Using chromogranin (CG) immunohistochemical staining, the prognostic significance of endocrine differentiation was investigated in 212 patients with primary colorectal adenocarcinoma (including 6 patients with mucosal carcinoma). CG‐immunoreactive cells were found to be an integral component of the tumor in 67 of 206 patients (32.5%, excluding mucosal carcinoma). The intra‐cellular localization of CG in the CG‐immunoreactive cells in cancer tissue was completely different from that in the normal endocrine cells of the large bowel. In addition, morphologic changes such as nuclear hyperchromasia and pleomorphism also indicated that the CG‐immunoreactive cells in the cancer tissue were malignant. The tumors were divided into three groups based on the frequency of CG‐immunoreactive cells: Group I (n = 139), negative; Group II (n = 38), less than 1 positive cell/mm2; and Group III (n = 29), more than 1 positive cell/mm2. No correlation was observed between CG‐immunoreactivity (CG‐IR) and tumor location, grade, depth of invasion, or stage, regardless of lymph node involvement. However, patients with numerous endocrine tumor cells (Group III) had a significantly worse prognosis compared with patients without endocrine cells (Group I) (multivariate Cox's model, P < 0.01). Similar findings were observed in patients with node‐negative tumor (multivariate Cox's model, P < 0.05). These results indicated that the neuroendocrine differentiation is an independent prognostic factor and that CG‐immunohistochemistry is useful for detecting a subgroup with a worse prognosis among patients with colorectal cancer.
Eighty-two cases of primary invasive breast carcinoma and adjacent "normal" mammary glands were examined immunohistochemically for tenascin expression and distribution. Formalin-fixed tissues pretreated with actinase were processed by the avidin-biotin complex method using anti-human tenascin monoclonal antibody (RBC1). In normal mammary glands, tenascin was distributed around the ducts and ductules but not around the acini. In carcinomas, a high incidence of tenascin-positive cases (greater than 67%) was seen with various histological appearances, with the exception of lobular carcinoma where a low incidence was found (25%). Although intense staining was seen around cancerous foci when compared with normal mammary glands, tenascin was often expressed at cancer-mesenchymal junctions with dense fibrotic stroma, but not at junctions with active inflammatory change and a loose fibrotic stroma. Tenascin, expression is not an all-or-none marker for mammary malignancy and the staining pattern suggests either a role in stimulating cancer cells or a host defence mechanism accompanied by a desmoplastic response to them.
We report 13 cases of breast carcinoma i n patients treated with neuroleptics (prolactin rdeasing drugs). Twelve of the patients were female and one was male. Nine patients had unicentric carcinoma, one had multicentric tumors arising synchronously, and three had bilateral tumors (synchronous i n one case and metachronous i n two cases). Thirteen tumors i n ten patients were invasive ductal carcinomas, two tumors i n one patient were rnucinous carcinomas, and the two other patients had lipid-secreting carcinomas. lmrnunohistochemical s t a i n i n g showed alpha lactalbumin ( a LA) i n the lipid-secreting carcinomas at sites exhibiting active lipid secretion. A precise cause effect relationship is difficult to elucidate, since the patients ranged in age from 40 t o 64 years (mean : 5 1 years) when cancer was first diagnosed. However, the relatively high incidence of multiple tumors and the production of lipid and (Y LA by the cancer cells were unusual features suggesting an association with neuroleptic therapy. Acta Pathol Jpn 42: 494-499, 1992. Previous studies have clearly demonstrated a causal relationship between prolactin and mammary tumor [genesis in rodents (1) Hypothalamic (median em1 nence) lesioned and pituitary-transplanted rats and mice show enhanced mammary tumor development and accel eration of tumor growth in response t o prolactin secre tion Neuroleptics are used extensively in the treatment of severe psychiatric disturbances, and have been demonstrated t o cause elevated serum prolactin levels both in rodents (2) and humans (3, 4), presumably by
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