The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda

Abstract Introduction In Uganda, colorectal cancer (CRC) is steadily increasing according to the Kampala Cancer Registry. In the West, microsatellite instability is detected in 90% of hereditary nonpolyposis colon cancers (HNPCC) which account for 1–2% of all CRC, and 15% of sporadic CRC. Germline m...

Full description

Saved in:
Bibliographic Details
Main Authors: Richard Wismayer, Rosie Matthews, Celina Whalley, Julius Kiwanuka, Fredrick Elishama Kakembo, Steve Thorn, Henry Wabinga, Michael Odida, Ian Tomlinson
Format: Article
Language:English
Published: BMC 2025-04-01
Series:BMC Cancer
Subjects:
Online Access:https://doi.org/10.1186/s12885-025-14195-9
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850042063523938304
author Richard Wismayer
Rosie Matthews
Celina Whalley
Julius Kiwanuka
Fredrick Elishama Kakembo
Steve Thorn
Henry Wabinga
Michael Odida
Ian Tomlinson
author_facet Richard Wismayer
Rosie Matthews
Celina Whalley
Julius Kiwanuka
Fredrick Elishama Kakembo
Steve Thorn
Henry Wabinga
Michael Odida
Ian Tomlinson
author_sort Richard Wismayer
collection DOAJ
description Abstract Introduction In Uganda, colorectal cancer (CRC) is steadily increasing according to the Kampala Cancer Registry. In the West, microsatellite instability is detected in 90% of hereditary nonpolyposis colon cancers (HNPCC) which account for 1–2% of all CRC, and 15% of sporadic CRC. Germline mutations in MLH1 and MSH2 account for 90% of HNPCC in the West, whilst the remainder of cases are due to mutations in MSH6 and PMS2. The aim of this study was to determine the microsatellite instability (MSI) status and determine the proportions of MLH1, MSH2, and MSH6 pathological mutations in Ugandan CRC patients. Methodology This was a cross-sectional study carried out between 1st January 2008 to 15th September 2021. Patients were recruited prospectively from 16th September 2019 to 16th September 2021, from Masaka Regional Referral Hospital, Mulago National Referral Hospital, Uganda Martyrs’ Hospital Lubaga and Mengo Hospital. From 1st January 2008 to 15th September 2019, CRC FFPE tissue blocks were obtained from the archives of the Department of Pathology, Makerere University. Data was abstracted from the medical case files for demographics, topography and stage. The histopathological subtype and grade of CRC were obtained by two consultant pathologists from the H&E slides. DNA was extracted from CRC formalin-fixed paraffin-embedded (FFPE) tissue blocks. Library preparation was completed using the Qiagen custom design panel. The custom panel represented 56 genes. The MLH-1, MSH2, MSH6, BRAF and KRAS genes were sequenced using the above library preparation and NGS sequencing. The MSI status was obtained if one of the MSI genes, MLH1, MSH2 or MSH6 was pathologically mutated. If none of the genes was pathologically mutated it was considered MSI negative, microsatellite stable (MSS). Immunohistochemistry was carried out to determine whether MLH1 and PMS2 was MMR proficient or deficient. Categorical data was summarized using frequencies and proportions corresponding to each of the three histopathological subtypes and MSI status subtypes. Continuous and categorical variables were analyzed using the chi-square and Fischer’s exact tests. A p -value ≤ 0.05 was considered statistically significant for all the analyses. Results Out of 127 CRC patients, the mean(SD) age of MSI cases was 55.6(16.9) years and of MSS cases was 55.4(15.5) years. The majority were MSS, 75(59.06%) followed by MSI, 52(40.9%). There were 14(11.02%) MLH-1 mutations, 30(23.62%) MSH2 mutations, and 26(20.47%) MSH6 mutations. BRAF mutational analysis showed only 5(3.9%) having pathologic missense BRAF V600 mutations. KRAS mutations consisted of only 8(6.3%) having pathologic missense KRAS mutations. Conclusions The high rate of MSI in Ugandan colorectal tumours was mainly associated with a lack of BRAF mutations and a high frequency of MSH2 and MSH6 MMR gene mutations. In CRC patients, identification of the causative mutation is recommended, however in a resource-limited setting, MSI testing and immunohistochemistry is more cost effective. In Ugandan CRC patients who meet at least one of the Bethesda criteria, MSI testing and immunohistochemistry may therefore be offered to obtain the MSI status of the tumour.
format Article
id doaj-art-bbc667f7901c4ebb8a2345df5bbb94b1
institution DOAJ
issn 1471-2407
language English
publishDate 2025-04-01
publisher BMC
record_format Article
series BMC Cancer
spelling doaj-art-bbc667f7901c4ebb8a2345df5bbb94b12025-08-20T02:55:38ZengBMCBMC Cancer1471-24072025-04-0125111310.1186/s12885-025-14195-9The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in UgandaRichard Wismayer0Rosie Matthews1Celina Whalley2Julius Kiwanuka3Fredrick Elishama Kakembo4Steve Thorn5Henry Wabinga6Michael Odida7Ian Tomlinson8Department of Surgery, Masaka Regional Referral HospitalInstitute of Genetics and Cancer, College of Medicine and Veterinary Medicine, University of EdinburghInstitute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of BirminghamDepartment of Epidemiology and Biostatistics, College of Health Sciences, Makerere UniversityDepartment of Immunology and Molecular Biology, School of Biomedical Sciences, College of Health Sciences, Makerere UniversityInstitute of Genetics and Cancer, College of Medicine and Veterinary Medicine, University of EdinburghDepartment of Pathology, School of Biomedical Sciences, College of Health Sciences, Makerere UniversityDepartment of Pathology, School of Biomedical Sciences, College of Health Sciences, Makerere UniversityInstitute of Genetics and Cancer, College of Medicine and Veterinary Medicine, University of EdinburghAbstract Introduction In Uganda, colorectal cancer (CRC) is steadily increasing according to the Kampala Cancer Registry. In the West, microsatellite instability is detected in 90% of hereditary nonpolyposis colon cancers (HNPCC) which account for 1–2% of all CRC, and 15% of sporadic CRC. Germline mutations in MLH1 and MSH2 account for 90% of HNPCC in the West, whilst the remainder of cases are due to mutations in MSH6 and PMS2. The aim of this study was to determine the microsatellite instability (MSI) status and determine the proportions of MLH1, MSH2, and MSH6 pathological mutations in Ugandan CRC patients. Methodology This was a cross-sectional study carried out between 1st January 2008 to 15th September 2021. Patients were recruited prospectively from 16th September 2019 to 16th September 2021, from Masaka Regional Referral Hospital, Mulago National Referral Hospital, Uganda Martyrs’ Hospital Lubaga and Mengo Hospital. From 1st January 2008 to 15th September 2019, CRC FFPE tissue blocks were obtained from the archives of the Department of Pathology, Makerere University. Data was abstracted from the medical case files for demographics, topography and stage. The histopathological subtype and grade of CRC were obtained by two consultant pathologists from the H&E slides. DNA was extracted from CRC formalin-fixed paraffin-embedded (FFPE) tissue blocks. Library preparation was completed using the Qiagen custom design panel. The custom panel represented 56 genes. The MLH-1, MSH2, MSH6, BRAF and KRAS genes were sequenced using the above library preparation and NGS sequencing. The MSI status was obtained if one of the MSI genes, MLH1, MSH2 or MSH6 was pathologically mutated. If none of the genes was pathologically mutated it was considered MSI negative, microsatellite stable (MSS). Immunohistochemistry was carried out to determine whether MLH1 and PMS2 was MMR proficient or deficient. Categorical data was summarized using frequencies and proportions corresponding to each of the three histopathological subtypes and MSI status subtypes. Continuous and categorical variables were analyzed using the chi-square and Fischer’s exact tests. A p -value ≤ 0.05 was considered statistically significant for all the analyses. Results Out of 127 CRC patients, the mean(SD) age of MSI cases was 55.6(16.9) years and of MSS cases was 55.4(15.5) years. The majority were MSS, 75(59.06%) followed by MSI, 52(40.9%). There were 14(11.02%) MLH-1 mutations, 30(23.62%) MSH2 mutations, and 26(20.47%) MSH6 mutations. BRAF mutational analysis showed only 5(3.9%) having pathologic missense BRAF V600 mutations. KRAS mutations consisted of only 8(6.3%) having pathologic missense KRAS mutations. Conclusions The high rate of MSI in Ugandan colorectal tumours was mainly associated with a lack of BRAF mutations and a high frequency of MSH2 and MSH6 MMR gene mutations. In CRC patients, identification of the causative mutation is recommended, however in a resource-limited setting, MSI testing and immunohistochemistry is more cost effective. In Ugandan CRC patients who meet at least one of the Bethesda criteria, MSI testing and immunohistochemistry may therefore be offered to obtain the MSI status of the tumour.https://doi.org/10.1186/s12885-025-14195-9Colorectal cancerMicrosatellite instability (MSI)Microsatellite stable (MSS)ImmunohistochemistryUganda
spellingShingle Richard Wismayer
Rosie Matthews
Celina Whalley
Julius Kiwanuka
Fredrick Elishama Kakembo
Steve Thorn
Henry Wabinga
Michael Odida
Ian Tomlinson
The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda
BMC Cancer
Colorectal cancer
Microsatellite instability (MSI)
Microsatellite stable (MSS)
Immunohistochemistry
Uganda
title The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda
title_full The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda
title_fullStr The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda
title_full_unstemmed The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda
title_short The role of MLH1, MSH2 and MSH6 in the development of colorectal cancer in Uganda
title_sort role of mlh1 msh2 and msh6 in the development of colorectal cancer in uganda
topic Colorectal cancer
Microsatellite instability (MSI)
Microsatellite stable (MSS)
Immunohistochemistry
Uganda
url https://doi.org/10.1186/s12885-025-14195-9
work_keys_str_mv AT richardwismayer theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT rosiematthews theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT celinawhalley theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT juliuskiwanuka theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT fredrickelishamakakembo theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT stevethorn theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT henrywabinga theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT michaelodida theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT iantomlinson theroleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT richardwismayer roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT rosiematthews roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT celinawhalley roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT juliuskiwanuka roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT fredrickelishamakakembo roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT stevethorn roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT henrywabinga roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT michaelodida roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda
AT iantomlinson roleofmlh1msh2andmsh6inthedevelopmentofcolorectalcancerinuganda