Muhammad Abbas’s scientific contributions

In the current study, the role of cell division cycle-associated 8 (CDCA8) in colon adenocarcinoma (COAD) was analyzed through comprehensive expression and methylation analysis, genetic mutation inquiry, and prognostic assessment. Utilizing the UALCAN database, CDCA8 expression analysis revealed significant overexpression in carcinogenic cells compared to normal control samples, suggesting its involvement in COAD proliferation. Further examination of CDCA8 expression across various clinical parameters showed significant upregulation in different cancer development stages, racial groups, genders, and age classes within COAD patients, highlighting its critical role in cancer proliferation. Validation using the GEPIA2.0 tool confirmed that CDCA8 was highly expressed in COAD compared to normal controls. Additionally, analysis of CDCA8 expression across different cancer stages revealed dysregulation in all four stages, with the highest expression in stage I and the lowest in stage III. The study also investigated the promoter methylation level of CDCA8, finding a significant association between COAD samples and normal controls. Analysis of promoter methylation across various clinical parameters showed significant variations, with distinct methylation patterns observed across cancer stages, racial groups, genders, and age groups. Overall survival (OS) and disease-free survival (DFS) analyses using the KM plotter tool demonstrated that low CDCA8 expression was associated with shorter OS compared to high CDCA8 expression. In terms of DFS, COAD patients with higher CDCA8 expression experienced better DFS than those with low CDCA8 expression. Further validation of CDCA8 expression against survival data indicated that high CDCA8 expression was associated with better OS and DFS in COAD. Lastly, mutational assessment using the cBioPortal platform showed no significant mutations in COAD samples. Overall, these findings highlight the complex role of CDCA8 in COAD pathogenesis, underscoring its potential as a prognostic biomarker and therapeutic target in COAD management.

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor dysfunction and the loss of dopaminergic neurons. Emerging evidence suggests that immune system dysregulation and neuroinflammation play key roles in PD pathogenesis. In this study, we aimed to explore immune-related hub genes and associated signaling pathways using bioinformatics analysis of the GSE20141 dataset. We identified 250 differentially expressed genes (DEGs) and constructed a protein-protein interaction (PPI) network to pinpoint key hub genes. Four hub genes, FGF17, MED26, LCK, and RPS12, were identified as central players in the network, and functional enrichment analysis revealed significant involvement of several immune-related pathways.Key pathways enriched in our analysis included the JAK-STAT signaling pathway, NF-kappa B signaling pathway, and T cell receptor signaling pathway, all of which are known to regulate immune responses and inflammation in neurodegenerative diseases. Interestingly, our study also identified pathways less commonly associated with PD, such as the adipocytokine signaling pathway and osteoclast differentiation, suggesting a potential link between metabolic dysregulation and neuroinflammation. Our findings highlight both established and novel immune mechanisms in PD, suggesting potential therapeutic targets aimed at modulating immune responses. This study provides valuable insights into the complex immune landscape of PD and emphasizes the importance of immune modulation in understanding and treating this debilitating disease. Further research is needed to validate the role of the identified hub genes and pathways and to explore their potential as targets for PD therapy.