8-Nitroguanine as a potential biomarker for progression of malignant fibrous histiocytoma, a model of inflammation-related cancer

Hoki, Yoko; Murata, Mariko; Hiraku, Yusuke; Ma, Ning; Matsumine, Akihiko; Uchida, Atsushi; Kawanishi, Shosuke

doi:10.3892/or.18.5.1165

Cited by 7 publications

(3 citation statements)

References 22 publications

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“…The presence of 8-nitroguanine has been shown in hepatocytes, Kuppfer's cells, and inflammatory cells of patients with chronic hepatitis C [187]. 8-Nitroguanine can lead to the formation of tumors and is detected in cancer cells [188,189].…”

Section: -Nitroguaninementioning

confidence: 99%

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

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Schizophrenia is a neurodevelopmental disorder featuring chronic, complex neuropsychiatric features. The etiology and pathogenesis of schizophrenia are not fully understood. Oxidative-antioxidant imbalance is a potential determinant of schizophrenia. Oxidative, nitrosative, or sulfuric damage to enzymes of glycolysis and tricarboxylic acid cycle, as well as calcium transport and ATP biosynthesis might cause impaired bioenergetics function in the brain. This could explain the initial symptoms, such as the first psychotic episode and mild cognitive impairment. Another concept of the etiopathogenesis of schizophrenia is associated with impaired glucose metabolism and insulin resistance with the activation of the mTOR mitochondrial pathway, which may contribute to impaired neuronal development. Consequently, cognitive processes requiring ATP are compromised and dysfunctions in synaptic transmission lead to neuronal death, preceding changes in key brain areas. This review summarizes the role and mutual interactions of oxidative damage and impaired glucose metabolism as key factors affecting metabolic complications in schizophrenia. These observations may be a premise for novel potential therapeutic targets that will delay not only the onset of first symptoms but also the progression of schizophrenia and its complications.

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Section: -Nitroguaninementioning

confidence: 99%

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

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“…8-nitroguanine is a mutagenic nitrative DNA lesion for med during chronic inflammation. [ 4 ] In this study, 8-nitroguanine was colocalized with iNOS and NF-kB in tumour cells of MFH patients. NF-kB expression in the nucleus of tumour cells was closely correlated with iNOS expression in MFH patients.…”

mentioning

confidence: 53%

Malignant Fibrous Histiocytoma of Scalp after Repeated Infection

Liu

Chen

et al. 2022

Indian Journal of Dermatology

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“…In contrast, the HR pathway's downregulation could sensitize cells to DNA crosslinking agents (Chan et al 2009). Studies suggest that iNOS-dependent 8-nitroguanine formation by HIF-1α and NF-κB plays an essential role in tumor progression, and 8nitroguanine can be a potential biomarker for inflammationrelated cancer (malignant fibrous histiocytoma) (Hoki et al 2007). Furthermore, results show that HIF-1α and iNOS have the probability of activating or influencing each other to handle fixed DNA damage, resulting in accumulation of mutation, acquiring tumor invasiveness, and poor prognosis (Kawanishi et al 2017).…”

Section: Hypoxia-induced Dna Damagementioning

confidence: 99%

Unboxing the molecular modalities of mutagens in cancer

Kumari

Sharma

Advani

et al. 2021

Environ Sci Pollut Res

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Graphical abstract The etiology of the majority of human cancers is associated with a myriad of environmental causes, including physical, chemical, and biological factors. DNA damage induced by such mutagens is the initial step in the process of carcinogenesis resulting in the accumulation of mutations. Mutational events are considered the major triggers for introducing genetic and epigenetic insults such as DNA crosslinks, single- and double-strand DNA breaks, formation of DNA adducts, mismatched bases, modification in histones, DNA methylation, and microRNA alterations. However, DNA repair mechanisms are devoted to protect the DNA to ensure genetic stability, any aberrations in these calibrated mechanisms provoke cancer occurrence. Comprehensive knowledge of the type of mutagens and carcinogens and the influence of these agents in DNA damage and cancer induction is crucial to develop rational anticancer strategies. This review delineated the molecular mechanism of DNA damage and the repair pathways to provide a deep understanding of the molecular basis of mutagenicity and carcinogenicity. A relationship between DNA adduct formation and cancer incidence has also been summarized. The mechanistic basis of inflammatory response and oxidative damage triggered by mutagens in tumorigenesis has also been highlighted. We elucidated the interesting interplay between DNA damage response and immune system mechanisms. We addressed the current understanding of DNA repair targeted therapies and DNA damaging chemotherapeutic agents for cancer treatment and discussed how antiviral agents, anti-inflammatory drugs, and immunotherapeutic agents combined with traditional approaches lay the foundations for future cancer therapies.

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8-Nitroguanine as a potential biomarker for progression of malignant fibrous histiocytoma, a model of inflammation-related cancer

Cited by 7 publications

References 22 publications

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

Malignant Fibrous Histiocytoma of Scalp after Repeated Infection

Unboxing the molecular modalities of mutagens in cancer

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