Fidelis Charles Bugoye

Mr. Fidelis Charles Bugoye


Research Focus & Metrics

Academic Career Length

9Years (2018-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
3 December 2019 in Prostate Cancer
Verified
Journal Article
Open access
PDF file
FBFidelis Charles Bugoye
Fidelis Charles Bugoye
GLGermana Henry Leyna
Germana Henry Leyna
KMKåre MOEN
Kåre MOEN
EMElia John Mmbaga
Elia John Mmbaga
Background. Late diagnosis of prostate cancer is common in low and middle income countries and contributes to high morbidity and mortality of the disease. Utilization of prostate cancer screening services plays a major role in prevention of adverse outcomes. However, there is limited information on the knowledge about, the perceived risk of, and the utilization of prostate cancer screening in Tanzania. Objective. To determine knowledge and perceived risk of prostate cancer, and the utilization of prostate cancer screening services, and associated factors, among men in Dar es Salaam, Tanzania. Design. A population-based cross-sectional study involving men aged 40 years and above living in Dar es Salaam was conducted between May and August, 2018. Methodology. Participants were recruited through multistage random sampling and took part in structured face-to-face interviews. Categorical variables were summarized using proportions while continuous variables were summarized as medians and inter-quarterly range (IQR). Chi square test was used to compare differences between proportions, and logistic regression modelling was used to determine factors associated with utilization of prostate cancer screening. Both crude and adjusted odds ratios (OR), with corresponding 95% confidence intervals, are reported. All analyses were two-tailed and the significance level set at 5%. Results. A total of 388 men with a median age of 53 years (IQR 44–55) participated. Half (52.1%) had poor knowledge about prostate cancer and prostate cancer screening. A third (32.3%, n=125) perceived the risk of prostate cancer to be low. Only 30 respondents (7.7%) had ever been screened for prostate cancer. Utilization of prostate cancer screening services was independently associated with age above 60 years [AOR = 21.46, 95% CI: 6.23, 73.93], monthly income above 305 US Dollars [AOR = 15.68, 95% CI: 4.60, 53.48], the perceived risk of prostate cancer [AOR = 16.34, 95% CI: 7.82, 14.92] and knowledge about prostate cancer [AOR = 67.71, 95% CI: 8.20, 559.57]. Conclusions. Knowledge about prostate cancer and prostate cancer screening services was low among men in Dar es Salaam with a third perceiving themselves to be at no risk for the disease. Utilization of screening services was low and associated with low income, younger age, low perceived risk of prostate cancer and low knowledge about the disease. Intervention measures aiming to increase knowledge about prostate cancer and screening services, and affordable provision of services, are urgently called for.

4 September 2023 in Frontiers in Genetics
Verified
Journal Article
Open access
FBFidelis Charles Bugoye
Fidelis Charles Bugoye
RTRispah Torrorey-Sawe
Rispah Torrorey-Sawe
RBRichard Biegon
Richard Biegon
NDNazima Dharsee
Nazima Dharsee
FMFidelice M. S. Mafumiko
Fidelice M. S. Mafumiko
SMSimeon K. Mining
Simeon K. Mining
Over the past few years, a number of studies have revealed that a significant number of men with prostate cancer had genetic defects in the DNA damage repair gene response and mismatch repair genes. Certain of these modifications, notably gene alterations known as homologous recombination (HRR) genes; PALB2, CHEK2 BRCA1, BRCA2, ATM, and genes for DNA mismatch repair (MMR); MLH1, MSH2, MSH6, and PMS2 are connected to a higher risk of prostate cancer and more severe types of the disease. The DNA damage repair (DDR) is essential for constructing and diversifying the antigen receptor genes required for T and B cell development. But this DDR imbalance results in stress on DNA replication and transcription, accumulation of mutations, and even cell death, which compromises tissue homeostasis. Due to these impacts of DDR anomalies, tumor immunity may be impacted, which may encourage the growth of tumors, the release of inflammatory cytokines, and aberrant immune reactions. In a similar vein, people who have altered MMR gene may benefit greatly from immunotherapy. Therefore, for these treatments, mutational genetic testing is indicated. Mismatch repair gene (MMR) defects are also more prevalent than previously thought, especially in patients with metastatic disease, high Gleason scores, and diverse histologies. This review summarizes the current information on the mutation spectrum and clinical significance of DDR mechanisms, such as HRR and MMR abnormalities in prostate cancer, and explains how patient management is evolving as a result of this understanding.

17 March 2025 in Frontiers in Oncology
Verified
Journal Article
Open access
PDF file
FBFidelis Charles Bugoye
Fidelis Charles Bugoye
RTRispah Torrorey-Sawe
Rispah Torrorey-Sawe
RBRichard Biegon
Richard Biegon
NDNazima Dharsee
Nazima Dharsee
FMFidelice Mafumiko
Fidelice Mafumiko
SMSimeon Mining
Simeon Mining
Background: Prostate cancer is defined by the suppression of genes that suppress tumours and the activation of proto-oncogenes. These are the hallmarks of prostate cancer, and they have been linked to numerous genomic variations, which lead to unfavourable treatment outcomes. Prostate cancer can be categorised into various risk groups of tumour molecular subtypes grounded in the idea of genomic structural variations connected to TMPRSS2:ERG fusion and loss of PTEN. Research suggests that certain genomic alterations may be more prevalent or exhibit different patterns in prostate cancer tumours across populations. Studies have reported a higher frequency of PTEN loss and TMPRSS2:ERG fusion in prostate tumours of Black/African American men, which may contribute to the more aggressive nature of the disease in this population. Thus, therapeutically important information can be obtained from these structural variations, including correlations with poor prognosis and disease severity.Methods: Peer-reviewed articles from 1998 to 2024 were sourced from PubMed and Google Scholar. During the review process, the following search terms were employed: “Tumour suppressor genes OR variations OR alterations OR oncogenes OR diagnostics OR ethnicity OR biomarkers OR prostate cancer genomics OR prostate cancer structural variations OR tumour and molecular subtypes OR therapeutic implications OR immunotherapy OR immunogenetics.”Results: There was a total of 13,012 results for our search query: 5,903 publications from Google Scholar with the patent and citation unchecked filer options, and 7127 articles from PubMed with the abstract, free full text, and full-text options selected. Unpublished works were not involved. Except for four articles published between 1998 and 1999, all other selected articles published in 2000 and later were considered. However, papers with irrelevant information or redundant or duplicate content were not chosen for this review. Thus, 134 met the inclusion criteria and were ultimately retained for this review.Conclusion: This review extracted 134 relevant articles about genomic structure variations in prostate cancer. Our findings demonstrate the importance of PTEN and TMPRSS2:ERG fusion and tumour molecular subtyping in prostate cancer precision medicine.

6 August 2018 in Genetics Research International
Verified
Journal Article
Open access
FBFidelis Charles Bugoye
Fidelis Charles Bugoye
EMElias Mulima
Elias Mulima
Gerald MisinzoGerald Misinzo
Gerald Misinzo
Hundred unrelated father-son buccal swab sample pairs collected from consented Tanzanian population were examined to establish mutation rates using 17 Y-STRs loci DYS19, DYS389I, DYS389II, DYS390, DYS391, DYS392, DYS393, DYS385a, DYS385b, DYS437, DYS438, DYS439, DYS448, DYS456, DYS458, DYS635, and Y-GATA-H4 of the AmpFlSTRYfiler kit used in forensics and paternity testing. Prior to 17 Y-STRs analysis, father-son pair biological relationships were confirmed using 15 autosomal STRs markers and found to be paternally related. A total of four single repeat mutational events were observed between father and sons. Two mutations resulted in the gain of a repeat and the other two resulted in a loss of a repeat in the son. All observed mutations occurred at tetranucleotide loci DYS389II, DYS385a, and DYS385b. The locus specific mutation rate varied between 0 and 1.176 x10−3 and the average mutation rate of 17Y-STRs loci in the present study was 2.353x10−3 (6.41x10−4 - 6.013x10−3) at 95% CI. Furthermore the mean fathers’ age with at least one mutation at son’s birth was 32 years with standard error of 2.387 while the average age of all fathers without mutation in a sampled population at son’s birth was 26.781 years with standard error of 0.609. The results shows that fathers’ age at son’s birth may have an effect on Y-STRs mutation rate analysis, though this age difference was statistically not significant using unpaired samples t-test (p = 0.05). As a consequence of observed mutation rates in this study, the precise and reliable understanding of mutation rate at Y-chromosome STR loci is necessary for a correct evaluation and interpretation of DNA typing results in forensics and paternity testing involving males. The criterion for exclusion in paternity testing should be defined, so that an exclusion from paternity has to be based on exclusion constellations at a minimum of two 17 Y-STRs loci.

7 February 2026 in Scientific African
Verified
Journal Article
Open access
AKAlly O Kanenda
Ally O Kanenda
LWLeticia N Waitara
Leticia N Waitara
DNDaud J Ngasa
Daud J Ngasa
SKSosthenes R Kusekwa
Sosthenes R Kusekwa
NSNsanya J Sote
Nsanya J Sote
FMFidelice M S Mafumiko
Fidelice M S Mafumiko

19 March 2026 in Frontiers in Oncology
Verified
Journal Article
Open access
PDF file
FBFidelis Charles Bugoye
Fidelis Charles Bugoye
RBRichard Biegon
Richard Biegon
NDNazima Dharsee
Nazima Dharsee
FMFidelice Mafumiko
Fidelice Mafumiko
HKHerry Kibona
Herry Kibona
RTRispah Torrorey-Sawe
Rispah Torrorey-Sawe
Background: Prostate cancer (PCa) is a leading cause of cancer-related morbidity and mortality among men globally. The prevalence is disproportionate among men of African descent and more specifically, in East Africa, where it is characterized by aggressive tumour biology and poor survival outcomes. Despite its high burden, the risk factors underlying its disproportionate prevalence remain understudied in this population. This study investigated lifestyle risk and protective factors among prostate cancer (PCa) patients, including demographic, dietary, lifestyle, and family cancer history, at Muhimbili National Hospital (MNH) and Ocean Road Cancer Institute (ORCI) in Dar es Salaam, Tanzania. Methods: This case-control study compared PCa patients with non-PCa controls. Data on sociodemographic, lifestyle, diet, and family history were collected using a standardized questionnaire. Multivariate logistic regression identified significant risk and protective factors for PCa from each of these factors. Several statistical approaches were used to rank a Tanzanian urban population’s significant risk or protective factors. Results: Ranking of broad classes of factors revealed that diet, lifestyle, sociodemographic, family, and patient history of cancer and other disease factor groups, in order of importance, were associated with PCa in men. However, the single best model explaining the odds of being PCa had intake of red meat, coffee, alcohol, tomato, and marital status as independent variables. Specifically, increased intake of red meat (AOR = 5.248), and alcohol (AOR = 2.189) were associated with a high PCa incidence while increased intake of soya (AOR = 0.248), coffee (AOR = 0.603), tomato (AOR = 0.188), and not being married (AOR = 0.147) were associated with lower incidence of PCa in the Tanzanian urban population. Conclusion: The findings suggest that dietary and lifestyle factors have a significant association with PCa incidence in a Tanzanian population compared to sociodemographic, family cancer history, and exposure to infectious and other lifestyle diseases. We recommend further research, including prospective studies or randomized controlled trials with large sample sizes, to confirm these findings, as they suggest health initiatives for the prevention of PCa among high-risk populations, such as urban male populations.