic variation data pertinent to CRC in Uganda.

Indexed as

Adenomatous Polyposis Coli ProteinClass I Phosphatidylinositol 3-KinasesColorectal NeoplasmsMutationSmad4 ProteinAdultAgedFemaleHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedUgandaAdenomatous Polyposis Coli ProteinAPC protein, humanClass I Phosphatidylinositol 3-KinasesPIK3CA protein, humanSmad4 ProteinSMAD4 protein, humanAfricaAPCColorectal cancerGeneticsMutationPIK3CASMAD4UgandaVariants

Identifiers

PMID39350061
PMCPMC11440721

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.