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1

Mitochondrial DNA mutations in human neoplasia

100%
Czarnecka A. M., Golik P., Bartnik E.
Journal of Applied Genetics
|
2006
|
vol. 47
|
issue 1
67-78
EN
Many models of tumour formation have been put forth so far. In general they involve mutations in at least three elements within the cell: oncogenes, tumour suppressors and regulators of telomere replication. Recently numerous mutations in mitochondria have been found in many tumours, whereas they were absent in normal tissues from the same individual. The presence of mutations, of course, does not prove that they play a causative role in development of neoplastic lesions and progression; however, the key role played by mitochondria in both apoptosis and generation of DNA-damaging reactive oxygen species might indicate that the observed mutations contribute to tumour development. Recent experiments with nude mice have proven that mtDNA mutations are indeed responsible for tumour growth and exacerbated ROS production. This review describes mtDNA mutations in main types of human neoplasia.
2

Mitochondria and aging: innocent bystanders or guilty parties?

100%
Tonska K., Solyga A., Bartnik E.
Journal of Applied Genetics
|
2009
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vol. 50
|
issue 1
55-62
EN
. There are many theories of aging and a number of them encompass the role of mitochondria in this process. Mitochondrial DNA mutations and deletions have been shown to accumulate in many tissues in mammals during aging. However, there is little evidence that these mutations could affect the functioning of aging tissues.
3

Human mitochondria in health, disease, ageing and cancer

100%
Bartnik E., Lorenc A., Mroczek K.
Journal of Applied Genetics
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2001
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vol. 42
|
issue 1
65-71
EN
In every human cell there are hundreds of mitochondria, which are required for oxidative phosphorylation as well as many other metabolic processes. Each mitochondrion contains approximately 5 mitochondrial DNA molecules. These circular DNAs of 16.5 kb in size contain only 39 genes . Mutations in mitochondrial DNA are responsible for many diseases. Alterations in these molecules may also play a role in ageing and in tumour formation.
4

Leber hereditary optic neuropathy ? a disease with a known molecular basis but a mysterious mechanism of pathology

100%
Mroczek-Tonska K., Kisiel B., Piechota J., Bartnik E.
Journal of Applied Genetics
|
2003
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vol. 44
|
issue 4
529-538
EN
Leber hereditary optic neuropathy is a maternally inherited type of blindness caused by degeneration of the optic nerve. It is caused by point mutations in mitochondrial DNA. Like in other mitochondrial diseases, its penetrance and inheritance is complicated by heteroplasmy, tissue distribution, and the bottleneck phenomenon in oocyte maturation. On the cellular level, the mechanism of the disease development is still mysterious. Currently three theories of pathomechanism of LHON are considered: biochemical, ROS (reactive oxygen species) and apoptotic.
5

MELAS as an example of a mitochondrial disease

88%
Piechota J., Mroczek M. K., Mroczek K., Bartnik B. E., Bartnik E.
Journal of Applied Genetics
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2001
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vol. 42
|
issue 3
351-358
EN
MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) is a disease mainly due to a mutation at position 3243 (A G) in the leucine tRNA gene in mitochondrial DNA. Symptoms of the disorder are complex and the exact pathogenesis is not understood. A review of the literature on the subject is presented.
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