Evaluation of Prediction of Polymorphisms of DNA Repair Genes on the Efficacy of Platinum‐Based Chemotherapy in Patients With Non‐Small Cell Lung Cancer: A Network Meta‐Analysis

Yu, Shiying; Liu, Gui‐Feng; Li, Xuefeng; Fu, Bo; Dong, Longlong; Zhang, Shuhua

doi:10.1002/jcb.26147

Cited by 19 publications

(12 citation statements)

References 46 publications

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“…These 11 gene sets were then subjected to survival analysis for a better understanding of their role according to a clinical perspective. LIHC, LUAD and PAAD networks, which were composed of bad prognostic genes in high percentages, confirmed previous studies on the important role of APE1 in these cancers [52][53][54][55][57][58][59][60][61][62][63][64][65] . Kaplan-Meier estimation was used to calculate survival probability associated with these genes; the ones having significantly lower survival prognosis (p < 0.05) were used to create cancer-specific PPI subnetworks ( Fig.…”

Section: Discussionsupporting

confidence: 88%

“…In order to focus our attention on the most relevant cancer types, we based our bioinformatic analysis on the eleven datasets having the highest number of bad prognostic genes. Among those, we were interested in particular in liver (LIHC) [52][53][54][55][56] , lung (LUAD) [57][58][59][60] and pancreatic (PAAD) [61][62][63][64][65] cancer datasets, as the essential role of APE1 in the tumorigenic processes of these cancer types is already well established. Notably, the LUAD dataset was the third having the highest number of bad prognostic genes (n = 153).…”

Section: Upstream Regulators Analysismentioning

confidence: 99%

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Architecture of The Human Ape1 Interactome Defines Novel Cancers Signatures

Ayyildiz

Antoniali

D’Ambrosio

et al. 2020

Sci Rep

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APE1 is essential in cancer cells due to its central role in the Base Excision Repair pathway of DNA lesions and in the transcriptional regulation of genes involved in tumor progression/chemoresistance. Indeed, APE1 overexpression correlates with chemoresistance in more aggressive cancers, and APE1 protein-protein interactions (PPIs) specifically modulate different protein functions in cancer cells. Although important, a detailed investigation on the nature and function of protein interactors regulating APE1 role in tumor progression and chemoresistance is still lacking. The present work was aimed at analyzing the APE1-PPI network with the goal of defining bad prognosis signatures through systematic bioinformatics analysis. By using a well-characterized HeLa cell model stably expressing a flagged APE1 form, which was subjected to extensive proteomics analyses for immunocaptured complexes from different subcellular compartments, we here demonstrate that APE1 is a central hub connecting different subnetworks largely composed of proteins belonging to cancer-associated communities and/or involved in RNA-and DNA-metabolism. When we performed survival analysis in real cancer datasets, we observed that more than 80% of these APE1-PPI network elements is associated with bad prognosis. Our findings, which are hypothesis generating, strongly support the possibility to infer APE1-interactomic signatures associated with bad prognosis of different cancers; they will be of general interest for the future definition of novel predictive disease biomarkers. Future studies will be needed to assess the function of APE1 in the protein complexes we discovered. Data are available via ProteomeXchange with identifier PXD013368.Alteration of DNA repair mechanisms is an important hallmark of cancer cells, and plays a role both in the onset of an initial cancerous phenotype and in tumor progression. Tumor cells can develop drug resistance through repair mechanisms that counteract the DNA damage induced by chemotherapy or radiotherapy 1,2 . Thus, specific DNA repair inhibitors are often combined with DNA-damaging agents to improve therapy efficacy. Emerging evidences in tumor biology suggest that: i) protein-protein interactions (PPIs) specifically modulate both canonical and non-canonical roles of DNA repair enzymes; ii) RNA processing pathways participate in DNA-Damage Response (DDR); iii) defects in the above-mentioned regulatory mechanisms are associated with cancer genomic instability 3 . Very recent studies clearly show that many DNA repair proteins are associated with those involved in RNA metabolism, proving a role of their interactome network in undertaking non-canonical functions affecting gene expression in tumors. In addition, novel studies have shown that interaction of DDR components and miRNA biogenesis process is linked to cancer development 2 . In the context of these emerging lines, we already demonstrated the crucial role that enzymes belonging to the base excision DNA repair (BER) pathway play 4 . In particular, we showe...

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Section: Discussionsupporting

confidence: 88%

Section: Upstream Regulators Analysismentioning

confidence: 99%

Architecture of The Human Ape1 Interactome Defines Novel Cancers Signatures

Ayyildiz

Antoniali

D’Ambrosio

et al. 2020

Sci Rep

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“…In addition, variants of the ERCC2 gene at codons 312 and 751 might alter the mutational spectrum of tumors in these patients and thereby modify the sensitivity toward radiochemotherapy [34]. In nonsmall-cell lung cancer lower response rates to palliative cisplatin-based chemotherapy were found in rs13181 [35] and rs1799793 minor variants [36] using a recessive model in concordance with the findings of the present study.…”

Section: Discussionsupporting

confidence: 90%

ERCC2 gene single-nucleotide polymorphism as a prognostic factor for locally advanced head and neck carcinomas after definitive cisplatin-based radiochemotherapy

et al. 2020

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Identifying patients with locally advanced head and neck carcinoma on high risk of recurrence after definitive concurrent radiochemotherapy is of key importance for the selection for consolidation therapy and for individualized treatment intensification. In this multicenter study we analyzed recurrence-associated single-nucleotide polymorphisms (SNPs) in DNA repair genes in tumor DNA from 132 patients with locally advanced head and neck carcinoma (LadHnSCC). Patients were treated with definitive radiotherapy and simultaneous cisplatin-based chemotherapy at six partner sites of the German Cancer Consortium (DKTK) Radiation Oncology Group from 2005 to 2011. For validation, a group of 20 patients was available. Score selection method using proportional hazard analysis and leave-one-out cross-validation were performed to identify markers associated with outcome. The SNPs rs1799793 and rs13181 were associated with survival and the same SNPs and in addition rs17655 with freedom from loco-regional relapse (ffLRR) in the trainings datasets from all patients. The homozygote major rs1799793 genotype at the ERCC2 gene was associated with better (Hazard ratio (HR): 0.418 (0.234–0.744), p = 0.003) and the homozygote minor rs13181 genotype at ERCC2 with worse survival (HR: 2.074, 95% CI (1.177–3.658), p = 0.017) in comparison to the other genotypes. At the ffLRR endpoint, rs1799793 and rs13181 had comparable prognostic value. The rs1799793 and rs13181 genotypes passed the leave-one-out cross-validation procedure and associated with survival and ffLRR in patients with LadHnSCC treated with definitive radiochemotherapy. While findings were confirmed in a small validation dataset, further validation is underway within a prospective biomarker study of the DKTK.

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“… The best predictor factor for evaluating the efficacy of PBC in the NSCLC is ERCC1(rs11615), XRCC1(rs25487, rs1799782) and XPD (rs13181). [ 52 ] 5 1004 patients, Pulmonary cancer Asian 173 SNPs from 27 genes ERCC5 rs2296147 has a RR significance This study suggests that SNPs in the NER pathway could be potential predictors for clinical outcomes of platinum-based chemotherapy among NSCLC. [ 47 ] GTF2H4 rs3218804 against clinical benefit is significant.…”

Section: Methodsmentioning

confidence: 97%

“…The XPA protein binds to damaged sites that have been “marked” by XPE and XPC and then unwinds the DNA in conjunction with the TFIIH complex 50 , 51 ( Figure 3 ). XPA is one of the platinum efficacy predictors 52 ( Table 1 ). Other meta-analysis studies have concluded that XPD is one of the proteins that has a significant association with PBC outcome 53 ( Table 1 ).…”

Section: Methodsmentioning

confidence: 99%

<p>Genetic Polymorphisms and the Efficacy of Platinum-Based Chemotherapy: Review</p>

Afifah

Diantini

Intania³

et al. 2020

PGPM

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Previous studies have indicated that genetic variations in individuals may result in changes in gene expression and amino acids. The effect of these changes may lead to different responses to platinum-based chemotherapy. A vast response rate interval and a short survival rate indicate that the efficacy and efficiency of the selection of chemotherapy have not been optimized. This article aims to illustrate the potential relationship of various genetic polymorphisms in response to platinum-based chemotherapy for several types of cancer. This review was conducted using articles from the last three-and five-year periods (2014-2019) that use gene polymorphism and its relationship to the efficacy of platinumbased chemotherapy as their theme. A total of 26 out of 488 relevant articles were included based on specific criteria. Through various mechanisms, genes, including ERCC1, ERCC2/ XPD,

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Evaluation of Prediction of Polymorphisms of DNA Repair Genes on the Efficacy of Platinum‐Based Chemotherapy in Patients With Non‐Small Cell Lung Cancer: A Network Meta‐Analysis

Cited by 19 publications

References 46 publications

Architecture of The Human Ape1 Interactome Defines Novel Cancers Signatures

Architecture of The Human Ape1 Interactome Defines Novel Cancers Signatures

ERCC2 gene single-nucleotide polymorphism as a prognostic factor for locally advanced head and neck carcinomas after definitive cisplatin-based radiochemotherapy

<p>Genetic Polymorphisms and the Efficacy of Platinum-Based Chemotherapy: Review</p>

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