DNA Damage Is a Potential Marker for TP53 Mutation in Colorectal Carcinogenesis

Scalise, José Ricardo; Poças, Regina Caeli Guerra; Caneloi, T.P.; Lopes, C.; Kanno, Danilo Toshio; Marques, Mayara Gonçalves; Valdivia, Júlio Cesar Martins; Máximo, Felipe Rodrigues; Pereira, José Aires; Ribeiro, Marcelo Lima; Priolli, Denise Gonçalves

doi:10.1007/s12029-016-9846-0

Cited by 12 publications

(7 citation statements)

References 27 publications

(73 reference statements)

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“…In all of the samples, the authors recorded the link between oxidative DNA damage and TP53 mutation. The authors concluded that oxidative DNA damage along with TP53 mutation are important contributors to colorectal adenoma-carcinoma transition [82]. Apart from somatic mutations in the gene, polymorphic features (germline variants including single nucleotide polymorphisms) of the gene may also modulate its function [83].…”

Section: Studies On the Interactions Of Dna Repair Telomere Homeostasis And P53 Mutational Status In Cancer Riskmentioning

confidence: 99%

The Interactions of DNA Repair, Telomere Homeostasis, and p53 Mutational Status in Solid Cancers: Risk, Prognosis, and Prediction

Vodička

Anděra

Opattová

et al. 2021

Cancers

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The disruption of genomic integrity due to the accumulation of various kinds of DNA damage, deficient DNA repair capacity, and telomere shortening constitute the hallmarks of malignant diseases. DNA damage response (DDR) is a signaling network to process DNA damage with importance for both cancer development and chemotherapy outcome. DDR represents the complex events that detect DNA lesions and activate signaling networks (cell cycle checkpoint induction, DNA repair, and induction of cell death). TP53, the guardian of the genome, governs the cell response, resulting in cell cycle arrest, DNA damage repair, apoptosis, and senescence. The mutational status of TP53 has an impact on DDR, and somatic mutations in this gene represent one of the critical events in human carcinogenesis. Telomere dysfunction in cells that lack p53-mediated surveillance of genomic integrity along with the involvement of DNA repair in telomeric DNA regions leads to genomic instability. While the role of individual players (DDR, telomere homeostasis, and TP53) in human cancers has attracted attention for some time, there is insufficient understanding of the interactions between these pathways. Since solid cancer is a complex and multifactorial disease with considerable inter- and intra-tumor heterogeneity, we mainly dedicated this review to the interactions of DNA repair, telomere homeostasis, and TP53 mutational status, in relation to (a) cancer risk, (b) cancer progression, and (c) cancer therapy.

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Section: Studies On the Interactions Of Dna Repair Telomere Homeostasis And P53 Mutational Status In Cancer Riskmentioning

confidence: 99%

The Interactions of DNA Repair, Telomere Homeostasis, and p53 Mutational Status in Solid Cancers: Risk, Prognosis, and Prediction

Vodička

Anděra

Opattová

et al. 2021

Cancers

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“…Patients with PTEN expression showed significantly longer overall survival compared to patients with PTEN loss tumor[88]; other studies reported an association with poor prognosis in stage II patients only[86] or in CRC patients with liver metastasis[89]. PTEN could represent a useful predictive marker for KRAS -WT patients treated with anti-EGFR therapy[90].…”

Section: Other Promising Biomarkers For Crcmentioning

confidence: 99%

Biomarkers in colorectal cancer: Current clinical utility and future perspectives

Vacante

Borzì

Burzotta

et al. 2018

WJCC

106

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Colorectal cancer (CRC) is a major cause of cancer death worldwide. CRC has poor prognosis and there is a crucial need for new diagnostic and prognostic biomarkers to avoid CRC-related deaths. CRC can be considered a sporadic disease in most cases (75%-80%), but it has been suggested that crosstalk between gene mutations (i.e., mutations of BRAF, KRAS, and p53 as well as microsatellite instability) and epigenetic alterations (i.e., DNA methylation of CpG island promoter regions) could play a pivotal role in cancer development. A number of studies have focused on molecular testing to guide targeted and conventional treatments for patients with CRC, sometimes with contrasting results. Some of the most useful innovations in the management of CRC include the possibility to detect the absence of KRAS, BRAF, NRAS and PIK3CA gene mutations with the subsequent choice to administer targeted adjuvant therapy with anti-epidermal growth factor receptor antibodies. Moreover, CRC patients can benefit from tests for microsatellite instability and for the detection of loss of heterozygosity of chromosome 18q that can be helpful in guiding therapeutic decisions as regards the administration of 5-FU. The aim of this review was to summarize the most recent evidence on the possible use of genetic or epigenetic biomarkers for diagnosis, prognosis and response to therapy in CRC patients.

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“…Mutated TP53 can be spotted in both malignant cells and in adenomas, and is expressed in about 60% of CRC. Point mutation in codon 72 - resulting in the substitution of proline to arginine - leads to dysfunction of the cell cycle “gatekeeper” that promotes the malignant process [ 69 - 70 ].…”

Section: Tp53-apc/β-cateninmentioning

confidence: 99%

Current and future biomarkers in colorectal cancer

Zarkavelis¹

2017

aog

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Colorectal cancer (CRC), one of the leading causes of death among cancer patients, is a heterogeneous disease and is characterized by diversions in multiple molecular pathways throughout its evolutionary process. To date, specific mutations in RAS and RAF genes are tested in everyday clinical practice along with mismatch repair gene deficiency, serving either as prognostic or predictive biomarkers, providing information for patient risk stratification and the choice of appropriate therapy. However, ongoing studies are focusing on the potential role of recently discovered genetic and epigenetic alterations in the management of CRC patients and their potential prognostic or predictive value. To overcome the problem of tumor heterogeneity as well as the practical obstacles of access to tumor tissue, and to achieve real-time monitoring of disease and therapy efficacy, liquid biopsies constitute a novel technology worth exploring. CRC screening and management is entering a new era where molecular testing will be applied to genomic material extracted from easily accessible bodily fluids.

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DNA Damage Is a Potential Marker for TP53 Mutation in Colorectal Carcinogenesis

Abstract: Oxidative DNA damage is an intervening variable for TP53 mutation in colorectal adenoma-carcinoma. Our data suggests that oxidative DNA damage is a potential marker of TP53 mutation in colorectal carcinogenesis.

Cited by 12 publications

References 27 publications

The Interactions of DNA Repair, Telomere Homeostasis, and p53 Mutational Status in Solid Cancers: Risk, Prognosis, and Prediction

The Interactions of DNA Repair, Telomere Homeostasis, and p53 Mutational Status in Solid Cancers: Risk, Prognosis, and Prediction

Biomarkers in colorectal cancer: Current clinical utility and future perspectives

Current and future biomarkers in colorectal cancer

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