Genomic Analysis Reveals Heterogeneity Between Lesions in Synchronous Primary Right-Sided and Left-Sided Colon Cancer
| Autor: | Feng Gao, Qian Zhang, Weiyuan Zhang, Hanqing Hu, Ziming Yuan, Tianyu Qiao, Zhifeng Gao, Guiyu Wang, Tianyi Ma, Rui Huang, Qingchao Tang, Meng Wang, Yinghu Jin |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty QH301-705.5 Colorectal cancer Sequencing data left-sided colon cancer clonality colorectal cancer Biology Gene mutation Biochemistry Genetics and Molecular Biology (miscellaneous) Biochemistry Left sided Genome Loss of heterozygosity metachronous colorectal cancer 03 medical and health sciences 0302 clinical medicine medicine Molecular Biosciences Copy-number variation Biology (General) right-sided colon cancer genome Molecular Biology Original Research General Commentary synchronous multiple primary cancer Clonal architecture synchronous colorectal cancer medicine.disease 030104 developmental biology 030220 oncology & carcinogenesis heterogeneity |
| Zdroj: | Frontiers in Molecular Biosciences Frontiers in Molecular Biosciences, Vol 8 (2021) |
| ISSN: | 2296-889X |
| DOI: | 10.3389/fmolb.2021.689466 |
| Popis: | Background: The synchronous primary right-sided and left-sided colon cancer (sRL-CC) is a peculiar subtype of colorectal cancer. However, the genomic landscape of sRL-CC remains elusive.Methods: Twenty-eight paired tumor samples and their corresponding normal mucosa samples from 14 patients were collected from the Second Affiliated Hospital of Harbin Medical University from 2011 to 2018. The clinical–pathological data were obtained, and whole-exome sequencing was performed based on formalin-fixed and paraffin-embedded samples of these patients, and then, comprehensive bioinformatic analyses were conducted.Results: Both the lesions of sRL-CC presented dissimilar histological grade and differentiation. Based on sequencing data, few overlapping SNV signatures, onco-driver gene mutations, and SMGs were identified. Moreover, the paired lesions harbored a different distribution of copy number variants (CNVs) and loss of heterozygosity. The clonal architecture analysis demonstrated the polyclonal origin of sRL-CC and inter-cancerous heterogeneity between two lesions.Conclusion: Our work provides evidence that lesions of sRL-CC share few overlapping mutational signatures and CNVs, and may originate from different clones. |
| Databáze: | OpenAIRE |
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