Background/Objectives: The tumor suppressor gene TP53 is one of the most frequently mutated genes in human cancers, with alterations predominantly affecting its DNA-binding domain (DBD). However, the mutational landscape and functional consequences of TP53 variants remain poorly characterized in African populations. This study aimed to characterize mutations in exons 5-6 of TP53 in oral cavity cancer (OCC), prostate cancer (PC), and breast cancer (BC) in a Senegalese population, and to assess their structural effects, functional consequences, and impact on protein-protein interactions with BCL-2. Methods: Seventy-eight archived tumor DNA samples from Senegalese patients with OCC, PC, and BC were analyzed. Variants were annotated using COSMIC and dbSNP databases. Functional impact was evaluated with PolyPhen-2. Structural stability changes (ΔΔG) were predicted using FoldX, conformational dynamics (ΔΔSvib) were assessed with ENCoM, and effects on the p53-BCL-2 interaction were analyzed using DDMut-PPI. Statistical analyses were also performed. Results: BC exhibited the highest TP53 mutation frequency, whereas OCC showed greater mutational diversity. Exon-level analysis revealed a significant enrichment of exon 6 mutations in BC. Structural analyses indicated that exon 5 mutations across all cancers and mutations in OCC were predominantly destabilizing and associated with loss-of-function effects. In contrast, recurrent exon 6 mutations in PC and BC, particularly V217L and V218M, were predicted to stabilize the p53 structure. Conformational dynamics differences between exons were significant only in PC. All analyzed mutations were predicted to stabilize the p53-BCL-2 interaction. Conclusions: This integrative in silico study identified cancer and exon-specific TP53 mutation patterns in a Senegalese population, highlighting exon 6 as a context-dependent hotspot with potential oncogenic implication in PC and BC. Despite its computational nature, the study provides valuable insights that merit further investigation.

Introduction: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with significant morbidity and mortality. In sub-Saharan Africa, AF frequently occurs at a younger age, most often in the context of rheumatic mitral valve disease (RMVD), and is characterized by advanced atrial remodeling. Genetic studies have identified the Paired-like Homeodomain Transcription Factor 2 (PITX2) gene at the 4q25 locus as a major susceptibility factor for AF. Objective: to investigate genetic variability within exon 4 of the PITX2 gene in African patients with RMVD and to explore its potential role in AF susceptibility. Materials and Methods: this prospective observational study was conducted at the Cuomo Cardiac Surgery Center, Aristide Le Dantec University Hospital (Dakar, Senegal). Forty-five patients undergoing surgery for RMVD were included, along with 15 control subjects without documented AF. Intraoperative left atrial endocardial biopsies were obtained in operated patients. Genomic Deoxyribonucleic Acid (DNA) extracted from atrial tissue and control blood samples was used for targeted amplification and Sanger sequencing of exon 4 of PITX2. Identified variants were annotated using public databases and evaluated with in silico prediction tools. Variants were classified according to the American College of Medical Genetics and Genomics (ACMG) guidelines. Results: the study population was young (mean age 31 years) and predominantly female. AF was present in 56% of patients and was associated with marked left atrial dilatation and preserved left ventricular systolic function. Sequencing identified four rare missense variants (c.59C>T, c.97A>G, c.121C>G, and c.149G>T) located within the conserved homeobox domain of PITX2. All variants were heterozygous and showed extremely low allele frequencies in population databases. In silico predictions were heterogeneous, and all variants were classified as variants of uncertain significance. Genetic diversity analyses revealed slightly higher haplotype and nucleotide diversity in AF patients, without significant genetic differentiation between groups. Conclusion: rare variants in exon 4 of PITX2 were identified in African patients with RMVD. Although their functional significance remains uncertain, these findings support a potential modulatory role of PITX2 in susceptibility to atrial fibrillation and highlight the importance of genetic studies in underrepresented African populations.

Prostate tumors are more common worldwide, with 60% of men over the age of 50 affected by benign prostatic hyperplasia (BPH) and 1.5 million new cases and 397,000 deaths from prostate cancer (PCa), which ranks as the second most common cancer globally. Although age is the most significant factor, other factors are associated with their development, and genetic factors appear to play a major role. This study aimed to evaluate the involvement of TP53 gene mutations in cases of prostate tumors among Senegalese men while contributing to the understanding of the mutational link between the two tumors. sixteen BPH tissue samples and seventeen PCa tissue samples were collected via biopsy from Senegalese patients following informed consent. DNA extraction followed by PCR amplification and sequencing were performed. Mutation Surveyor was used to identify mutations. Mutation Taster, Polyphen-2, SIFT, and SNP & GO were used to assess pathogenicity predictions. I-Mutant2, MuPro, and Dynamut2 were used to predict the stability, flexibility, and dynamics of the mutated p53 protein. MutPred2 and Mutation3D were used to predict physicochemical properties and map risk mutations. Variability, diversity, and genetic structure were determined using MEGA, BioEdit, DnaSP, and Arlequin. A total of 32 TP53 mutations were identified in the two tumors. These mutations were predominant in prostate cancer. No mutations shared between the two tumor types were found; however, shared mutations within each tumor type were observed, particularly one mutation (c.652G>A p.218Val>Met) present in all prostate cancer patients. Most non-synonymous mutations are predicted to be pathogenic and destabilizing for the mutated p53 protein in both tumors. Low polymorphism and a short genetic distance were observed between the two prostate tumors. This study provided insight into the potential impact of TP53 gene mutations on prostate tumors. Despite their low frequency in the Senegalese population, which may be explained by the small sample size, they play a role in the development and aggressiveness of prostate tumors. Therefore, special attention is required in patients carrying these mutations, particularly for the c.652G>A p.218Val>Met mutation, as the latter could influence management.

Background: The Arg72Pro (R72P) polymorphism of the TP53 tumor suppressor gene has been controversially associated with breast cancer risk, with significant variations depending on ethnic origin. Little data exists for West African populations. This study seeks to evaluate the distribution and association of the R72P polymorphism of exon 4 of the TP53 gene with benign and malignant breast tumors in the Senegalese population. Methodology: The study was conducted on 48 Senegalese women: 17 with breast cancer (malignant), 12 with benign tumors, and 19 healthy controls. The polymorphism was genotyped by PCR followed by restriction fragment analysis. Polymorphism and allelic diversity, as well as genetic differentiation parameters and correspondence factor analysis, were generated using Genetix software version 4.05.2 and Bayesian inference with STRUCTURE. Hardy-Weinberg equilibrium was tested using GenePop software version 4.3. Results: The analysis revealed a distinct allele distribution, with a predominant frequency of the C allele (Pro72) in controls (77.7%) and an increased frequency of the G allele (Arg72) in patients with tumors (25% malignant, 12.5% benign). Statistically, no significant association was found between genotypes and the risk of developing malignant or benign breast tumors. Hardy-Weinberg equilibrium tests showed a significant imbalance in the patient populations, unlike in the controls. Finally, population genetic analyses (low FST differentiation indices, negligible genetic distances, and genetic structure in two clusters) indicated high genetic homogeneity between the three groups for this specific locus. Conclusion: Although differences in allele frequency were observed, the R72P polymorphism of TP53 is not an independent and significant risk factor for breast cancer in this Senegalese cohort. The high genetic homogeneity observed suggests that this variant alone is probably not a key determinant of breast pathology in this population. These results highlight the importance of local studies and the need for broader research incorporating other genetic and environmental factors.

Background WHO reports in 2024 revealed that breast cancer affects women of all ages from puberty onward, with incidence increasing with age. Approximately 2.3 million new cases were recorded. In 2022, this disease caused 670,000 deaths worldwide. Low-penetrance genes, although not systematically associated with a high risk of breast cancer, appear to play an important role. These genes, frequently mutated in the general population, contribute significantly to breast cancer susceptibility, particularly when they interact with environmental factors or other genetic mutations. This study aims to evaluate the involvement of MT-CYB gene mutations in the progression of breast cancer among Chadian women. Methods We analyzed the variability of the MT-CYB gene in 43 patients using the PCR-sequencing technique. First, raw sequencing data were processed through the Mutation Surveyor software, which compares submitted chromatograms with the reference sequence. Next, we identified present mutations and assessed their potential impact on pathogenicity. Results Our findings highlight the potential role of the MT-CYB gene in the development of breast cancer in Chadian women. We identified 53 mutations, including 21 (39.62%) homozygous and 32 (60.37%) heterozygous mutations. Among them, 14 were already listed in the dbSNP database, while 39 were novel, with the majority found in cancerous tissues. Among these mutations, 69.81% (37/53) were non-synonymous substitutions, resulting in an amino acid change in 86.04% (37/43) of cases. Pathogenicity analysis revealed that 48.64% (18/37) were potentially deleterious, while 51.35% (19/37) were classified as neutral polymorphisms according to prediction software that considers protein structure. A detailed evaluation of the non-synonymous mutations showed that, of the 37 analyzed, 67.56% (25/37) were considered pathogenic, and 32.43% (12/37) were deemed benign. Conclusion These results highlight the crucial importance of prevention, early detection and genetic research to better understand and treat breast cancer.

OBJECTIVE:This study aimed to understand the effect of nucleotide mutations and microsatellite locus instability on breast cancer in Senegalese women. METHODS:A total of 120 healthy and cancerous tissue samples were analyzed. After PCR/sequencing analysis, the nucleotide variability of two mitochondrial genes (MTCYB and D-loop) and polymorphisms of two microsatellite loci (BAT-25 and BAT-26) were determined. Additionally, structural and correlation analyses were performed between the clinicopathological features and polymorphisms of the genes studied. RESULT:Multiple variations in MTCYB and the D-loop were identified with much higher frequencies in cancerous tissues. However, MTCYB appeared more affected than the D-loop during carcinogenesis. Regarding the BAT-25 and BAT-26 loci, breast carcinogenesis was associated with instability of these microsatellite loci, with an MSI-H phenotype in 60.71% of tumors. Furthermore, the number of pears and the histological grade impacted patient survival. In addition, mutations at D-loop sites 150 and 152 and BAT-25 stability negatively impacted patient survival. In contrast, BAT-26 instability conferred the advantage of longer post-operative survival. Molecular variance analysis revealed that the clinical heterogeneity of the tumors was a function of the number of invading lymph nodes. CONCLUSION:This study highlights the high penetrance of mitochondrial mutations in breast cancer in Senegalese women, as well as the predominant role of BAT-25 marker stability and BAT-26 marker instability in breast carcinogenesis.

A cancer is said to be hormone-dependent when hormones influence the carcinogenesis process. Studies suggest a possible protective effect of hormone treatment in colorectal cancer. Given the hormone treatment, a thorough study of CYP17A1 is necessary. This study aims to assess the penetrance of CYP17A1 in the development of colorectal cancer. This study involved 24 colorectal cancer patients and 24 controls. For each sample, DNA extraction was performed, followed by CYP17A1 gene amplification and Sanger sequencing. The nature and position of mutations were identified using Mutation Surveyor version 5.1.2. DnaSP version 5.10, MEGA version 7.014, and the Arlequin program version 3.1 were used to highlight the parameters of variability, differentiation, and demogenetic evolution of the study population. The results revealed heterozygous mutations in the CYP17A1 gene and a substitution at the c.-34T>C promoter region. The absence of nonsynonymous mutations was revealed by very low genetic variability in the cancer population compared with controls. There was also little genetic differentiation and distance between the two populations. The frequent c.-34T>C mutation suggests that this polymorphism may modulate the transcriptional activity of CYP17A1 and consequently the hormones under this gene's control, and therefore colorectal tumor growth.

Cancer is the leading cause of death and a major obstacle to increasing life expectancy worldwide in the 21st century. Oral cavity cancers are the most common type of head and neck cancers. This study aimed to determine the polymorphism and genetic diversity of the tumor protein P53 (TP53) in oral cavity cancers in Senegal. From a total of 40 patients with oral cavity cancer, we collected 40 cancerous tissue samples, 20 adjacent healthy tissue samples, and 15 blood samples. Blood samples were collected from participants in the control group. Tissue samples were obtained from each patient during a biopsy after obtaining informed consent. DNA extraction, polymerase chain reaction (PCR), and sequencing were performed. MEGA, BioEdit, and DnaSP software were used to analyze polymorphisms and genetic diversity. A total of 36.80%, 22.27%, and 7.74% polymorphic sites were found in cancerous tissues, healthy tissues, and blood samples, respectively. Nine amino acids showed significant differences in distribution between participants in the control group and patients. Significant differences were also observed within and between populations. This study revealed an increasing number of oral cancer cases in Senegal. Moreover, healthy tissues exhibited the same genetic alterations as cancerous tissues.

Breast cancer refers to a malignant tumour resulting from the uncontrolled proliferation of epithelial cells in the mammary gland. It is the leading cause of cancer in women. In Senegal, regional disparities remain marked by differences in access to screening, diagnosis, and treatment. Proteomics provides a direct reflection of the functional state of tissues and biological pathways and captures the functional effects of molecular alterations. In order to better understand the relationship between the pathogenesis of breast cancer and the existence of potential biomarkers based on each underlying clinical and sociodemographic parameter, this study performs correlation analyses. Proteins were extracted from healthy and cancerous tissues. The analytical workflow showed 30 proteins that were statistically deregulated between those under and over 50 years of age, 5 proteins between married and unmarried patients, 37 proteins between women with fewer than 7 children and those with more than 7 children, six proteins between the early stage and the locally advanced stage, and treatment response showed that 17 proteins were statistically deregulated. The results of this study have identified numerous proteins with high prognostic value associated with robust statistics and significantly overexpressed according to the parameters.

Cytokines are proteins involved in cellular communication, particularly in the immune system. They are ambivalent and can promote or inhibit tumor progression. Their stimulation represents a promising strategy against cancer, particularly in the context of immunotherapy. To highlight the link between cytokines and tumorigenesis, polymorphisms of IL8 (-251T/A) and IL6 (-174G/C) were studied in Senegalese patients. The analysis of the polymorphism of interleukins IL6 (-174 G/C) and IL8 (-251 T/A) in 24 patients with colorectal cancer and 20 control individuals was performed by the PCR-RFLP method. Polymorphism and allelic diversity as well as genetic differentiation parameters and factorial correspondence analysis were generated by Genetix software version 4.05.2. Linkage equilibrium was sought using GenePop software version 4.3. Analysis of interleukin polymorphism showed a higher frequency of mutant genotypes CC (60%) and AA (54%) of interleukins IL6 and IL8 respectively. The frequency of these mutant genotypes was higher in controls with (85%) for IL6 and (80%) for IL8. The distribution of allelic and genotypic frequencies of the two loci are not in Hardy-Weinberg equilibrium. Poor discrimination between cancer cases and controls was observed. The low frequency of mutant alleles in the cancer population suggests a reduction in the transcriptional activity of the promoter of these genes and may compromise the antitumor immune response. The low distribution of these mutant alleles between the two populations shows that polymorphisms of IL6 (-174 G/C) and IL8 (-251 T/A) exert reduced penetrance of these genes in the occurrence of colorectal cancer.

Our study aimed to determine the genetic variability of the D-loop region in a Senegalese population with ovarian cancer. This research involved healthy and cancerous tissue samples obtained from Senegalese women diagnosed with ovarian cancer. Extraction of mtDNA from the D-loop region, followed by sequencing, yielded 49 nucleotide sequences. These sequences will be utilized to investigate several parameters of genetic variability: allelic frequencies, nucleotide frequencies, and mutation rates. Additionally, we will explore intra- and inter-individual diversity, assess genetic variability between different tissue types from distinct individuals, and illustrate both intra- and inter-individual haplotypic diversity.

In Senegal, ovarian cancer is the 3rd most common cancer in women with an incidence of 5.0/100,000 women. Thirty-five cancerous tissues, twenty-seven healthy tissues were included in this study. Due to the anatomical position of the ovary, the removal of a sample of suspicious tissue from each patient involves surgery through laparotomy or laparoscopy after obtaining consent. DNA extraction, polymerase chain reaction (PCR) and sequencing were performed to obtain sequences. BioEdit version 7.0.5.3 2005, Harlequin version 3.0, DnaSP version 5.10.01, MEGA 6 were used to perform the analyses. The results show a higher percentage of transition in cancerous tissues (91.45) than in healthy tissues (75.19) in contrast to transversions which are greater in healthy tissues (24.84) than in cancerous tissues (8.54), and the mutation rate (R) is also higher in cancerous tissues (10.712) than in healthy tissues (3.079). Analysis of the polymorphism revealed high values of haplotypic diversity in both cancerous tissues (0.662±0.085) and healthy tissues (0.997±0.011), and low nucleotide diversity values in both tissues (cancerous tissues=0.00922±0.00175; healthy tissues=0.01539±0.00175), these results show us that the genetic evolution of mutations in ovarian cancer has a strong polymorphism. It was also found that the value of the genetic distance between healthy tissues (0.016) was higher than that observed between cancerous tissues (0.009). The genetic distance between healthy and cancerous tissues is 0.015 closer than that observed between healthy tissues. The value of genetic differentiation between healthy and cancerous tissues is significant; this demonstrates a much faster proliferation of cancer cells. The objective of this study is, on the one hand, to better understand the target population by clearly identifying demographic parameters and on the other hand, to evaluate the involvement of somatic mutations and mitochondrial DNA gene expression in the occurrence of ovarian cancer in women in Senegal. The specific objectives are to search for mutations of interest by sequencing mtDNA genes with quasi-maternal inheritance and the impact of these mutations in the D-loop region in healthy and diseased tissues in the patient, but also to learn about the diversity, differentiation and genetic evolution of ovarian cancer in Senegalese women.

Oral cavity cancers appear to be more common among head and neck cancers (HNCs). Its incidence and etiology vary from country to country. In this study, the aim is to describe the epidemiological profile and emerge the risk factors for oral cancer in Senegal and their association with genetic alterations. The study is prospective and was conducted on 54 patients and 54 controls. Epidemiological and clinicopathological data were entered into Microsoft Excel. Descriptive and association analyses were determined using R software. Differentiation and genetic distance factors were performed with the Arlequin software. The results showed a female predominance, with a sex ratio of 0.86 and a mean age of 57.11 years. Age between 50 and 70 years, poor oral hygiene, smoking and cola consumption are risk factors for OCCs. Gum and cheek cancers as well as smokers and nonsmokers are genetically different. In view of these results, it seems that Senegalese patients have epidemiological profiles different to those of patients from other countries. The TP53 variants found in this study could be used as a biomarker in at-risk populations. Key words: Epidemiology, risk factors, TP53, mutations, cancer, oral cavity.

Introduction: Breast cancer is the most common malignant tumor in women and the leading cause of cancer-related death among female populations worldwide. Neoadjuvant chemotherapy is a systematic treatment administered before radiotherapy or surgery. It remains a preferred treatment option in cancer management, given its relevant results. However, certain single-nucleotide polymorphisms (SNPs) of the MDR1 gene are cited as factors that can induce differences between individuals in response to neoadjuvant chemotherapy. Objectives: The aim of this study was to evaluate the possible association between SNPs of the ABCB1 gene, specifically the polymorphisms C1236T and C3435T, and the response to neoadjuvant chemotherapy in Senegalese women with breast cancer. Methods: Our study included 60 senegalese patients diagnosed with breast cancer and treated with four different neoadjuvant chemotherapy protocols (AC, FAC, CARBO and TXT). Wealso included 15 healthy women as a control group. The sample type was a cytological biopsy. The C1236T and C3435T polymorphisms were genotyped using the PCR-RFLP method with respectively the following primers 5′-TTTTTCTCACGGTCCTGGTAG-3′; 5′-CATCCCCTCTGTGGTCATA-3′; and 5CAAAGAAATAAAGC-3′; 5′-CTTACATTAGGCAGTGACT CG-3′. As for restriction enzymes, we used HaeIII for exon 12 and DpnII for exon 26. Genotypic data was recorded in an Excel spreadsheet, and the results were analyzed using R Studio software, version 3.4.2. The genotypic frequencies were determined using GenePop software, version 4.3. Linear regression tests were conducted to determine association between the MDR1 gene polymorphisms and neoadjuvant chemotherapy using XLSTAT software (Lumivero, 2023), version 2023.2.0 (1411). Results: The CC genotype was found in a proportion of 58.3% for the C1236T SNP and 61.6% for the C3435T SNP. Healthy women were exclusively (100%) of the CC genotype for exons 12 and 26. The heterozygous CT genotype was not detected in any of the participants in our study. Linear regression tests mostly showed no association between chemotherapy protocols and the C1236T and C3435T polymorphisms of the ABCB1 gene. In the cases where the P-value was significant, the association was weak. Conclusion: In the present study, no significant association was found between the C1236T and C3435T polymorphisms of the MDR1 gene and neoadjuvant chemotherapy regimens in Senegalese women with breast cancer. Keywords: Breast Cancer, ABCB1, polymorphism, association, Senegal. Impact of Employee Compensation and Benefits on Operating Performance This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. Copyright © Author(s) retain the copyright of this article.

In Senegal in particular, ovarian cancer, which is one of the most common gynecological cancers, accounts for 2.8% of deaths. The most important risk factor is genetic, with 10% of cases occurring in a context of genetic predisposition. The sequencing of the human genome, which has led to the discovery of millions of sequence variations, makes it possible to study variations within sequences. These variations are limited to Single Nucleotide Polymorphisms (SNPs) and this common form of polymorphism occurs approximately every 1000 bases in the human genome and 1.8 million SNPs are currently listed according to [1]. The aim of this study is to gain a better understanding of the impact of mutations in the D-loop region of mtDNA on ovarian cancer in Senegalese women. This study involved searching for mutations in our study population after DNA extraction and sequencing. Mutations were found after a comparison of our sequences with the Cambridge reference sequence (NC_012920). The mutations found in the DNA studied extend from position 7 to position 16568 and most of these mutations are located in the hypervariate zones (HV1 and HV2). Heteroplasmy with three mutant alleles was also found in certain variants. Common mutations were found in both healthy and cancerous tissues, with almost identical frequencies in both types of tissue. This enabled us to understand the spread of tumor cells throughout the ovary.

Background: Acute rheumatic fever (ARF) is a systemic inflammatory disease resulting from an abnormal immune response to group A β-hemolytic streptococci. ARF is a major public health problem in developing countries, particularly in Senegal. The aim of this study was to evaluate the mutation penetrance and genetic diversity of exon 2 of the HLA-DRB1 gene in Senegalese patients with ARF. Results: DNA was extracted from the blood of patients with ARF. Exon 2 of the HLA-DRB1 gene was amplified by polymerase chain reaction and sequenced using the Sanger method. Bioinformatics software and databases (polyphen-2, SIFT and ProVean) were used to assess the pathogenicity of missense mutations. The results revealed a high level of polymorphism in exon 2 of the HLA-DRB1 gene, with 73 non-synonymous mutations between codons 21 and 89, which lie in the hypervariable region encoded by exon 2. Of the 73 variants tested, 44% were pathogenic, indicating their potential involvement in ARF onset. Conclusion: Our results indicate that the HLA-DRB1 mutations involvement in the onset of rheumatic fever.

Genetic factors have been implicated in the predisposition to cancer in Senegalese women. The arginine allele at codon 72 of exon 4 of the TP53 gene has been associated with a predisposition to several cancers in different populations. The objective of this study was to determine the effect of this polymorphism in a Senegalese population located in the locality of Widou Thiengoly. Two hundred and six (206) women living in Widou were recruited as well as thirty-two (32) control women, all assumed to be healthy. Genotyping of codon 72 of exon 4 of the TP53 gene was performed by Polymerase Chain Reaction and Restriction Fragment Length Polymorphism (PCR-RFLP) in 122 women. A significant association was found in the distribution of allelic and genotypic frequencies depending on the locality (p value: 5.6 x 10- 09; OR: 0.015; IC95: 3.5e-04-11e-02). However, no correlation was found between the risk factors (age, menopause, oral contraception, parity, gestational age, date of onset of first menstrual period, marital status) and the distribution of the allele frequency in the Widou locality. Due to the strong presence of the Arg allele in the Widou locality, a vast screening campaign for female cancers would be recommended.

Oral cavity cancers (OCC) are the most common malignancies in the subcategory of head and neck cancers, and represent the 6th most common cancer in the world. These cancers have become more frequent in individuals without a history of alcohol-tobacco abuse, which are the major risk factors. Other factors have been suggested, such as viral infections, but especially genetic alterations. This work establishes the epidemiological profile and researches the presence of viral DNA in OCCs. The epidemiology was highlighted with 105 patients using the Epi Info software. HPV DNA was sought in 50 samples of diseased tissue and blood by attempting to amplify its L1 region by PCR. At the epidemiological level, the results show a mean age of 53.2 years, a sex ratio of 0.8 and a low consumption of tobacco (16.2%) and alcohol (4.8%). HPV was not detected in any of the samples. Thus, the epidemiological profile of OCCs in Senegal is different from that in other countries, and HPV is not associated with its occurrence.