Pontin J E, Hamed H, Fentiman I S, Idle J R
Department of Pharmacology and Toxicology, St. Mary's Hospital Medical School, London, U.K.
Eur J Cancer. 1990;26(7):790-2. doi: 10.1016/0277-5379(90)90153-k.
129 female patients with breast cancer and 79 controls undergoing biopsy for benign breast conditions had debrisoquine hydroxylator phenotype established. 129 female hospital patients with known hydroxylator phenotype were used as another control group. The breast cancer cases differed significantly from the benign controls in their debrisoquine phenotype, with 10% being poor metabolisers compared with none of the controls (P less than 0.01). However, while a comparison of the distributions of metabolic ratio (an inverse measure of debrisoquine metabolism) of breast cancer patients and hospital controls showed a significant difference by rank, there was no significant difference in the proportion of poor metabolisers in these two groups. The cases with benign disease differed from the hospital controls in both metabolic ratio distribution (P less than 0.001) and frequency of poor metabolisers (P less than 0.05). Although there was a shift in metabolic ratio distribution, debrisoquine hydroxylator phenotype was not a genetic marker for breast cancer. Why no patients undergoing biopsies for benign conditions were poor metabolisers is unknown.
对129例乳腺癌女性患者以及79例因乳腺良性疾病接受活检的对照者进行了异喹胍羟化酶表型测定。将129例已知羟化酶表型的女性住院患者作为另一对照组。乳腺癌病例在异喹胍表型方面与良性对照组有显著差异,10%为代谢不良者,而对照组无代谢不良者(P<0.01)。然而,虽然乳腺癌患者与住院对照组的代谢率(异喹胍代谢的反向指标)分布比较显示秩次有显著差异,但两组代谢不良者的比例无显著差异。良性疾病患者在代谢率分布(P<0.001)和代谢不良者频率(P<0.05)方面均与住院对照组不同。虽然代谢率分布有偏移,但异喹胍羟化酶表型并非乳腺癌的遗传标志物。为何因良性疾病接受活检的患者中没有代谢不良者尚不清楚。