Quantitative analysis of numerical chromosome aberrations in various morphological types of colorectal carcinomas

Abstract

Quantitative analysis by fluorescence in situ hybridization (FISH) on thin paraffin-embedded tissue sections, using specific probes for chromosomes 11, 17, and 18 was employed in various morphological types of early and advanced colorectal cancer to clarify tumor cytogenetics. The chromosome index (CI) was calculated as a quantitative measure of the chromosome copy number. Compared with the CI of normal epithelium, the CI of chromosome 11 in villous components of adenomas or polypoid early cancers was decreased, while the CI in flat type or advanced colorectal cancers, conversely, was increased (P < 0.05). The CI of chromosome 17 in villous components of adenomas and all cancers was higher than that of normal epithelium (P < 0.05), but the differences were not significant. In protruding advanced cancers, the CI of chromosome 18 was significantly decreased (P < 0.01) compared to the CI of normal epithelium. There was no significant chromosomal heterogeneity between the superficial and the deepest layer in each cancer. In mucosa adjacent to sessile and flat type cancers, the CI of chromosome 17 was significantly higher than the CI in normal epithelium or adenomas (P < 0.05). These results suggest that numerical chromosome aberrations are associated with the histological type of adenoma and the morphological diversity of cancer in the colorectum, and that chromosome 17 abnormality occurs in mucosa adjacent to sessile and flat cancers.

Different Expression of Sialyl Tn Antigen between Polypoid and Nonpolypoid Growth Types of Advanced Colorectal Carcinoma

“…Such morphologic differences between cancers may reflect differences in the biological characteristics of the individual cancer cells. Compared with PG-type cancers, NPG-type cancers possess a low incidence of K- ras mutation [6, 8, 9], different cellular proliferation activity [10], different numerical chromosome aberrations [11, 12], and a lack of a pericryptal fibroblast network [26]. The current study reveals the difference in sialyl Tn expression during tumor development between two growth types.…”

“…Such morphologic differences between PG-type and NPG-type cancers may reflect differences in biological characteristics of the cancer cells themselves. In keeping with this hypothesis, characteristics such as a low incidence of K- ras mutation [6, 8, 9], different cellular proliferation activity [10], and distinct chromosomal aberrations [11, 12]have all been reported. However, other cellular features of PG-type and NPG-type colorectal cancers remain unknown, including the processes of cellular transformation during carcinogenesis and tumor progression.…”

“…The transitional mucosa did not show any microscopic features of malignancy, but increased histochemically detectable sialomucins [21]. Although the possibility that changes in transitional mucosa are a secondary rather than a primary phenomenon has been considered [20], the characteristics of transitional mucosa have been recently revealed using molecular analysis, including deoxyribonucleic acid ploidy [28], mucosal cell proliferation [29], proliferation-specific genes [30], and numerical aberrations of chromosomes [12]. These reports have led to the suggestion that transitional mucosa may be in the hyperproliferative and preneoplastic state.…”

Comparison of the expression of ABH/Lewis‐related antigens in polypoid and non‐polypoid growth types of colorectal carcinoma

“…The difference in the morphology of PG‐type and NPG‐type cancers may reflect differences in the biological characteristics of the cancer cells themselves. Recently, we reported the results of molecular analysis of the cellular features of PG‐type and NPG‐type colorectal carcinomas and found alteration of chromosomes and cellular proliferation activity 6,7 . The K ‐ ras mutation is present in a small percentage of NPG‐type colorectal cancers 2 .…”

Colorectal carcinoma: contribution of growth pattern on prognosis

“…Further studies have described differences in the biologic behaviour as well as in the cellular and genetic features of PG-type and NPG-type carcinomas, indicating a difference in the pathway of colorectal carcinogenesis [2][3][4][5][6][7][8].…”