结直肠癌（CRC）是一种癌症形式，其特点是许多症状，并且容易转移到身体的不同器官。循环节律是在受CRC影响的患者中观察到的多个过程之一，这些循环节律的过程被发现失调。本研究旨在确定受CRC影响的患者中失调的生理过程，并将循环节律基因的表达谱与CRC患者的生存率进行关联。我们进行了广泛的微阵列基因表达流程，鉴定了471个差异表达的基因（DEGs），然后缩小了我们的搜索范围，挑选了43个对循环节律产生影响的DEGs。我们访问了循环基因数据库以获取循环节律特异基因。然后对DEGs进行了多层次功能注释，即通过ClueGO/CluePedia进行初步分析，并使用DAVID进行通路富集分析。我们的研究结果非常有意思，我们观察到受CRC影响的患者的生存率在约100个月时显著下降。此外，我们发现激素活性、异物代谢和PI3K-Akt信号通路经常失调。此外，我们还检测到ZFYVE基因家族和两个基因，即MYC和CDK4与CRC的发病和进展相关。本研究揭示了生物信息学对于简化我们对控制不同表型的不同基因相互作用的理解的重要性。 版权© 2023 Elsevier Inc. ISSN 12345678.

Colorectal cancer (CRC) is a form of cancer characterized by many symptoms and readily metastasizes to different organs in the body. Circadian rhythm is one of the many processes that is observed to be dysregulated in CRC-affected patients. In this study, we aim to identify the dysregulated physiological processes in CRC-affected patients and correlate the expression profiles of the circadian clock genes with CRC-patients' survival rates. We performed an extensive microarray gene expression pipeline, whereby 471 differentially expressed genes (DEGs) were identified, following which, we streamlined our search to 43 circadian clock affecting DEGs. The Circadian Gene Database was accessed to retrieve the circadian rhythm-specific genes. The DEGs were then subjected to multi-level functional annotation, i.e., preliminary analysis using ClueGO/CluePedia and pathway enrichment using DAVID. The findings of our study were interesting, wherein we observed that the survival percentage of CRC-affected patients dropped significantly around the 100th-month mark. Furthermore, we identified hormonal activity, xenobiotic metabolism, and PI3K-Akt signaling pathway to be frequently dysregulated cellular functions. Additionally, we detected that the ZFYVE family of genes and the two genes, namely MYC and CDK4 were the significant DEGs that are linked to the pathogenesis and progression of CRC. This study sheds light on the importance of bioinformatics to simplify our understanding of the interactions of different genes that control different phenotypes.Copyright © 2023. Published by Elsevier Inc.