Suleiman Zakari

Malaria remains a major global health challenge, particularly in sub‐Saharan Africa where Anopheles mosquitoes transmit the Plasmodium parasites. Resistance to insecticides remains an obstacle in spite of the efforts to control malaria vector. The interaction between Plasmodium parasites and mosquito vectors, with a focus on the immunity of mosquitoes and approaches to combat malaria, is examined in this review. This review explores the potential of genetic approaches including CRISPR‐Cas9, Wolbachia , RNA interference (RNAi), and symbiont‐based strategies for the control of malaria vector. The innate immune system of Anopheles mosquitoes that identify, recognize, and limit Plasmodium infection through pathogen recognition receptors, signaling pathways, and effector mechanisms like antimicrobial peptides and melanization is well developed. However, Plasmodium has developed several evasion mechanisms to establish infection. This led to various genetic modification techniques being designed to reduce vector population and transmission. Gene drive such as CRISPR‐Cas9 can introduce genetic alterations to interfere with the transmission of malaria; Wolbachia interferes with vector competence, RNAi‐mediated gene to target relevant genes involved in reproduction and survival. Self‐limiting strategies such as RIDL and pgSIT genetically modified insect releasement to the environment. mosGILT is an emerging immune regulator which has shown relevance in blocking transmission. This review explores the potential of these genetic approaches in malaria vector control efforts, highlighting their advantages and imitations. Further research should explore mosquito immune genes and pathways in developing innovative and acceptable genetic vector control approaches.

The unchecked growth and spread of aberrant cells describe a widely diverse collection of disorders that collectively constitute cancer. Conventional therapies for cancer, including radiation therapy, chemotherapy, and surgery, have increased the chances of survival significantly in most patients. These traditional methods usually result in low tumor or tumor cell specificity, significant systemic toxicity, and the development of drug resistance. This review summarizes updates in cancer therapy, some of which include cutting‐edge therapies represented by CAR‐T therapy, targeted therapies, gene therapy, arginine‐depriving therapy, mitochondria‐targeted therapies, neutrophil‐targeted therapies, and the latest PROTAC technology for proteolysis‐targeting chimera. It has emphasized mechanisms underlying these new therapeutic strategies and their translational potential for treating human cancers. We further discuss, for each approach, the challenges, limitations, side effects, and delivery systems. The review proceeds with a dynamic change in the landscape of cancer research in biology, where machine learning and artificial intelligence are increasingly important to improve our understanding of the mechanisms of cancer and treatment responses. We also describe the potential of stem cell therapy, metabolomics, and novel drug delivery systems toward better patient outcomes. The paper pulls together some of the current research findings and results of clinical trials in new therapeutic developments and emerging areas of research that hold out exciting promises for the future progress of cancer treatment.

Speckle‐type pox virus and zinc finger protein (SPOP) has emerged as a key focus in prostate cancer research due to its critical role in regulating the androgen receptor (AR) signaling pathway. This review aims to comprehensively summarize current knowledge on SPOP gene mutations in prostate cancer, emphasizing their importance in disease characterization and identification of therapeutic targets. A systematic literature search was conducted across multiple databases, including PubMed, Web of Science, Scopus, and Google Scholar. In addition, this study uses computational approaches and data from the TCGA cBioPortal database to explore the landscape of SPOP mutations in prostate cancer. After screening 682 articles and following systematic selection steps, 56 high‐quality articles were included. Computational analysis of TCGA cBioPortal data revealed a SPOP mutation prevalence of 5%‐6%, along with significant alterations in AR signaling and epigenetic regulation. SPOP mutations disrupt substrate recognition, leading to dysregulation of downstream pathways such as AR signaling and chromatin remodeling. Notably, SPOP‐mutant prostate cancers are mutually exclusive with TMPRSS2‐ERG fusions and enriched for Wnt pathway alterations. Patients with SPOP mutations demonstrate prolonged responses to androgen deprivation therapy (ADT), although concurrent mutations in TP53 or DNA repair genes negatively impact outcomes. While their prognostic significance continues to evolve, their impact on the AR pathway highlights their potential as therapeutic targets. The clinical implications of SPOP mutations are substantial, as they are linked to variations in treatment response and disease progression, thus serving as valuable biomarkers for risk stratification and prognosis.

Study’s Excerpt: Full Abstract: The escalating challenge of bacterial resistance to antibiotics has prompted interest in exploring the antibacterial potential of Calotropis procera. To investigate the antibacterial efficacy of C. procera, the leaves and stems of the plant were collected and macerated in ethanol to obtain crude extracts. Using GC-MS analysis, we identified key phytochemicals in the leaf and stem extracts of the plant. Escherichia coli, Pseudomonas aeruginosa, Bacillus subtilis, and Staphylococcus aureus were selected for the study. We used the Kirby Bauer disc diffusion test to evaluate bacterial susceptibility to C. procera extracts, while the minimum inhibitory concentration (MIC) was determined using microdilution plates. Additionally, time-kill kinetics were assessed for each bacterium. The stem extract demonstrated superior activity, achieving complete bactericidal effects against Pseudomonas aeruginosa and Escherichia coli within 20 hours. Phytochemicals such as Lupenyl Acetate and Phytol were identified as key bioactive compounds. These findings highlight the potential of C. procera as a natural source for developing antimicrobial agents. Statistical analysis strongly suggests that C. procera extracts the test bacteria (p = 0.001). In conclusion, the leaf and stem extracts of C. procera exhibit distinct variations in the relative abundance of bioactive compounds and further demonstrate multiple antimicrobial mechanisms. These properties of the plant highlight its potential as a valuable resource in addressing antibiotic-resistant bacterial strains.

Study’s Excerpt/Novelty Full Abstract It is believed that among others, magnetic nanoparticles possess the ability for stability, biocompatibility, and cost-effectiveness in biomedicine. Despite many types of magnetic materials, including non-noble metals like iron, cobalt, and nickel, the potential applications seem not to have been as explored as with noble metals like gold. This review aimed to give a broad overview of magnetic nanoparticles, more so their synthesis, characterization, and various applications in disease detection, such as cancer diagnostics. This was a literature review design; the data were sourced from peer-reviewed articles published within the last ten years. The criteria for selecting studies included that they had to directly address magnetic nanoparticle synthesis, design, and application. For this purpose, databases such as PubMed, Scopus, and Google scholar were tapped into to ensure the widest possible relevant coverage. Different approaches, such as chemical or mechanical ones, are used to create magnetic nanoparticles. The paper outlines the advantages of magnetic nanoparticles in the treatment of diseases. Furthermore, as most of the categorization techniques now in use are found to be inaccurate and unreliable, they have now shown certain flaws. Therefore, the use of magnetic nanoparticles in biomedical applications, especially in diagnosing and treating diseases, holds great promise. However, improvement in the methodology for the classification of nanoparticles is quite necessary. Such standard protocols for synthesizing and characterizing magnetic nanoparticles should be developed in the near future, with new therapeutic applications being explored in this domain.

Context: Prostate cancer remains a significant global health concern, and understanding the molecular drivers of this disease is crucial for developing effective diagnostic and therapeutic strategies. Steroid receptor coactivator-3 (SRC-3), a member of the SRC family, has emerged as a key player in prostate cancer pathogenesis. Aims: To examine the role of SRC-3 in prostate cancer, encompassing molecular mechanisms, clinical implications, and therapeutic opportunities. Methods: A systematic literature search following PRISMA guidelines was conducted in PubMed, PMC, and other relevant databases to identify studies that investigate SRC-3 in prostate cancer. Results: 785 articles were retrieved from databases using specific keywords and MeSH terms related to SRC-3 and Prostate Cancer. After removing 461 duplicates, 260 articles were excluded based on title and abstract review. Subsequently, a comprehensive screening by three researchers resulted in 47 relevant articles for this systematic review. Evidence suggests that SRC-3 expression correlates with prostate cancer aggressiveness, disease recurrence, and poor patient outcomes. Its potential as a diagnostic biomarker and therapeutic target if explored, offers insights into personalized medicine approaches. Conclusions: SRC-3 plays a pivotal role in prostate cancer, influencing disease progression and clinical outcomes. Understanding the molecular intricacies of SRC-3 in prostate cancer offers new opportunities for precision medicine and innovative therapeutic approaches. This review provides a comprehensive overview of SRC-3's involvement in prostate cancer, emphasizing its clinical relevance and potential as a therapeutic target, ultimately contributing to improved patient care in the era of personalized oncology.

Background: Prostate cancer remains a significant global health concern, and understanding the molecular drivers of this disease is crucial for developing effective diagnostic and therapeutic strategies. Steroid Receptor Coactivator-3 (SRC-3), a member of the SRC family, has emerged as a key player in prostate cancer pathogenesis. This review comprehensively examine the role of SRC-3 in prostate cancer, encompassing molecular mechanisms, clinical implications, and therapeutic opportunities. Methods: A systematic literature search following PRISMA guidelines was conducted in PubMed, PMC, and other relevant databases to identify studies that investigate SRC-3 in prostate cancer. A total of 67 articles were selected based on predetermined inclusion criteria. Results: 785 articles were retrieved from databases using specific keywords and MeSH terms related to SRC-3 and Prostate Cancer. After removing 461 duplicates, 260 articles were excluded based on title and abstract review. Subsequently, a comprehensive screening by three researchers resulted in 47 relevant articles for this systematic review. We summarize its contributions to AR-mediated transcriptional regulation, tumor growth, and metastasis. Evidence suggests that SRC-3 expression correlates with prostate cancer aggressiveness, disease recurrence, and poor patient outcomes. Its potential as a diagnostic biomarker and therapeutic target is explored, offering insights into personalized medicine approaches. Conclusions: SRC-3 plays a pivotal role in prostate cancer, influencing disease progression and clinical outcomes. Understanding the molecular intricacies of SRC-3 in prostate cancer offers new opportunities for precision medicine and innovative therapeutic approaches. This review provides a comprehensive overview of SRC-3's involvement in prostate cancer, emphasizing its clinical relevance and potential as a therapeutic target, ultimately contributing to improved patient care in the era of personalized oncology.

Background: Prostate cancer is a global health concern, necessitating ongoing research to enhance our comprehension of its molecular foundations and develop more efficacious therapeutic approaches. Among the emerging protagonists in this arena is Speckle-type POZ (pox virus and zinc finger protein) (SPOP), an E3 ubiquitin ligase substrate adaptor protein. SPOP's recent ascent to prominence in prostate cancer research is attributed to its crucial role in regulating the Androgen Receptor (AR) signaling pathway. This systematic review aims to provide a comprehensive synthesis of existing knowledge concerning SPOP mutations in prostate cancer. It seeks to elucidate their significance in characterizing the disease and their potential as therapeutic targets. Methods: A systematic literature search was conducted in multiple databases, including PubMed, Web of science, Scopus and google scholar to identify relevant studies published up to September 2023. Eligible studies included investigations of SPOP mutations in prostate cancer and their implications. Data extraction, quality assessment, and synthesis were performed in conformity to the PRISMA guidelines. Results: The review revealed that SPOP mutations are recurrent events in prostate cancer, with a notable prevalence in specific molecular subtypes. These mutations primarily affect the MATH domain of SPOP, disrupting its substrate recognition function. Notably, SPOP mutations have profound consequences on the AR signaling pathway, leading to increased AR protein stability and transcriptional activity. The clinical implications of SPOP mutations remain diverse, with varying associations with prognostic outcomes. Conclusion: SPOP mutations represent a significant facet of prostate cancer biology, influencing disease heterogeneity and clinical behavior. While their precise prognostic significance is evolving, their functional impact on the AR pathway highlights their potential as therapeutic targets. This systematic review provides a comprehensive overview of SPOP mutations in prostate cancer, contributing to our understanding of the disease's molecular landscape and therapeutic avenues.