Detection of Mitochondrial DNA Mutations in Nonmuscle Invasive Bladder Cancer

Güney, Ahmet İlter; Ergeç, Deniz; Tavukçu, Hasan Hüseyin; Koç, Gülşah; Kıraç, Deniz; Ulucan, Korkut; Javadova, Dilara; Türkeri, Levent

doi:10.1089/gtmb.2011.0227

Cited by 27 publications

(17 citation statements)

References 21 publications

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“…The present results are consistent with a previous study by the present authors, in which mtDNA mutations were examined in TCC patients and healthy individuals. In that study, a total of 68 mutations were identified, a number of which are similar to the ones reported in the present study (30). The D-loop region, while being non-coding, has been demonstrated to have a higher mutation rate than coding mtDNA within cancer patients.…”

Section: Discussionsupporting

confidence: 84%

Investigation of the association between mitochondrial DNA and p53 gene mutations in transitional cell carcinoma of the bladder

et al. 2016

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Abstract. Bladder carcinoma is the most common malignancy of the urinary tract. The major aim of the present study is to investigate the association between mitochondrial DNA (mtDNA) and p53 gene mutations in bladder carcinoma. A total of 30 patients with transitional cell carcinoma and 27 controls were recruited for the study. Bladder cancer tissues were obtained by radical cystectomy or transurethral resection. Genomic DNA was extracted from peripheral blood. mtDNA and p53 genes were amplified by polymerase chain reaction and sequenced directly. A total of 37 polymorphisms were identified, among which, 2 mutations were significant in the patient group, and 1 mutation was significant in the control group. Additionally, 5 different moderate positive correlations between mtDNA mutations and 3 different positive correlations between p53 gene and mtDNA mutations were detected. The high incidence of mtDNA and p53 gene mutations in bladder cancer suggests that these genes could be important in carcinogenesis.

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Section: Discussionsupporting

confidence: 84%

Investigation of the association between mitochondrial DNA and p53 gene mutations in transitional cell carcinoma of the bladder

et al. 2016

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“…In 31 urothelial cell carcinoma patients, tumor cells contain ND1 (n = 2), ND2 (n = 3), ND4 (n = 2), and ND6 (n = 1) frequency variations [53]. In a study examining 38 bladder tumors, 73% contain at least one base-pair alteration in the ND1 gene [54].…”

Section: Alterations In Nd Genesmentioning

confidence: 99%

“…Tumor cells from 3 of 31 patients with urothelial cell carcinoma contain CYTB alterations [53]. In 81% of bladder carcinomas, at least one base-pair substitution is present in the CYTB gene [54]. In a human bladder cancer model, CYTB alteration is shown to generate higher levels of ROS and lead to increased tumor growth [55].…”

Section: Alterations In the Cytb Genementioning

confidence: 99%

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Mitochondrial Markers for Cancer: Relevance to Diagnosis, Therapy, and Prognosis and General Understanding of Malignant Disease Mechanisms

Paepe

2012

ISRN Pathology

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Cancer cells display changes that aid them to escape from cell death, sustain their proliferative powers, and shift their metabolism toward glycolytic energy production. Mitochondria are key organelles in many metabolic and biosynthetic pathways, and the adaptation of mitochondrial function has been recognized as crucial to the changes that occur in cancer cells. This paper zooms in on the pathologic evaluation of mitochondrial markers for diagnosing and staging of human cancer and determining the patients’ prognoses.

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“…These mutations form the maternal backgrounds of an individual and can affect the expression of different diseases (Fuku et al, 2007;Ji et al, 2008). Mutations in other cells in the body, except germ cells, are not passed to next generation, but can cause dysfunction in mtDNA genomes and result in various diseases (Zanssen and Schon, 2005;Chatterjee et al, 2006), including bladder cancer (Fliss et al, 2000;Guney et al, 2012), head and neck cancer (Mizumachi et al, 2008), lung cancer (Fliss et al, 2000;Jin et al, 2007;Fang et al, 2015), pancreatic cancer (Navaglia et al, 2006), hepatocellular carcinomas (Okochi et al, 2002), colorectal cancer (Feng et al, 2012), thyroid cancer (Abu-Amero et al, 2005), breast cancer (Cai et al, 2011;Fendt et al, 2011;Alhomidi et al, 2013), prostate cancer (Parr et al, 2006;Ashtiani et al, 2012), and gastric carcinomas (Hung et al, 2010;Bi et al, 2011). Somatic mutation may arise from oxidative damage caused by the accumulation of ROS in tissues and the deficiency of mtDNA repair systems (Croteau and Bohr, 1997;Yakes and Van Houten, 1997).…”

Section: Introductionmentioning

confidence: 99%

Deciphering the spectrum of somatic mutations in the entire mitochondrial DNA genome

Chen

Shi

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The mitochondrion is a crucial intracellular organelle responsible for regulating cellular energy metabolism, producing free radicals, initiating and executing the apoptotic pathways. Previous studies have shown that somatic mutations in mitochondrial DNA are associated with various tumors, which may be involved during carcinogenesis and tumor progression. To examine the mutation pattern in cancer, 625 reported somatic mutations in the mitochondrial DNA genome were analyzed. We found that, except for deletions and insertions, most somatic mutations were point mutations, accounting for 89.44% of somatic mutations. Transition was the predominant form of X.Z. Chen et al. 4332©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (2): 4331-4337 (2015) somatic mutation in the entire mitochondrial DNA genome, accounting for 87.12% of point mutations, most of which were homoplastic. Frequency statistics analysis of point mutations indicated that, except for 3 tRNA genes, the mutations were distributed on all resting genes and in the D-loop region, with the latter showing the highest frequency of somatic mutation (19.34%), followed by the tRNA leucine 2 gene and non-coding regions between base pairs 5892 and 5903, while 13 coding-region genes and 2 rRNA genes showed a relatively lower frequency of somatic point mutations. Nonsynonymous mutations and terminal amino acid changes were the primary point somatic mutations detected from 13 coding-region genes, which may cause mitochondrial dysfunction in cancer cells. We found that the somatic mutations may affect the mitochondrial DNA genome; the non-coding region should be examined to identify somatic mutations as potential diagnostic biomarkers for early detection of cancer.

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Detection of Mitochondrial DNA Mutations in Nonmuscle Invasive Bladder Cancer

Cited by 27 publications

References 21 publications

Investigation of the association between mitochondrial DNA and p53 gene mutations in transitional cell carcinoma of the bladder

Investigation of the association between mitochondrial DNA and p53 gene mutations in transitional cell carcinoma of the bladder

Mitochondrial Markers for Cancer: Relevance to Diagnosis, Therapy, and Prognosis and General Understanding of Malignant Disease Mechanisms

Deciphering the spectrum of somatic mutations in the entire mitochondrial DNA genome

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