The transition of
CML to the blastic phase represents a critical factor leading to mortality inthis cancer, and its underlying mechanisms remain poorly understood.CDC۲۷, a component of the APC/C complex, plays a vital role in precisely controlling transitions inthe cell cycle, which is essential for normal cell division and development. When
CDC۲۷ and theAPC/C complex are dysregulated, the development and progression of cancer may occur. The CDC۲۷gene has eleven pseudogenes.Pseudogene is a DNA sequence that mimics a functional gene but has either lost its capability to codefor proteins or remains unexpressed. Changes in the expression of pseudogenes have been identifiedacross different cancer types, and their irregular activity can affect critical cellular processes like cellproliferation, apoptosis, and metastasis.In this study, RNA-seq data from the EGA with accession EGAS۰۰۰۰۱۰۰۳۰۷۱ were employed. TheGRCh۳۸ was used as reference genome and HISAT۲ as the mapper. Stringtie which is equipped withefficient algorithms for recovering transcript structure and estimating abundance, was employed toanalyze the bulk
RNA-Seq reads aligned to the reference genome. We utilized both DESeq۲ and edgeRpackages for the analysis of Differentially Expressed Genes (DEGs). Analyses were conducted in bothpaired and unpaired approaches.As a result, in all blastic phase
CML patients, the expression of three pseudogenes including CDC۲۷P۹,CDC۲۷P۱۰, and CDC۲۷P۱۱, with a False Discovery Rate (FDR) less than ۰.۰۱ and Log۲FC>۱ washigher than chronic phase of CML, while the expression of other
CDC۲۷ pseudogenes between thesetwo groups was not significantly different. Continuous and thorough investigations are required toassess target molecules whose expression is influenced by these three pseudogenes including CDC۲۷gene that plays pivotal role in regulating cell cycle and other cellular processes. Furthermore, it willhelp explore potential therapeutic options.