Imtiaz Ali Soomro’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.

Liver hepatocellular carcinoma (LIHC) is a prevalent and deadly form of liver cancer characterized by significant genetic and epigenetic alterations. This study focuses on the role of COL1A1, a gene implicated in various cancers, by analyzing its expression, promoter methylation, and genetic mutations in LIHC. Using the UALCAN database, we observed a significant upregulation of COL1A1 in LIHC samples compared to normal controls, suggesting its involvement in cancer progression. This finding was corroborated by GEPIA2 analysis, which also showed elevated COL1A1 expression in LIHC. Further analysis using UALCAN revealed that COL1A1 expression was consistently upregulated across different cancer stages, races, ages, and genders of LIHC patients, indicating its broad role in tumor development. Validation with GEPIA2 confirmed these observations at individual cancer stages. Methylation analysis showed that COL1A1 was hypomethylated in LIHC samples relative to normal controls, a factor known to enhance tumor development. Interestingly, stage-specific analysis indicated hypermethylation of COL1A1 in stage 4 LIHC, reflecting its complex regulatory mechanisms. Survival analysis using KM plotter and GEPIA2 indicated that higher COL1A1 expression was associated with lower overall survival (OS) rates in LIHC patients, although the results were not statistically significant. Genetic alteration analysis via cBioPortal identified a low mutation frequency (3%) in COL1A1, suggesting limited impact on LIHC through genetic mutations alone. In conclusion, our comprehensive analysis highlights COL1A1 as a potentially significant player in LIHC progression through its aberrant expression and methylation, although its direct genetic mutations appear to have minimal effect. These findings underscore the need for further research to fully elucidate COL1A1's role and therapeutic potential in LIHC.

The investigation focused on explaining the role of PIM1 expression and its regulatory mechanism in liver hepatocellular carcinoma (LIHC). Using the UALCAN database, PIM1 expression assessment revealed a critical down-regulation in malignant cells as compared with normal controls, suggesting its contribution in LIHC proliferation. Further, taking apart PIM1 expression across various boundaries showed unsurprising down-regulation in different cancer development stages, racial groups, genders and age classes inside LIHC patients, characteristics for its essential role in cancer proliferation. Validation of PIM1 expression done by Utilizing the GEPIA2.0 database, which showed PIM1 was lowly expressed in LIHC cancer as compared to normal control samples. Additionally, dismantling PIM1 validation across different stages of cancer showed dysregulation in all four stage with highest expression in stage III and the lowest expression in stage IV. Subsequently, this study investigated the promoter methylation level of PIM1, elucidating a critical correlation between LIHC samples and normal control samples. Analyzing promoter methylation across v 1 arious clinical parameters uncovered huge variations, with particular methylation patterns seen across cancer stages, race groups, genders and age groups. Survival analysis(OS and RFS) utilizing the KM plotter tool showed an epic association between PIM1 expression levels in LIHC patients, with low PIM1 expression exhibited with higher overall survival (OS) while high PIM1 expression experienced shorter DFS. Further upon validation of results of PIM1 expression level. We divided the LIHC patients into low and high expression groups of PIM1. In LIHC, high PIM1 expression level was associated with good overall survival (OS) while low PIM1 expression level was associated with good DFS in LIHC patients. Additionally, et al. 1235 Migration Letters mutational analysis utilizing the cBioPortal stage revealed that no critical change found in LIHC samples. Overall, these findings cause to notice the intricate contribution of PIM1 in LIHC pathogenesis, underlining its importance as a prognostic biomarker and supportive therapeutic agent in LIHC management.