Alteration of mitochondrial DNA sequence and copy number in nasal polyp tissue

Park, Sang-Young; Shin, Myung‐Geun; Kim, Hye‐Ran; Oh, Jiyeon; Kim, Soohyun; Shin, Jong‐Hee; Cho, Yong-Bum; Suh, Soon Pal; Ryang, Dong‐Wook

doi:10.1016/j.mito.2009.04.006

Cited by 24 publications

(33 citation statements)

References 27 publications

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“…Numerous studies have revealed that the change of mtDNA copy number is correlated with tumor progression (6,22). In this study, the relative mtDNA copy number was measured by real-time quantitative PCR and the relative mtDNA copy numbers were found to be significantly increased in colon and rectal tumor tissues compared to corresponding non-cancerous ones.…”

Section: A B Cmentioning

confidence: 82%

Correlation between increased copy number of mitochondrial DNA and clinicopathological stage in colorectal cancer

Yang¹

2011

Oncol Lett

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Abstract. Change of mitochondrial DNA (mtDNA) copy numbers is considered to be an important hallmark of cancers. However, whether quantitative changes in mtDNA occur during the initiation and progression of colorectal cancer remains to be determined. Quantitative change in mtDNA was observed during the initiation and progression of colorectal cancer and possible correlations of the mtDNA copy number in colorectal cancer with the clinicopathological stage were investigated. Tumor tissues and the corresponding noncancerous tissues were surgically resected from 24 colon and 20 rectal patients between 2008 and 2009. β-actin expression was quantified in all of the specimens, and the copy numbers were calculated. In colorectal cancer, the quantitative changes of mtDNA exhibited a significant increase. In 24 cases of colon cancer, the average relative mtDNA copy number ratios were 115.15±31.57 in cancer tissues and 54.09±13.22 in the corresponding non-cancerous tissues (p<0.01). Furthermore, in 20 cases of rectal cancer, the ratios were 145.6±43.83 in cancer tissues and 55.58±12.47 in the corresponding non-cancerous tissues (p<0.001). Following correlation with clinicopathological data, change of the mtDNA copy number in colorectal cancer exhibited a significant association with clinicopathological stage, but no association with gender. Moreover, this increase was particularly marked in stages Ⅰ and Ⅱ. Our results indicate that mtDNA copy number plays a significant role during the initiation and progression of colorectal cancer, particularly during early clinicopathological stages.

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Section: A B Cmentioning

confidence: 82%

Correlation between increased copy number of mitochondrial DNA and clinicopathological stage in colorectal cancer

Yang¹

2011

Oncol Lett

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“…The mutation rate in homoplasmy (all mitochondria contain the same mutation) was only slightly increased. Previous literature has found that in a variety of cancers, cells have an increased rate of mtDNA homoplasmic mutations [6], while in benign nasal polyps, there is an increase in heteroplasmic mutations [17]. The authors concluded that the absence of morphologic features of malignancy and the presence of mtDNA mutations in heteroplasmy are indicative of a benign lesion.…”

Section: Discussionmentioning

confidence: 95%

Sinonasal Seromucinous Hamartoma: A Review of the Literature and a Case Report with Focal Myoepithelial Cells

Fleming

Perez-Ordoñez

Nasser

et al. 2012

Head and Neck Pathol

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Seromucinous hamartoma is a benign lesion of the sinonasal tract. Since its description in 1974, only a small number of additional cases have been reported. It is composed of a proliferation of seromucinous glands and ducts within a variable fibrous stroma. The serous component typically stains positively for S100 (at least focally) and lacks p63 positive abluminal cells. The lack of myoepithelial/basal cells is an important diagnostic feature of seromucinous hamartoma; their absence could lead to an incorrect diagnosis of low-grade sinonasal adenocarcinoma. We report the case of a polypoid mass resected from the posterior nasal cavity and nasopharynx of a 54-year-old woman. The lesion contained a population of small and large glands lined by cuboidal to flattened cells within a hypocellular stroma varying from dense and sclerotic to myxoid. Additionally, there was a superficial focus of ciliated invaginated surface epithelium and glands. Throughout the lesion there were no cytologic or architectural features of malignancy. The histologic features were diagnostic of seromucinous hamartoma. Immunohistochemistry showed focal S100 positivity of the serous glands. However, in contrast to previously reported cases, the glands focally showed an outer basal layer that was calponin, p63 and actin positive. Our case demonstrates two important points. First, complete absence of p63 staining should not necessarily be a required feature in the diagnosis of seromucinous hamartoma. Second, the ciliated larger glands-in keeping with respiratory epithelial adenomatoid hamartoma (REAH)-support the suggestion that seromucinous hamartoma and REAH are a spectrum of lesions, often seen together.

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“…Another example of inflammation can cause increased mtDNA content is nasal polyps, which is believed being caused by inflammation mainly. In 2009, Park et al tested the inflammatory tissue of nasal polyps and non-polyp tissue found that the mtDNA content is markedly increased [51] . The data above indicates that unlike high oxidative stress the inflammation regulates mtDNA content downwards.…”

Section: Mtdna Content and Human Diseasesmentioning

confidence: 99%

Mitochondrial DNA alteration and pathological progression in colorectal cancer

et al. 2016

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Mitochondrion, the major organelle involved in cell energy metabolism, plays important roles in many human diseases. Nowadays, its dysfunction during initation and progression of cancers is calling more and more attention. Since Otto Warburg brought out his hypothesis, mitochondrial DNA (mtDNA) may affect on cancer development by regulating oxidative phosphorylation, many important findings have been discovered. It is widely recognized that research the potential correlations between mitochondrion and mtDNA in cancers are of great importance. And the trends of change of mtDNA content are different in different cancers. Thus leaves us numerous works to do. Although some cancers have already been reported their relation with mtDNA alteration, different experimental methods or evidence may lead to different conclusions. This article presents a brief in summarizing the mitochondrion dysfunction in human disease and the alteration of mtDNA in cancers. Moreover, the recent highlighting achievements on colorectal cancer and mtDNA are also summarized to provide a discussion on possible pathological mechanism and clinical usage.

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Alteration of mitochondrial DNA sequence and copy number in nasal polyp tissue

Cited by 24 publications

References 27 publications

Correlation between increased copy number of mitochondrial DNA and clinicopathological stage in colorectal cancer

Correlation between increased copy number of mitochondrial DNA and clinicopathological stage in colorectal cancer

Sinonasal Seromucinous Hamartoma: A Review of the Literature and a Case Report with Focal Myoepithelial Cells

Mitochondrial DNA alteration and pathological progression in colorectal cancer

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