Marc Donald Wilfried Adico,1– 3 Tata Gnire Safiatou Coulibaly,4 Dramane Dagnogo,1 Mousso Savadogo,3 Wentoin Alimata Marie Pierre Daramcoum,1,5 Saraka Didier Martial Yao,1,5 Dougba Noel Dago,1,5 Foungotin Hamidou Coulibaly,6 Abdou Azaque Zouré Snr,1,2,7 Bagora Bayala,1,2,8 Nafan Diarrassouba,1,5 Wendkuuni Florencia Djigma,2,3 Jacques Simporé21Department of Genetics and Biochemistry, Peleforo GON COULIBALY University, Korhogo, Côte d’Ivoire; 2Department of Molecular Biology, Pietro Annigoni Biomolecular Research Center (CERBA), Ouagadougou, Burkina Faso; 3Department of Biochemistry-Microbiology, Laboratory of Molecular Biology and Molecular Genetics, Joseph KI-ZERBO University, Ouagadougou, Burkina Faso; 4Molecular Genetics Platform, Pasteur Institute, Abidjan, Côte d’Ivoire; 5Department of Genetics and Biochemistry, African Center for Shea Research and Applications (CRAK), Laboratory of Molecular Biology and Functional Genomics (BIOGEN-CRAK), Peleforo GON COULIBALY University, Korhogo, Côte d’Ivoire; 6Department of Biotechnology and Food Safety, Felix Houphouet Boigny University, Abidjan, Côte d’Ivoire; 7Department of Biomedical and Public Health, Research Institute for Health Sciences, Ouagadougou, Burkina Faso; 8Department Biochemistry, Ecole Normale Superieure, Koudougou, Burkina FasoCorrespondence: Abdou Azaque Zouré Snr, Department of Biomedical and Public Health, Research Institute for Health Sciences, Ouagadougou, Burkina Faso, Email abdouazaque@gmail.comAbstract: In recent decades, Africa has experienced an increase in cancer mortality rates. This challenge conducted to wide use of anticancer drugs but their efficacy and toxicity may vary depending on patient’s genetic characteristics. In this context, pharmacogenomics may play a crucial role in optimizing and personalizing these treatments in African populations, which have been very little studied so far in this field. The main objective of this scoping review is to identify clinical and molecular data concerning the influence of genetic variants on the efficacy and the toxicity of anticancer drugs in African populations. The scientific databases PubMed, Science Direct, and Google Scholar were used to search for articles published between January 2010 and December 2025. This review was conducted according to the Arksey and O’Malley framework in accordance with the PRISMA-ScR method (Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews). Data on genes, variants, cancer type, drug, country, year of study publication, and clinical effects on patients were extracted. This information was used to highlight the effect of pharmacogenes on the response of anticancer drugs and their implication for personalized medicine. A total of 2397 articles were identified in the three databases. After eliminating duplicates and off-topic articles, 59 articles were selected. Among them, 30 were examined in full text, of which two were excluded due to the unavailability of the full text. Finally, 28 articles were selected for the qualitative analysis of this review. From these 28 articles, 58 variants spread over 41 genes were identified. The results revealed a geographical disparity in importance of the included research, with a strong one coming from North and Southern Africa. The ABCB1, CYP3A5, CYP2D6, SLC28A3, CYP2C9, CYP2B6, TPMT and MTHFR genes have been the most studied. They were significantly associated with the efficacy and toxicity of chemotherapeutic drugs in most studies. The most frequently analyzed anticancer drugs for their drug-gene associations include imatinib, tamoxifen and doxorubicin. Breast cancer, chronic myeloid leukemia and acute lymphoblastic leukemia have been the most studied types of cancer. The available pharmacogenomic data for cancer drugs remain insufficient to allow a real application of personalized medicine in the treatment of cancer on the continent. This study provides an overview of the current state and gaps in pharmacogenomic research of anticancer drugs in Africa. It is particularly intended for pharmacologic clinicians, oncologists and health decision-makers involved in cancer management on the African continent.Keywords: pharmacogenomics, personalized medicine, genetic variants, cancers, anticancer drugs, Africa
Hu Zhang,1 Senyue Zhang,2 Tong Fu,3 Mingzhu Zhang,4 Cunyue Yu,5 Jianing Li,6 Ying Tong71Guang’anmen Hospital Heilongjiang China Academy of Chinese Medical Sciences, Harbin, People’s Republic of China; 2Jiamusi Hospital of Traditional Chinese Medicine, Jiamusi, People’s Republic of China; 3Department of Psychology, Brandeis University, Waltham, MA, USA; 4Department of Rheumatology, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, People’s Republic of China; 5Department of Geriatrics, Heilongjiang Academy of Traditional Chinese Medicine, Harbin, People’s Republic of China; 6China Academy of Chinese Medical Sciences, Beijing, People’s Republic of China; 7Department of Oncology, The First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, People’s Republic of ChinaCorrespondence: Ying Tong, Email tongying@hljucm.edu.cn Jianing Li, Email jianing9912@163.comBackground: Hyperuricemia is increasingly prevalent and is closely associated with gout and several cardiometabolic and renal disorders. Although pharmacological development in this field is expanding, the overall structure and recent evolution of the global development pipeline remain incompletely characterized. This study aimed to characterize recent trends in drug development and clinical research for hyperuricemia.Methods: Hyperuricemia-related drug-development records were retrieved from the Pharmaprojects database from database inception to July 31, 2025. Records were screened according to disease classification, pharmacological relevance, and development status. After screening and data verification, 69 eligible records were included. Development stage, geographical distribution, therapeutic class, mechanism of action, molecular target, and commencement date were analyzed descriptively.Results: A total of 69 eligible drug-development records were included. The pipeline was predominantly concentrated in preclinical and early clinical development, with preclinical programs accounting for 31.88%, Phase I for 20.29%, Phase II for 18.84%, and Phase III for 17.39%. China and the United States represented important contributors to the identified development activities. The development portfolio was dominated by gout-related therapies but showed increasing mechanistic diversity. URAT1-related approaches were prominent, and SLC22A12 was the most frequently represented molecular target. Xanthine oxidase-, uricase-, and inflammation-related mechanisms were also represented.Conclusion: The global development pipeline for hyperuricemia remains weighted toward preclinical and early clinical stages but is becoming increasingly diverse in therapeutic mechanisms and molecular targets. Further late-stage clinical evaluation, multicenter studies, and long-term safety assessment are required to establish the clinical value of emerging therapeutic strategies.Keywords: drug, treatment, hyperuricemia, clinical trials
Akash Kishor Rokade,1 Anna Meiliana,2,3 Vesara Ardhe Gatera,4 Edmund Ui-Hang Sim51Laboratory of Pesticide and Environmental Toxicology, Department of Plant Pests and Diseases, Faculty of Agriculture, Universitas Padjadjaran, Jatinangor, West Java, Indonesia; 2Department of Pharmacology and Clinical Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Jatinangor, West Java, Indonesia; 3Prodia Clinical Laboratory, Jakarta, Indonesia; 4Department of Biological Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Jatinangor, West Java, Indonesia; 5Faculty of Resource Science and Technology, Universiti Malaysia Sarawak, Kota Samarahan, MalaysiaCorrespondence: Anna Meiliana, Email anna.meiliana@unpad.ac.idAbstract: Personalized nutrition, guided by nutrigenetic insights, is a promising strategy for optimizing immune function through targeted dietary interventions. Peripheral blood mononuclear cells (PBMCs), comprising lymphocytes and monocytes, serve as a dynamic model for investigating gene–diet interactions because of their sensitivity to nutritional and genetic influences. This review aimed to synthesize current reports on the interplay between genetic variation, dietary components, and PBMC molecular responses and evaluate the clinical applicability of the interaction in the development of individualized nutritional strategies for immune optimization. A structured and narrative-focused method was used to synthesize the literature, showing the relationship between molecular knowledge and practical solutions in personalized nutrition as well as immune system optimization, with a focus on PBMCs. A thorough search was performed on PubMed, Scopus, and Google Scholar, encompassing the years 2006 to 2025. Genetic polymorphisms in the vitamin D receptor (VDR), peroxisome proliferator-activated receptor (PPAR), superoxide dismutase 2 (SOD2), and Toll-like receptor 4 (TLR4) modulated the response of PBMCs to nutrients, including vitamin D, omega-3 fatty acids, antioxidants, and polyphenols. The discussion encompassed molecular pathways involving cytokine modulation, oxidative stress, and epigenetic alterations, highlighting PBMCs as indicators of immunological resistance and chronic disease susceptibility. The exploration of multiomics integration to achieve precision nutrition holds significant implications for clinical practice and public health. By using PBMC-based nutrigenetic profiling as a monitoring and stratification tool, future interventions may move toward more focused immune optimization and improved health outcomes, pending further validation in longitudinal and interventional studies.Keywords: nutrigenomics, genetic polymorphism, personalized nutrition, functional foods
Abdkerem Abdulahi Abdi,1,2 Mohamed Mustaf Ahmed,3 Chalirmporn Atasilp,4 Abdinasir Mohamed Aray,3 Chonlaphat Sukasem21Department of Microbiology and Laboratory Sciences, Faculty of Medicine and Health Sciences, SIMAD University, Mogadishu, Somalia; 2Division of Pharmacogenomics and Personalized Medicine, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, 10400, Thailand; 3Faculty of Medicine and Health Sciences, SIMAD University, Mogadishu, Somalia; 4Chulabhorn International College of Medicine, Thammasat University, Pathum Thani, ThailandCorrespondence: Abdkerem Abdulahi Abdi, Email darwiish83@simad.edu.soIntroduction: Fluoropyrimidines are widely used against solid tumors, and severe treatment-related toxicity remains a major clinical problem. DPYD variants prioritized in predominantly European guidelines may not capture those most relevant elsewhere, and their predictive value in Asian and African study populations is unclear.Methods: We searched PubMed, Embase, Scopus, the Cochrane Library, and Google Scholar. Eligible studies reported DPYD variants with toxicity outcomes in Asian or African study populations receiving fluoropyrimidine-based chemotherapy. The risk of bias was assessed using the design-specific Joanna Briggs Institute tools, and findings were synthesized narratively by variant, following the PRISMA 2020.Results: Twenty-three studies published between 2007 and 2025, spanning 14 countries, were included, six at low risk of bias, nine at moderate, and eight at high. Recurrent variants were c.1627A>G (DPYD*5), c.85T>C (DPYD*9A), c.1905+1G>A (DPYD*2A), c.496A>G, c.1896T>C, and c.2194G>A (DPYD* 6). Associations were most consistent for c.85T>C, with unadjusted odds ratios of 2.3 for hand-foot syndrome and 2.7 for diarrhea in South India, and an adjusted odds ratio of 4.35 for mucositis in Tunisia, all for any-grade toxicity. For c.1905+1G>A, adjusted odds ratios were 6.47 for grade 3– 4 neutropenia and 5.76 for diarrhea in Bangladesh. Findings for c.1627A>G were inconsistent in direction. Only one study corrected for multiple testing, and the designs, regimens, grading systems, and genotyping platforms were highly heterogeneous.Conclusion: Evidence for population-specific DPYD variation is strongest in Asian populations. Data from the African populations represented in the available studies, confined to Tunisia, Algeria, Sudan, and Zimbabwe, are too sparse for strong conclusions. No carrier of the four guideline variants was found among 150 genotyped Zimbabwean patients, yet 36% of the 50 who received fluoropyrimidine had severe adverse events. Harmonized prospective studies reporting genotype-specific numerators and denominators are needed before population-specific variants can be considered clinically actionable.Keywords: fluoropyrimidine toxicity, dihydropyrimidine dehydrogenase, pharmacogenetics, Asian populations, African populations, study population
Background: Warfarin remains a widely used anticoagulant for long-term thromboprophylaxis, but its narrow therapeutic index and substantial interindividual variability increase the risk of bleeding complications. Functional variants in vascular endothelial growth factor A (VEGFA) may therefore influence vascular integrity during anticoagulant therapy. This study investigated the association between functional VEGFA polymorphisms and warfarin-associated bleeding in a Saudi cohort. Methods: In this retrospective cohort study, 161 Saudi patients receiving stable maintenance warfarin therapy were genotyped for five VEGFA single-nucleotide polymorphisms (SNPs): rs699947, rs833069, rs2010963, rs35410204, and rs866236. Clinical characteristics and bleeding events during warfarin therapy were obtained from electronic medical records. Bleeding status was determined from clinically documented bleeding events during warfarin therapy that required medical evaluation, hospitalization, or blood transfusion. Genotype-phenotype associations were assessed using chi-square analysis and a multivariable logistic regression model. Results: Bleeding occurred in 39% of the patients (63/161). Among the five VEGFA variants studied, rs699947 and rs833069 showed associations with bleeding in bivariate analysis. The rs699947 A/A genotype and rs833069 T/T genotype were less frequent in patients with bleeding than in those without bleeding (6.7% vs 25.5%, p = 0.009; and 16.4% vs 37.5%, p = 0.013, respectively). The rs833069 association did not survive Bonferroni correction for multiple testing and is therefore considered exploratory. Following adjustment for age, sex, body mass index, international normalized ratio, systolic blood pressure, and diastolic blood pressure, rs699947 remained significantly associated with bleeding. For rs833069, the overall genotype association remained statistically significant; however, individual genotype comparisons were not statistically significant. For rs699947, the A/A genotype was associated with lower odds of bleeding compared with the C/C genotype (OR 0.249, 95% CI 0.062-0.999; p = 0.050). No significant associations were observed for rs2010963, rs35410204, or rs866236. Conclusion: In this exploratory retrospective cohort study, VEGFA rs699947 and rs833069 showed possible associations with bleeding during warfarin therapy in Saudi patients. These findings provide preliminary evidence that VEGFA polymorphisms may contribute to bleeding susceptibility during warfarin therapy. Given the modest sample size, these findings should be interpreted cautiously and require validation in larger prospective studies. Bleeding occurred in 63 of the 161 patients. Two VEGFA gene changes, called rs699947 and rs833069, showed possible links with bleeding. One genetic pattern in rs699947 appeared less common in patients who experienced bleeding, suggesting it may be linked with lower bleeding risk. The other three VEGFA gene changes studied did not show clear associations with bleeding. These findings suggest that genes involved in blood vessel function may help explain why some patients are more likely to bleed during warfarin treatment. However, this was an exploratory study with a modest sample size, so the results need to be confirmed in larger studies before they can be used in clinical practice.
