van't Hof A, Gilissen K, Cohen R J, Taylor L, Haffajee Z, Thornley A L, Segal I
Department of Gastroenterology, Baragwanath Hospital, Johannesburg, South Africa.
Gut. 1995 May;36(5):691-5. doi: 10.1136/gut.36.5.691.
Most studies on colorectal carcinogenesis suggest a field defect, preceding overt development of cancer. The low incidence of adenomatous polyps in the African population, however, suggests that there may be an alternative route for cancer development. The aim of the study was to discover if the difference in incidence of colorectal cancer in Africans compared with the white population is reflected in a different pattern of cell proliferation. Histological normal mucosa from 30 patients (15 white South African (W), 15 South African Africans (A)) with confirmed colon cancer were examined. Proliferating cells were detected using the Ki-67 antigen. In addition, cell proliferation data were obtained, from 30 age matched controls (15 Africans, 15 white South Africans), without colorectal disease. The African controls were significantly younger (mean (SD) (A: 42 (20), W: 66 (13), p < 0.05)) than the white controls. The second control group had a significantly higher mean (SD) total labelling index (W: 11 (3), A: 6 (4), p < 0.05). In addition the proliferative pattern of the white group without evidence of colorectal cancer showed a comparatively large amount of dividing cells in compartment 2, compared with African controls (mean (SD) (W: 21 (8), A: 9 (8), p < 0.05)). Mucosa from Africans with cancer showed a proliferative pattern with the same increased total labelling index (A: 15 (5), W: 16 (6), p = NS, phase II proliferative lesion) and an even more pronounced upward expansion (phase I proliferative lesion) compared with white cancer patients. This suggests that the mechanism of colorectal carcinogenesis is similar in Africans and the white population. The lack of clinical evidence of the adenoma-carcinoma sequence, and the incidence of cancer at a comparatively young age in Africans may be explained by the fact that colorectal cancer in this ethnic group behaves more aggressively and that adenomatous polyps are rapidly converted into overt cancer before detection.
大多数关于结直肠癌发生机制的研究表明,在癌症明显发生之前存在一个场缺陷。然而,非洲人群中腺瘤性息肉的低发病率表明,癌症发展可能存在另一条途径。本研究的目的是探究与白种人群相比,非洲人结直肠癌发病率的差异是否反映在不同的细胞增殖模式上。对30例确诊为结肠癌的患者(15名南非白人(W),15名南非非洲人(A))的组织学正常黏膜进行了检查。使用Ki-67抗原检测增殖细胞。此外,从30名年龄匹配的无结直肠疾病的对照者(15名非洲人,15名南非白人)获取细胞增殖数据。非洲对照者比白人对照者明显年轻(平均值(标准差)(A:42(20),W:66(13),p<0.05))。第二个对照组的平均(标准差)总标记指数明显更高(W:11(3),A:6(4),p<0.05)。此外,与非洲对照者相比,无结直肠癌证据的白人群体的增殖模式显示,在第2区有相对大量的分裂细胞(平均值(标准差)(W:21(8),A:9(8),p<0.05))。患有癌症的非洲人的黏膜显示出增殖模式,其总标记指数增加相同(A:15(5),W:16(6),p=无显著性差异,II期增殖性病变),与白人癌症患者相比,甚至有更明显的向上扩展(I期增殖性病变)。这表明非洲人和白人群体中结直肠癌的发生机制相似。腺瘤-癌序列缺乏临床证据,以及非洲人在相对年轻时患癌的发病率,可能是因为该种族群体中的结直肠癌行为更具侵袭性,并且腺瘤性息肉在检测前迅速转化为明显的癌症。