Department of Biochemistry

Permanent URI for this communityhttp://itsupport.cu.edu.ng:4000/handle/123456789/28750

Welcome to the Department of Biochemistry

Browse

Author: search.filters.author.Zakari, SuleimanHas files: Yes

Search Results

Now showing 1 - 8 of 8
  • No Thumbnail Available
    Item
    Mechanisms of carbamate resistance in the malaria vector: Anopheles gambiae
    (Parasite Epidemiology and Control, 2026-02-18) Cleanclay, Wisdom D.; Akanni, Mosunmola H.; Bajepade, Tobiloba I.; Ajeoge, Joshua K.; Zakari, Suleiman
    In Africa, the female Anopheles gambiae is the primary malaria vector and a key target of vector control measures. The four principal classes of insecticides used in the control of these vectors are pyrethroids, organophosphates, carbamates and organochlorines. Historically, pyrethroids were the main type of insecticides employed to impregnate insecticide-treated nets because they are less toxic to humans and more effective against mosquitoes. The effectiveness of these interventions is however currently challenged by the development of pyrethroid-resistant mosquito populations. The World Health Organization recommends alternative or rotational use of carbamate insecticides in pyrethroid resistant areas. The mechanism of action of carbamates is to inhibit acetylcholinesterase reversibly to trigger the build-up of acetylcholine in mosquito nerves and consequent paralysis and death of the mosquito. However, carbamate resistance is also on the rise, and poses significant issues to malaria control systems. Notably, the mechanisms of carbamate resistance in Anopheles gambiae are target site mutations in the acetylcholinesterase gene and increased detoxification of carbamate by enzymes, including esterases and cytochrome P450s. This review presents a synthesis of existing information on the molecular and metabolic pathways of carbamate resistance in the Anopheles gambiae and discuss their consequences for the control of malaria vector. Understanding these resistance mechanisms is crucial for sustaining the effectiveness of IRS, informing insecticide resistance management strategies, and guiding malaria control policies in areas where pyrethroid resistance is increasing. AnophelesAnophelesAnophelesKeywords: Carbamate, Insecticide Resistance, female Anopheles gambiae, Malaria Vector
  • No Thumbnail Available
    Item
    Photosensitizers in photodynamic therapy: An advancement in cancer treatment
    (Results in Chemistry (Elsevier), 2024) Oluwajembola, Abimbola Mary; Cleanclay, Wisdom D.; Onyia, Abimbola F.; Chikere, Bruno N.; Zakari, Suleiman; Ndifreke, Ebong; De Campos, Opeyemi C.
    Photodynamic therapy (PDT) is a clinically proven advancement in cancer treatment that has progressively gained consideration as a possible method of cancer treatment over time. This therapy, which involves the administration of a photosensitizing drug before activation of the drug with light from a source such as a laser to produce a cytotoxic effect, is minimally invasive and could increase the life expectancy of cancer patients. Cancer has been a major threat to human health, and it affects the quality of life of cancer patients as it is one of the topmost causes of mortality worldwide. The burden of cancer has been projected to increase to 2.1 million new cases and 1.4 million deaths in Africa by 2040. It is therefore expedient to put in more effort in proffering preventive measures, more efficient treatments, and possible cures for this disease. Recent studies have shown that many types of tumors can be destroyed using PDT. Tumor cells are destroyed via apoptosis, necrosis, and autophagy through some mechanisms in PDT. The successful outcome of this therapy depends greatly on three components which are photosensitizer (PS), light and molecular oxygen. Out of these three, photosensitizer is the most essential. Among the characteristics of a potent PS are the presence of a tetrapyrrole structure and the ability to initiate a photodynamic reaction when irradiated typically at a wavelength between 600 nm and 800 nm, although some PS can function effectively outside this range. This review highlights the effectiveness of PDT in the treatment of cancer and emphasizes the importance of PS, with more focus on those derived from natural sources, in determining the outcome of the therapy.
  • No Thumbnail Available
    Item
    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
  • No Thumbnail Available
    Item
    A ReviewofNovelCancerTherapeuticsandCurrent Research Trends
    (Wiley The Scientific World Journal Volume 2025, 2025) Oluwajembola, Abimbola Mary; Zakari, Suleiman; Cleanclay, Wisdom D.; Ayeni, Timothy; Adebosoye, Adewale; Okoh, Olayinka S.; Folamade, Joshua; Bawa, Inalegwu; Ogunlana, OlubankeOlujoke
    The uncheckedgrowthandspreadofaberrantcellsdescribeawidelydiversecollectionofdisordersthatcollectivelyconstitute cancer. Conventionaltherapiesforcancer,includingradiationtherapy,chemotherapy,andsurgery,haveincreasedthechances of survivalsignificantly inmostpatients.Thesetraditionalmethodsusuallyresultinlowtumorortumorcellspecificity, significant systemictoxicity,andthedevelopmentofdrugresistance.Thisreviewsummarizesupdatesincancertherapy,some of whichincludecutting-edgetherapiesrepresentedbyCAR-Ttherapy,targetedtherapies,genetherapy,arginine-depriving therapy, mitochondria-targetedtherapies,neutrophil-targetedtherapies,andthelatestPROTACtechnologyforproteolysis- targeting chimera.Ithasemphasizedmechanismsunderlyingthesenewtherapeuticstrategiesandtheirtranslationalpotential for treatinghumancancers.Wefurtherdiscuss,foreachapproach,thechallenges,limitations,sideeffects, anddelivery systems. Thereviewproceedswithadynamicchangeinthelandscapeofcancerresearchinbiology,wheremachinelearning and artificial intelligenceareincreasinglyimportanttoimproveourunderstandingofthemechanismsofcancerandtreatment responses. Wealsodescribethepotentialofstemcelltherapy,metabolomics,andnoveldrugdeliverysystemstowardbetter patient outcomes.Thepaperpullstogethersomeofthecurrentresearch findings andresultsofclinicaltrialsinnew therapeutic developmentsandemergingareasofresearchthatholdoutexcitingpromisesforthefutureprogressofcancer treatment
  • No Thumbnail Available
    Item
    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.
  • No Thumbnail Available
    Item
    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
  • No Thumbnail Available
    Item
    Updates onSPOPGeneMutationsinProstateCancerand Computational InsightsFromTCGAcBioPortalDatabase
    (Wiley Scientifica Volume 2025, 2025) Zakari, Suleiman; Rotimi, Solomon O.; Bholah, Chandra Tatsha; Ogunlana, OlubankeO.
    Speckle-type poxvirusandzinc*ngerprotein(SPOP)hasemergedasakeyfocusinprostatecancerresearchduetoitscriticalrole in regulatingtheandrogenreceptor(AR)signalingpathway./isreviewaimstocomprehensivelysummarizecurrentknowledge on SPOPgenemutationsinprostatecancer,emphasizingtheirimportanceindiseasecharacterizationandidenti*cationof therapeutic targets.Asystematicliteraturesearchwasconductedacrossmultipledatabases,includingPubMed,WebofScience, Scopus, andGoogleScholar.Inaddition,thisstudyusescomputationalapproachesanddatafromtheTCGAcBioPortaldatabase to explorethelandscapeofSPOPmutationsinprostatecancer.Afterscreening682articlesandfollowingsystematicselection steps, 56high-qualityarticleswereincluded.ComputationalanalysisofTCGAcBioPortaldatarevealedaSPOPmutation prevalence of5%-6%,alongwithsigni*cantalterationsinARsignalingandepigeneticregulation.SPOPmutationsdisrupt substrate recognition,leadingtodysregulationofdownstreampathwayssuchasARsignalingandchromatinremodeling. Notably, SPOP-mutantprostatecancersaremutuallyexclusivewithTMPRSS2-ERGfusionsandenrichedforWntpathway alterations. PatientswithSPOPmutationsdemonstrateprolongedresponsestoandrogendeprivationtherapy(ADT),although concurrent mutationsinTP53orDNArepairgenesnegativelyimpactoutcomes.Whiletheirprognosticsigni*cancecontinuesto evolve, theirimpactontheARpathwayhighlightstheirpotentialastherapeutictargets./eclinicalimplicationsofSPOP mutations aresubstantial,astheyarelinkedtovariationsintreatmentresponseanddiseaseprogression,thusservingasvaluable biomarkers forriskstrati*cationandprognosis.
  • No Thumbnail Available
    Item
    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.