Xeroderma pigmentosum a2 arkadiy f, morgan f

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Xeroderma Pigmentosum Genetic Disorder Project by Morgan F. and Arkadiy F.

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Abstract: Xeroderma pigmentosum with squamous cell carcinoma of skin has been infreqently reported .Is a rare autosomal recessive disease characterized by defective DNA repair. . A seven year old boy having xeroderma pigmentosa presented with extensive ulceration of the face . On investigation, the ulceration was found to be squamous cell carcinoma. The details of the case are presented and its pathological findings are discussed

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Rare genetic disorder that occurs worldwide in all races and ethnic groups. First described by Hebra and Kaposi in 1874. Photosensitivity and premature onset of all major types of skin cancer . Inability of a cell to repair damage caused by UV leading to genetic instability and skin cancer. Responsible for removing the damaged segments of DNA and restoring the original sequence of DNA. The NER mechanism is composed of two types: Transcription coupled(TCR): Which rapidly repairs areas of DNA that are "active" and being transcribed into RNA Global genome(GGR): Which repairs damage in the rest of the genome more slowly Seven XP genes are central to NER which includes many other accessory proteins The term “complementation group” is based on cell fusion experiments. Cells from different XP patients are fused to investigate if the DNA repair defect in the fused cells is corrected. If DNA repair in the fused cell is increased, each cell provides proteins that the other is lacking and the cells “complement” each other and are in different complementation groups. If DNA repair in the fused cells is not normalized, the cells do not “complement” each other, meaning that both cells harbor mutations in the same DNA repair gene. Seven such complementation groups have been identified (XP-A to XP-G), which correspond with mutations in seven distinct genes that can cause XP. Severity changes is dependent on the amount of sun exposure and the degree of UVR protection Acute and severe sunburn on minimal sun exposure takes weeks to resolve. 50% of XP patients suffer from severe and prolonged sunburn reactions. Rest 50% have sunburn reactions that are normal and present with lentigines as well as hypopigmented macules. Development of many freckles at an early age. • Rough-surfaced growths (solar keratoses), and skin cancers • Blistering or freckling on minimum sun exposure • Telangiectasia (spider veins) • Limited growth of hair on chest and legs •

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DNA interacts with the environment, and sometimes that interaction can be detrimental to genetic information. In fact, every time you go outside, you put your DNA in danger, because ultraviolet (UV) light from the Sun can induce mutations in your skin cells. One type of UV-generated mutation involves the hydrolysis of a cytosine base to a hydrate form, causing the base to mispair with adenine during the next round of replication and ultimately be replaced by thymine. Indeed, researchers have found an extremely high rate of occurrence of this UV-induced C-to-T fingerprint-type mutation in genes associated with basal cell carcinoma, a form of skin cancer (Seidl et al., 2001). UV light can also cause covalent bonds to form between adjacent pyrimidine bases on a DNA strand, which results in the formation of pyrimidine dimers. Repair machinery exists to cope with these mutations, but it is somewhat prone to error, which means that some dimers go unrepaired. Furthermore, some people have an inherited genetic disorder called xeroderma pigmentosum (XP), which involves mutations in the genes that code for the proteins involved in repairing UV-light damage. In people with XP, exposure to UV light triggers a high frequency of mutations in skin cells, which in turn results in a high occurrence of skin cancer. As a result, such individuals are unable to go outdoors during daylight hours. In addition to ultraviolet light, organisms are exposed to more energetic ionizing radiation in the form of cosmic rays, gamma rays, and X-rays. Ionizing radiation induces double-stranded breaks in DNA, and the resulting repair can likewise introduce mutations if carried out imperfectly. Unlike UV light, however, these forms of radiation penetrate tissue well, so they can cause mutations anywhere in the body. Solution DNA interacts with the environment, and sometimes that interaction can be detrimental to genetic information. In fact, every time you go outside, you put your DNA in danger, because ultraviolet (UV) light from the Sun can induce mutations in your skin cells. One type of UV-generated mutation involves the hydrolysis of a cytosine base to a hydrate form, causing the base to mispair with adenine during the next round of replication and ultimately be replaced by thymine. Indeed, researchers have found an extremely high rate of occurrence of this UV-induced C-to-T fingerprint-type mutation in genes associated with basal cell carcinoma, a form of skin cancer (Seidl et al., 2001). UV light can also cause covalent bonds to form between adjacent pyrimidine bases on a DNA strand, which results in the formation of pyrimidine dimers. Repair machinery exists to cope with these mutations, but it is somewhat prone to error, which means that some dimers go unrepaired. Furthermore, some people have an inherited genetic disorder called xeroderma pigmentosum (XP), which involves mutations in the genes that code for the proteins involved in repairing UV-light damage. In people .

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