Evolutionary patterns of chromosomal instability and mismatch repair deficiency in proximal and distal colorectal cancer

Golas, Monika M.; Gunawan, Bastian; Cakir, Meliha; Cameron, Silke; Enders, Christina; Liersch, Torsten; Füzesi, L.; Sander, Bjoern

doi:10.1111/codi.15946

Cited by 13 publications

(6 citation statements)

References 82 publications

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“…Interestingly, our analysis of Boolean implication networks revealed a larger contribution of genes specifically present in Boolean implication networks in the case of COAD bearing GAIN-Chr20. Our result in COAD is in agreement with the observation that GAIN-Chr20 is a frequent and early-appearing abnormality in colon cancer [ 35 – 38 ], thus suggesting that GAIN-Chr20 exerts a stronger cancer driving force in the context of colon cancer in comparison to other cancer types, such as STAD, BLCA and CESC. Indeed, several research groups have reported the importance of Chr20 amplification in colon cancer, and attributed such effect to the location of multiple oncogenes such as BCL2L1, AURKA, TPX2, and SRC on this chromosome [ 39 – 43 ].…”

Section: Discussionsupporting

confidence: 91%

Measuring cancer driving force of chromosomal aberrations through multi-layer Boolean implication networks

Cosentini,

Condorelli,

Locicero

et al. 2024

PLoS ONE

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Multi-layer Complex networks are commonly used for modeling and analysing biological entities. This paper presents the advantage of using COMBO (Combining Multi Bio Omics) to suggest a new role of the chromosomal aberration as a cancer driver factor. Exploiting the heterogeneous multi-layer networks, COMBO integrates gene expression and DNA-methylation data in order to identify complex bilateral relationships between transcriptome and epigenome. We evaluated the multi-layer networks generated by COMBO on different TCGA cancer datasets (COAD, BLCA, BRCA, CESC, STAD) focusing on the effect of a specific chromosomal numerical aberration, broad gain in chromosome 20, on different cancer histotypes. In addition, the effect of chromosome 8q amplification was tested in the same TCGA cancer dataset. The results demonstrate the ability of COMBO to identify the chromosome 20 amplification cancer driver force in the different TCGA Pan Cancer project datasets.

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Section: Discussionsupporting

confidence: 91%

Measuring cancer driving force of chromosomal aberrations through multi-layer Boolean implication networks

Cosentini,

Condorelli,

Locicero

et al. 2024

PLoS ONE

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“…183, unpublished data). Gain for chromosomal region 13q11-q34 obviously represents an early event, since it was present in primary CRC and all metastatic sites (Golas et al 2022 ). Accordingly, this aberration had been described at the transition from adenoma to primary CRC (Hermsen et al 2002 ).…”

Section: Discussionmentioning

confidence: 99%

“…Gutenberg et al had identified 20q as the most frequently occurring copy number change in 11 patients with brain metastases (Gutenberg et al 2010 ). Additionally, this gain had often been detected in CRC primary tumors and been described as an early event in CRC tumor progress (Golas et al 2022 ).…”

Section: Discussionmentioning

confidence: 99%

“…Recent investigations suggest the accumulation of genetic alterations as an essential step for the tumor evolution of CRC. The timing of specific genetic events could influence the metastatic potential, whereby copy number aberrations already acquire early in tumor development (Golas et al 2022 ; Nguyen et al 2022 ). In comparison to CIN, MSI is less common and seems to be associated with a better prognosis (Christensen et al 2016 ; Guinney et al 2015 ; Knösel et al 2002 ; Watanabe et al 2001 ).…”

Section: Introductionmentioning

confidence: 99%

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SNP array genomic analysis of matched pairs of brain and liver metastases in primary colorectal cancer

Brandt,

Holland,

Wallenborn

et al. 2023

J Cancer Res Clin Oncol

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Purpose Brain metastasis formation is a rare and late event in colorectal cancer (CRC) patients and associated with poor survival. In contrast to other metastatic sites, the knowledge on chromosomal aberrations in brain metastases is very limited. Methods Therefore, we carried out single nucleotide polymorphism (SNP) array analyses on matched primary CRC and brain metastases of four patients as well as on liver metastases of three patients. Results Brain metastases showed more chromosomal aberrations than primary tumors or liver metastases. Commonly occurring aberrations were gain of 8q11.1-q24.3 (primary CRC), gain of 13q12.13-q12.3 (liver metastases), and gain of 20q11.1-q13.33 (brain metastases). Furthermore, we found one copy-neutral loss of heterozygosity (cn-LOH) region on chromosome 3 in primary CRC, three cn-LOH regions in liver metastases and 23 cn-LOH regions in brain metastases, comprising 26 previously undescribed sites. Conclusion The more frequent occurrence of cn-LOHs and subsequently affected genes in brain metastases shed light on the pathophysiology of brain metastasis formation. Further pairwise genetic analyses between primary tumors and their metastases will help to define the role of affected genes in cn-LOH regions.

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“…Previous studies showed that aberrant function of proteins involved in chromosome separation could induce aneuploidy which was found in many types of cancer (6,7). Aneuploidy is usually caused by an abnormal number and size of the centrosome, may accelerate tumorigenesis and carcinogenesis by causing chromosomes to separate unequally during mitosis (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

The prognostic value and mechanisms of centromere protein M in patients with lung adenocarcinoma

Qi¹,

Niu²,

Li³

et al. 2022

Transl Cancer Res TCR

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Background: Centromere protein M (CENPM) has been reported to exert important roles in promoting tumor initiation and progression. However, the expression, effect, impact on prognosis and underlying mechanism of CENPM in lung adenocarcinoma (LUAD) remain unclear. Methods: Seventy-eight paired clinical samples of LUAD and corresponding adjacent non-tumor (ANT) tissues were obtained. The clinical pathological data and clinical outcome were tested, including univariate and multivariate Cox regression model. The relationship between CENPM expression and LUAD prognosis were identified according to the data obtained from the Cancer Genome Atlas (TCGA) database. Then, we explored the protein and mRNA levels of CENPM in LUAD and paired ANT tissues, and analyzed the correlation between CENPM and LUAD overall survival in our patients. In vitro studies, LUAD cell lines were treated with CENPM-short hairpin RNA (shRNA) (shCENPM), or transfected with CENPM overexpression plasmids with or without LY294002 (PI3K inhibitor) treatment. Cell proliferation ability was determined through cell counting kit-8 (CCK-8) assays. Cell cycle and apoptosis were detected by flow cytometer. The migration and invasion ability were assessed through Transwell assay. In vivo studies, the growth of xenografts in nude mice were evaluated after shCENPM stimulated cells injection, and the proliferation and apoptosis of xenografts were also analyzed.Results: CENPM was significantly upregulated in LUAD patients compared with healthy controls, and CENPM upregulation was relevant to the higher pathological stages and poor survival rates in our LUAD patients. The bioinformatics analysis also revealed similar trends. CENPM could promote cell proliferation, cause alterations in cell cycle progression, enhance cell migration and invasion capacity, promote apoptosis in LUAD cell lines and promote the growth of xenografts in nude mice via regulation of AKT1/mTOR signaling pathway.Conclusions: CENPM was upregulated in LUAD patients, and it correlated with higher pathological stages and poor survival rates. CENPM could affect cell proliferation, cell cycle, cell migration and invasion capacity, and apoptosis in LUAD cell lines via regulation of AKT1/mTOR signaling pathway.

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Evolutionary patterns of chromosomal instability and mismatch repair deficiency in proximal and distal colorectal cancer

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Cited by 13 publications

References 82 publications

Measuring cancer driving force of chromosomal aberrations through multi-layer Boolean implication networks

Measuring cancer driving force of chromosomal aberrations through multi-layer Boolean implication networks

SNP array genomic analysis of matched pairs of brain and liver metastases in primary colorectal cancer

The prognostic value and mechanisms of centromere protein M in patients with lung adenocarcinoma

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