Background: The mutation of the KRAS proto-oncogene is frequently detected in various cancers, including hepatocellular carcinoma (HCC). This mutation often results in the failure of treatments based on tyrosine kinase receptor inhibitors. The study's objective was to investigate mutations of codon 12 and 13 of the KRAS gene and assess the risk of developing Hepatocellular Carcinoma. Methods: A prospective, cross-sectional, and analytical study was conducted from November 2018 to October 2021 at the biochemistry and molecular biology laboratory of Cheikh Anta Diop University’s Faculty of Medicine. Mutations of codons 12 and 13 were identified using High Resolution Melting and confirmed by sequencing. Hepatic assessments (transaminases, GGT, PAL, bilirubin, and AFP) were performed on all patients, and histopathological analysis was conducted. Results: The study consisted of 34 patients with an average age of 44±3.4 years and a sex ratio of 5.8. There was a predominance in the age group of 36 to 45 years (38.2%). The prevalence of the G12D mutation of the KRAS gene was 23.5% and was more common in subjects over 45 years (n=5; 11.7%). Hepatic impairments were less pronounced in carriers of the G12D mutation of the KRAS gene, albeit not significantly different. Additionally, tumors of grade 3 and type pT3 appeared more linked to the G12D mutation of the KRAS gene, with prevalences of 18.75% (n=3) and 30.8% (n=4), respectively. The relationship between chronic Hepatitis B Virus carriage and the KRAS gene mutation was not significant. Conclusion: Molecular biology significantly contributes to diagnosis and patient management by identifying molecular markers for pre-therapeutic evaluation.
| Published in | International Journal of Genetics and Genomics (Volume 14, Issue 4) |
| DOI | 10.11648/j.ijgg.20261404.12 |
| Page(s) | 154-160 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2026. Published by Science Publishing Group |
Codon 12 and 13 KRAS, HBV, Hepatocellular Carcinoma, Senegal
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APA Style
Thorpe, D. F. K. S., Souleymane, T., Abdourahmane, S., Yaya, S. I., Fatou, D., et al. (2026). Benefits of Testing for the G12D Mutation of the KRAS Gene in Hepatocellular Carcinoma (HCC) in Senegal. International Journal of Genetics and Genomics, 14(4), 154-160. https://doi.org/10.11648/j.ijgg.20261404.12
ACS Style
Thorpe, D. F. K. S.; Souleymane, T.; Abdourahmane, S.; Yaya, S. I.; Fatou, D., et al. Benefits of Testing for the G12D Mutation of the KRAS Gene in Hepatocellular Carcinoma (HCC) in Senegal. Int. J. Genet. Genomics 2026, 14(4), 154-160. doi: 10.11648/j.ijgg.20261404.12
AMA Style
Thorpe DFKS, Souleymane T, Abdourahmane S, Yaya SI, Fatou D, et al. Benefits of Testing for the G12D Mutation of the KRAS Gene in Hepatocellular Carcinoma (HCC) in Senegal. Int J Genet Genomics. 2026;14(4):154-160. doi: 10.11648/j.ijgg.20261404.12
@article{10.11648/j.ijgg.20261404.12,
author = {Dia Fatou Kine Sy Thorpe and Thiam Souleymane and Samba Abdourahmane and Soumah Idrissa Yaya and Diedhiou Fatou and Agossou Hortence Honorine Medece and Ka Ibrahima and Deguenonvo Gabriel Nougnignon Comlan and Cisse Fatou and Ndiaye Arame and Coly Najah Fatou and Dial Cherif Mouhamed and Diop Papa Saloum and Diallo Fatou},
title = {Benefits of Testing for the G12D Mutation of the KRAS Gene in Hepatocellular Carcinoma (HCC) in Senegal},
journal = {International Journal of Genetics and Genomics},
volume = {14},
number = {4},
pages = {154-160},
doi = {10.11648/j.ijgg.20261404.12},
url = {https://doi.org/10.11648/j.ijgg.20261404.12},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijgg.20261404.12},
abstract = {Background: The mutation of the KRAS proto-oncogene is frequently detected in various cancers, including hepatocellular carcinoma (HCC). This mutation often results in the failure of treatments based on tyrosine kinase receptor inhibitors. The study's objective was to investigate mutations of codon 12 and 13 of the KRAS gene and assess the risk of developing Hepatocellular Carcinoma. Methods: A prospective, cross-sectional, and analytical study was conducted from November 2018 to October 2021 at the biochemistry and molecular biology laboratory of Cheikh Anta Diop University’s Faculty of Medicine. Mutations of codons 12 and 13 were identified using High Resolution Melting and confirmed by sequencing. Hepatic assessments (transaminases, GGT, PAL, bilirubin, and AFP) were performed on all patients, and histopathological analysis was conducted. Results: The study consisted of 34 patients with an average age of 44±3.4 years and a sex ratio of 5.8. There was a predominance in the age group of 36 to 45 years (38.2%). The prevalence of the G12D mutation of the KRAS gene was 23.5% and was more common in subjects over 45 years (n=5; 11.7%). Hepatic impairments were less pronounced in carriers of the G12D mutation of the KRAS gene, albeit not significantly different. Additionally, tumors of grade 3 and type pT3 appeared more linked to the G12D mutation of the KRAS gene, with prevalences of 18.75% (n=3) and 30.8% (n=4), respectively. The relationship between chronic Hepatitis B Virus carriage and the KRAS gene mutation was not significant. Conclusion: Molecular biology significantly contributes to diagnosis and patient management by identifying molecular markers for pre-therapeutic evaluation.},
year = {2026}
}
TY - JOUR T1 - Benefits of Testing for the G12D Mutation of the KRAS Gene in Hepatocellular Carcinoma (HCC) in Senegal AU - Dia Fatou Kine Sy Thorpe AU - Thiam Souleymane AU - Samba Abdourahmane AU - Soumah Idrissa Yaya AU - Diedhiou Fatou AU - Agossou Hortence Honorine Medece AU - Ka Ibrahima AU - Deguenonvo Gabriel Nougnignon Comlan AU - Cisse Fatou AU - Ndiaye Arame AU - Coly Najah Fatou AU - Dial Cherif Mouhamed AU - Diop Papa Saloum AU - Diallo Fatou Y1 - 2026/10/29 PY - 2026 N1 - https://doi.org/10.11648/j.ijgg.20261404.12 DO - 10.11648/j.ijgg.20261404.12 T2 - International Journal of Genetics and Genomics JF - International Journal of Genetics and Genomics JO - International Journal of Genetics and Genomics SP - 154 EP - 160 PB - Science Publishing Group SN - 2376-7359 UR - https://doi.org/10.11648/j.ijgg.20261404.12 AB - Background: The mutation of the KRAS proto-oncogene is frequently detected in various cancers, including hepatocellular carcinoma (HCC). This mutation often results in the failure of treatments based on tyrosine kinase receptor inhibitors. The study's objective was to investigate mutations of codon 12 and 13 of the KRAS gene and assess the risk of developing Hepatocellular Carcinoma. Methods: A prospective, cross-sectional, and analytical study was conducted from November 2018 to October 2021 at the biochemistry and molecular biology laboratory of Cheikh Anta Diop University’s Faculty of Medicine. Mutations of codons 12 and 13 were identified using High Resolution Melting and confirmed by sequencing. Hepatic assessments (transaminases, GGT, PAL, bilirubin, and AFP) were performed on all patients, and histopathological analysis was conducted. Results: The study consisted of 34 patients with an average age of 44±3.4 years and a sex ratio of 5.8. There was a predominance in the age group of 36 to 45 years (38.2%). The prevalence of the G12D mutation of the KRAS gene was 23.5% and was more common in subjects over 45 years (n=5; 11.7%). Hepatic impairments were less pronounced in carriers of the G12D mutation of the KRAS gene, albeit not significantly different. Additionally, tumors of grade 3 and type pT3 appeared more linked to the G12D mutation of the KRAS gene, with prevalences of 18.75% (n=3) and 30.8% (n=4), respectively. The relationship between chronic Hepatitis B Virus carriage and the KRAS gene mutation was not significant. Conclusion: Molecular biology significantly contributes to diagnosis and patient management by identifying molecular markers for pre-therapeutic evaluation. VL - 14 IS - 4 ER -