Ultrastructure of villous adenomas of the large intestine

7 villous adenomas of the colon from patients of 44 to 63 years are studied electron-microscopically. Their cells are shown to preserve the capacity for specific differentiation. 4 types of differentiated cells are distinguished and changes connected with the processes of structural-functional restructuration are described. The existence of two ultrastructural variants of villous adenomas depending upon the proportion of differentiated and nondifferentiated cells is noted. Prognostic value of these findings is discussed.     

Lymphoreticular infiltrates in adenocarcinoma of the large intestine

Twenty-two invasive adenocarcinomas of the large intestine were investigated histologically and immunohistologically to determine the localisation and composition of the tumor-infiltrating lymphoreticular cells: The lymphoreticular cells were consistently more frequent in the intervening stroma than in the tumor foci. Monocytes/macrophages (Mono 1+), helper/inducer cells (Leu-3 a+), and T lymphocytes (Leu-1+) were mostly observed in large numbers, thus constituting the great majority of tumor-infiltrating cells. In most tumors, the suppressor/cytotoxic T lymphocytes (Leu-2a+), plasma cells, eosinophils, and tissue mast cells occurred in moderate numbers. T-accessory cells bearing the CD 1 surface-antigen (Leu-6+) were generally detected in low, or even very low numbers, while B lymphocytes (TO 15+) and natural killer cells (Leu-7+) were nearly, and dendritic reticulum cells (KiM 4+) were totally absent from the lymphoreticular infiltrates. Though an immunohistological in situ analysis of tumor-infiltrating cells allows only limited conclusions concerning their functional properties, the often dense and polymorphic infiltrates might reflect a relatively intensive interaction between the specific and non-specific host defense and the malignant tumor.     

Lymphocytic infiltration and mitotic activity of the epithelium in villous tumors of the large intestine

Morphostatistical analysis of the lymphocytic infiltration intensity and mitotic activity in 34 colon villous tumours is performed depending on the degree of dysplasia, the presence or the absence of invasive growth. The above parameters changed during the various stages of tumour progression and can be taken into account in the process of histological verification of difficult cases.     

Primary endometrioid adenocarcinoma of the large intestine arising in colorectal endometriosis

AIMS: Three cases of endometrioid adenocarcinoma arising in colorectal endometriosis are described with discussion of their macroscopic and microscopic pathology and diagnosis, using immunohistochemistry. METHODS AND RESULTS: Three middle-aged women presented with symptoms and signs of colorectal mass effect. Two had a preceding history of gynaecological endometriosis and all three had either been on hormone replacement therapy or had functioning ovaries prior to presentation with colorectal disease. Each underwent resection of tumours of the distal large intestine. The definitive diagnosis was dependent on histological examination and immunohistochemistry, which was used to demonstrate an origin in endometriotic tissue. CONCLUSIONS: Endometrioid adenocarcinoma is a rare complication of colorectal endometriosis, this report contributing to a total of 25 cases in the literature. Definitive diagnosis, aided by immunohistochemical studies, is important to enable the identification of the optimal management for this uncommon condition.     

Importance of apoptosis in the histopathology of drug related lesions in the large intestine.

AIM: To investigate the possibility that the incidence of apoptotic bodies in the cryptal epithelium might help to identify colonic lesions due to drugs, especially non-steroidal anti-inflammatory drugs (NSAIDs). METHODS: The apoptotic count (AC) the number of apoptotic bodies per 100 crypts was calculated in a series of colorectal biopsy specimens, stained with haematoxylin and eosin from patients with (a) known or suspected drug induced colitis and (b) inflammatory bowel disease before or after treatment with salazopyrine or corticosteroids. These specimens were compared with normal biopsy specimens from a control group of comparable age and sex distribution. RESULTS: Under normal conditions apoptotic bodies were seldom seen at all and the mean apoptotic count was less than 1.0. In untreated inflammatory bowel disease the mean apoptotic count was marginally increased (2.4), but when there was a partial response to drug treatment the apoptotic count rose to 13.1 (p 0.003). In colonic lesions directly attributable to drugs the apoptotic count was always increased, reaching its highest level (106) with 5-fluorouracil. In colitis related to NSAIDs apoptoses were associated with inflammation, most notably an increase in lymphocytes in both lamina propria and epithelium. CONCLUSION: The presence of crypt apoptoses in substantial numbers (with an apoptotic count in excess of 5) should always raise the possibility of drug effect. The mechanisms involved are not clear but with NSAIDs the changes might well be immunologically mediated.     

大肠癌和腺瘤中的细胞凋亡及其调控基因表达

目的通过观察结、直肠腺癌和腺瘤中的细胞凋亡及其调控基因ｐ５３、ｂｃｌ－２的表达状态，探讨细胞凋亡及其调控基因在大肠上皮恶性转化进程的不同阶段中的作用。方法利用ＤＮＡ缺口末端标记技术和ｐ５３、ｂｃｌ－２蛋白免疫组化染色，原位观察３２例大肠绒毛状腺瘤和３３例大肠乳头状腺癌中的凋亡细胞和ｐ５３、ｂｃｌ－２蛋白阳性表达细胞的密度与分布，以１５例非肿瘤大肠粘膜做为对照。结果腺瘤和腺癌中的凋亡细胞密度均显著高于非肿瘤粘膜（Ｐ＜０．０１）；腺瘤高于腺癌（Ｐ＜０．０１）。ｐ５３和ｂｃｌ－２蛋白的表达率和表达强度，腺癌和腺瘤高于非肿瘤粘膜（Ｐ＜０．０１），腺癌的表达强度也高于腺瘤（Ｐ＜０．０５）。腺瘤中ｂｃｌ－２蛋白表达阳性组的凋亡细胞密度显著低于ｂｃｌ－２阴性组（Ｐ＜０．０１）。结论细胞凋亡调控异常在大肠癌发病中可能起重要作用。ｂｃｌ－２蛋白在腺瘤和腺癌中均可抑制细胞凋亡，而突变型ｐ５３蛋白可能仅在腺癌中起抑制细胞凋亡的作用。     

Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma

The 2004 WHO classification of lung tumours recognised basaloid carcinoma as a variant of squamous and large cell carcinoma. We report a unique case of primary pulmonary adenocarcinoma with a basaloid component. An 82-year-old man underwent pulmonary lobectomy for a 2.8 cm tumour. The patient is disease-free 13 months after diagnosis. Histologically, an invasive carcinoma having a glandular and a solid component was observed. The former was an adenocarcinoma with mucus containing spaces lined by columnar mucinous cells and basaloid cells. The solid component was an organoid proliferation of basaloid-type cells, as in cutaneous basal cell carcinoma. Basaloid cells, but not mucinous cells, were immunoreactive for high molecular weight cytokeratins (CK), CK 7 and, focally, for TTF-1. High Ki67 index, p53 and EGFR expression were also found. This tumour is unique in several respects: (1) The solid areas resemble a conventional basaloid carcinoma, except for the presence of small mucin-containing spaces. (2) The mucinous adenocarcinoma areas contain two layers of columnar and basaloid cells. (3) Both components are neoplastic based on cell morphology, invasive properties and phenotypic profile. These findings indicate that a basaloid variant of adenocarcinoma is also existing in the spectrum of basaloid carcinomas of the lung.