Tumors without abnormality of the 11p15 region, mainly benign tumors, did not exhibit pathologic functional imprinting. Abnormalities of the 11p15 region, including LOH with the loss of the maternal allele and duplication of the paternal allele and/or IGF2 gene overexpression, are frequent features of the malignant state these abnormalities were found in 27 of 29 (93%) of the malignant tumors but in only 3 of 35 (9%) of the benign tumors. They screened for pathologic functional imprinting of the 11p15 region in tumors not exhibiting LOH and evaluated the expression of the H19 gene ( 103280) in these tumors. (1997) evaluated the frequency and distribution of 11p15 LOH and IGF2 gene ( 147470) overexpression in a series of 82 sporadic adrenocortical tumors. ( 1987, 1989) interpreted this as indicating the existence of a recessive oncogene responsible for hereditary ADCC on 11p, probably 11p15.5. Studies with 11p markers indicated loss of heterozygosity (LOH) in the tumor cells of both brothers furthermore, the chromosome 11 region that remained in the tumor was the same and was inherited from the same parent. (1987) described 2 brothers who developed ADCC with signs of virilism. One form of ADCC is caused by mutation in the TP53 gene, which maps to chromosome 17p13.
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