Browsing by Author "Ogunlana, Olubanke Olujoke"

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    Association between CYP17A1 and HSD3B1 gene polymorphisms and testosterone levels in Nigerian prostate cancer patients
    (Scientific Reports, 2025) Ekenwaneze, Christogonus Chichebe; Zakari, Suleiman; Amadi, Emmanuel Chimuebuka; Okesola, Mary; Rotimi, Solomon Oladapo; Oyekan, Ademola; Fatiregun, Olamijulo; Iweala, Emeka Eze Joshua; Odedina, Folakemi T.; Ogunlana, Olubanke Olujoke
    Prostate cancer (PCa) is a primary global health concern and the leading cause of cancer-related deaths in men. Genetic variation in androgen pathways is essential in PCa development and progression. Cytochrome P450 17A1 (CYP17A1) gene encodes a critical metabolic enzyme involved in testosterone (TT) synthesis, as it converts cholesterol into androstenedione. Similarly, the 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) gene encodes an enzyme that catalyses the conversion of dehydroepiandrosterone (DHEA) to androstenedione, a critical precursor for TT production. The case-control study was conducted on 40 PCa patients and 40 healthy males with matching ages. Detection of CYP17A1 and HSD3B1 polymorphisms was done using the TaqMan genotyping assay, and estimation of TT levels in serum was done using the enzyme-linked immunosorbent assay technique. Detected genotypes were AA, AG, and GG for CYP17A1, and AA and CA for HSD3B1; the adrenalpermissive CC genotype of HSD3B1 was absent. The TT levels were significantly lower in PCa patients (p = 0.00148). No significant associations were found between polymorphisms in CYP17A1, HSD3B1 and TT levels. The HSD3B1 CA genotype showed a non-significant trend toward increased PCa risk (OR = 2.39, p = 0.183) that requires validation in larger studies before any clinical relevance can be established.
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    Association between CYP17A1 and HSD3B1 gene polymorphisms and testosterone levels in Nigerian prostate cancer patients
    (Scientific reports, 2025) Ekenwaneze, Christogonus Chichebe; Zakari, Suleiman; Amadi, Emmanuel Chimuebuka; Okesola, Mary; Rotimi, Solomon Oladapo; Oyekan, Ademola; Fatiregun, Olamijulo; Iweala, Emeka Eze Joshua; Odedina, Folakemi T.; Ogunlana, Olubanke Olujoke
    Prostate cancer (PCa) is a primary global health concern and the leading cause of cancer-related deaths in men. Genetic variation in androgen pathways is essential in PCa development and progression. Cytochrome P450 17A1 (CYP17A1) gene encodes a critical metabolic enzyme involved in testosterone (TT) synthesis, as it converts cholesterol into androstenedione. Similarly, the 3β-hydroxysteroid dehydrogenase type 1 (HSD3B1) gene encodes an enzyme that catalyses the conversion of dehydroepiandrosterone (DHEA) to androstenedione, a critical precursor for TT production. The case-control study was conducted on 40 PCa patients and 40 healthy males with matching ages. Detection of CYP17A1 and HSD3B1 polymorphisms was done using the TaqMan genotyping assay, and estimation of TT levels in serum was done using the enzyme-linked immunosorbent assay technique. Detected genotypes were AA, AG, and GG for CYP17A1, and AA and CA for HSD3B1; the adrenalpermissive CC genotype of HSD3B1 was absent. The TT levels were significantly lower in PCa patients (p = 0.00148). No significant associations were found between polymorphisms in CYP17A1, HSD3B1 and TT levels. The HSD3B1 CA genotype showed a non-significant trend toward increased PCa risk (OR = 2.39, p = 0.183) that requires validation in larger studies before any clinical relevance can be established.
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    Surveillance of Wolbachia infection in mosquito species in Ota, Ogun State, Nigeria
    (Discover Applied Sciences, 2025-03-27) Tebamifor, Mercy Eyitomi; Cleanclay, Wisdom D.; Mamudu, Collins Ojonugwa; Ogunlana, Olubanke Olujoke
    Introduction In light of climate change, proliferation of mosquito-borne diseases like dengue and malaria is a mounting concern, driven by expanding mosquito populations as a result of favorable environment for their survival. Addressing public health challenges caused by mosquitoes demands constant innovation and sustainable solutions. Objective This study responds to recent reports of Wolbachia infections in West African mosquito species, suggesting their potential as biocontrol agents for disease vectors. We seek to detect the presence of Wolbachia pipientis in different mosquito species in Ota and identify mosquito species present in the area. Method We conducted a comprehensive mosquito larval surveillance in Ota, Ogun State, Nigeria using a systematic stratified random sampling method from November 2022 to March 2023 to assess mosquito species distribution and Wolbachia infection. During this period, we surveyed mosquito larvae in various sites, rearing them to adulthood. We meticulously identified species, sex, and collection locations then, stored specimens at − 20 °C. Sodium chloride precipitation protocol was employed to extract DNA from the mosquitoes individually. Polymerase chain reaction (PCR) analysis was carried out using one to one point five microliter of DNA, with distilled water as negative control. Results Out of 1265 emerging young adult mosquitoes, 62.1% were females, while 37.1% were males. Aedes species constituted 22.2%, Anopheles 37.2%, and Culex 40.6% of the population. DNA analysis identified Wolbachia infection in Ae. albopictus and Ae. aegypti, with wsp gene sizes ranging from 590 to 632 bp, confirming Wolbachia presence by sequencing. Conclusion Our study is the first report on Wolbachia presence in Aedes sp within this region, which suggests that this mosquito species is a less likely vector for dengue virus and other related infectious agents. The study highlights the importance of continuous mosquito population and breeding site monitoring for potential biocontrol interventions against disease vectors.
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    Unraveling the potential of USP8 as a therapeutic target for overcoming c-Met-mediated resistance in breast cancer: A review
    (Cancer Treatment and Research Communications, 2026) Amuji, Doris Nnenna; Zakari, Suleiman; Pirisola, Ayomikun Joshua; Ogunlana, Olubanke Olujoke; Iweala, Emeka E.J.
    Therapeutic resistance remains a serious challenge in breast cancer, and abnormal c-mesenchymal epithelial transition factor (c-Met) receptor tyrosine kinase (RTK) activation contributes to therapeutic resistance in many. Ubiquitin-specific peptidase 8 (USP8) has emerged as a modulator of RTK stability through deubiquitination and endosomal trafficking, and preclinical studies show that inhibition of USP8 speeds up ubiquitin-dependent degradation of RTKs, including c-Met and EGFR, suppresses PI3K/Akt and MAPK signaling, and reverses resis tance phenotypes. In this review, we summarize mechanistic evidence for USP8 regulation of c-Met and related RTKs, explore preclinical studies that assess inhibition of USP8 as a strategy to sensitize RTK-driven tumors, and highlight translational limitations such as drug selectivity, toxicity, dosing, pharmacodynamics biomarkers, and patient selection that must be addressed prior to a clinical trial in breast cancer. While the therapeutic targeting of USP8 is promising, direct validation in breast cancer models and the development of robust pharmacodynamic markers and inhibitors that are clinically graded remain crucial next phase
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    Unraveling the potential of USPS as a therapeutic target for overcoming c-Met-mediated resistnce in breast cancer: A view
    (Cancer Treatment and Research Communication, 2026) Amnji, Doris Nnenna; Zakari, Suleiman; Pirisola, Ayomikun Joshua; Ogunlana, Olubanke Olujoke