Contribution of the activation of the ras oncogene to the evolution of aldosterone- and renin-secreting tumors.
The possible point-mutational activation of the ras oncogene, which probably contributes to the evolution of aldosterone-producing adenomas and ectopic reninoma, was evaluated. Chromosomal DNA was extracted from six aldosterone-producing adenomas and one renin-secreting liver carcinoma, using the standard method with phenol:chloroform:isoamyl alcohol. One microgram of sample DNA, forward and reverse primers, Taq I polymerase and deoxyribonucleotide triphosphates (dNTPs) were mixed and the ras gene was amplified by the polymerase chain reaction. Point mutations at ras-12 or ras-61 sites of amplified DNA were tested by dot-blotting, using H-, N- and K-ras oligonucleotide probes with mutations at codons 12 or 61. However, there were no point mutations at amino acid codons 12 or 61 of c-Hi-ras, c-Ki-ras and N-ras oncogenes in all aldosterone-producing adenomas and the one ectopic reninoma. These results indicate that point-mutational activation of ras oncogenes does not contribute, at least in this series, towards the evolution of aldosterone-producing adenomas and the reninoma.
Higaki
J
J
Department of Geriatric Medicine, Osaka University Medical School, Japan.
Miya
A
A
Miki
T
T
Morishita
R
R
Mikami
H
H
Takai
S
S
Ogihara
T
T
D000236:Adenoma / Q000235:genetics* / Q000378:metabolism; D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000378:metabolism; D004273:DNA, Neoplasm / Q000032:analysis; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology*; D011905:Genes, ras / Q000502:physiology*; D006801:Humans; D006929:Hyperaldosteronism / Q000235:genetics; D008113:Liver Neoplasms / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000378:metabolism*
D004273:DNA, Neoplasm; D000450:Aldosterone; D012083:Renin