The distribution of myofibroblasts and CD34-positive stromal cells in normal renal pelvis and ureter and their cancers.

In this article, we examined the distribution of myofibroblasts and CD34-positive stromal cells in normal renal pelvis and ureter and their cancers using immunohistochemistry. Eighteen tumors and normal tissues apart from the main tumor were examined. In the wall of normal renal pelvis and ureter, no myofibroblasts were observed through all layers, but CD34-positive stromal cells were observed in the deep area of lamina propria, muscular layer and adventitia. In the stroma of renal pelvic and ureteral cancers, myofibroblasts were distributed in fifteen tumors and were absent in three tumors. All three tumors containing no myofibroblasts in the stroma were non-invasive type and all invasive cancers contained myofibroblasts in the stroma. CD34-positive stromal cells were consistently absent in the stroma of cancers, irrespective of the invasiveness. Finally, myofibroblasts are major stromal components in renal pelvic and ureteral cancers, particularly in invasive cancers, and CD34-positive stromal cells are consistently absent or lost in the stroma of their cancers. These findings suggest that the invasion of renal pelvic and ureteral cancers may cause the phenotypic change of stromal cells.

Pulmonary adenocarcinoma with micropapillary component: an immunohistochemical study. Case report.

Micropapillary carcinoma has been described in various organs, including the breast, urinary bladder, ovary and lung. We here present a case of pulmonary micropapillary carcinoma in a 72-year-old Japanese man who died of respiratory failure and septic shock, following which autopsy was performed. A mass measuring 2.5 x 2.5 x 2.5 cm was observed in the left lower lobe of the lung. The tumor showed moderately differentiated papillary adenocarcinoma with a focal micropapillary component. Carcinomatous lymphangiosis was also observed in the left lung and metastatic lesions were observed in the bilateral lung, liver, vertebra, muscle layer of the urinary bladder, right adrenal gland, spleen and lymph nodes. The micropapillary component was predominant at some metastatic sites. Immunohistochemically, both the adenocarcinoma and micropapillary components were positive for cytokeratin (CK) 7, CK19, TTF (thyroid transcription factor)-1, carcinoembryonic antigen (CEA) and surfactant apoprotein A (SP-A), and negative for CK20, estrogen receptor, progesterone receptor, uroplakin III, and CA125. The invasive area of the conventional adenocarcinoma component contained a large number of myofibroblasts, whereas the stroma of the micropapillary component contained a small number of myofibroblasts. However, no myofibroblasts were observed in the stroma of the central core of the non-invasive micropapillary carcinoma. Several lymphatic invasions by neoplastic cells were identified in the peripheral area of the micropapillary component using D2-40 antibody. The immunohistochemical profile may be helpful in determining the primary location of the neoplasm containing micropapillary features. Myofibroblasts are present in the stroma of the invasive neoplastic nests in the micropapillary component as well as the conventional adenocarcinoma component, and D2-40 monoclonal antibody may be useful for evaluating the lymphatic invasion of pulmonary micropapillary carcinoma.

Consistent lack of CD34-positive stromal cells in the stroma of malignant breast lesions.

To examine the distribution of CD34-positive and ASMA-positive stromal cells in various breast lesions, we performed immunohistochemical assays (using a streptavidin-biotin immunoperoxidase technique) of tissue specimens, obtained by excisional biopsy and partial or total mastectomy, from 62 patients with breast lesions. Specimens were obtained from 64 lesions as follows: fibrocystic disease (n=12), intraductal papilloma (n=4), fibroadenoma (n=17), invasive lobular carcinoma (n=6), invasive ductal carcinoma (n=20) and invasive micropapillary carcinoma (n=5). In normal breast tissue (controls), CD34-positive spindle cells were abundant in the intralobular stroma, but no ASMA-positive stromal cells were identified except myoepithelial cells. Small to large numbers of CD34-positive cells were observed in the stroma of 29 of 33 benign diseases. In all invasive carcinomas (lobular, ductal and micropapillary), no CD34-positive stromal cells were observed in the stroma. In the stroma of benign lesions, the number of ASMA-positive stromal cells was various, but the stroma of all invasive breast cancers contained ASMA-positive stromal cells. The present results indicate that disappearance of CD34-positive stromal cells consistently occurs in the stroma of invasive carcinoma of the breast, irrespective of histological type and may be associated with the presence of ASMA-positive stromal cells.

The appearance of myofibroblasts and the disappearance of CD34-positive stromal cells in the area adjacent to xanthogranulomatous foci of chronic cholecystitis.

We investigated the distribution of myofibroblasts and CD34-positive stromal cells in normal gallbladder and its pathological conditions (cholecystitis, n=25) using immunohistochemistry and in situ hybridization. In the wall of normal gallbladder, myofibroblasts were generally absent from all layers, but many CD34-positive stromal cells were observed in the connective tissue layer. In chronic cholecystitis with mild perimuscular fibrosis, a small to moderate number of myofibroblasts appeared in the mucosal layer. In chronic cholecystitis with marked perimuscular fibrosis, a small to large number of myofibroblasts appeared predominantly in the connective tissue layer, whereas the number of CD34-positive stromal cells decreased at the same location, although the number of myofibroblasts increased. In chronic cholecystitis with xanthogranulomatous foci, a small to large number of myofibroblasts were observed in the periphery of the xanthogranulomatous reaction and adjacent area. In contrast, CD34-positive stromal cells were completely absent or were limited to the area just around the xanthogranulomatous reaction. Induction of collagen type I and III mRNA was predominantly observed in the cytoplasm of myofibroblasts associated with the marked fibrosis, which consisted primarily of mature collagen fibers, and in the cytoplasm of myofibroblasts around the xanthogranulomatous reaction, respectively. Finally, myofibroblasts were observed in all subtypes. The increased number of myofibroblasts was most prominent in the connective tissue layer of chronic cholecystitis with marked perimuscular fibrosis or in the area adjacent to xanthogranulomatous foci of chronic cholecystitis. Under these conditions, CD34-positive stromal cells tended to disappear from the connective tissue layer, which exhibited an increase in myofibroblasts.

Intestinal Behçet's disease associated with non-Hodgkin's lymphoma.

A 45-year-old man with intestinal Behçet's disease noticed an enlarged right cervical lymph node, and was diagnosed with diffuse large cell type, non-Hodgkin's lymphoma. The intrapelvic lymph tract was markedly deformed because of recurrent ileocecal ulceration, and conventional lymphoscintigraphy with a common tracer did not abolish the suspicion that lymphoma cells may have invaded the lymph nodes. Dynamic lymphoscintigraphy with a new tracer, 99mtechnetium-diethylene triamine pentaacetic acid-human serum albumin, because of its high detection sensitivity, was very useful for excluding this suspicion, and for determining the clinical stage of lymphoma. Combination induction chemotherapy led to complete remission without any adverse effects, but subsequent supportive therapy with same protocol could not be completed because of progression of the intestinal lesions. Special management for the intestinal lesions, such as bowel rest, may be essential with chemotherapy for patients with intestinal Behçet's disease.

[A case of flomoxef-induced pneumonitis].

We report a case of flomoxef-induced pneumonitis. A 22-year-old man was treated with flomoxef following liver biopsy. A few days later he developed a high fever and severe dyspnea, and his chest X-ray film revealed diffuse reticulo-nodular shadows in both lung fields. We suspected interstitial pneumonitis due to flomoxef, and pulse therapy with methylprednisolone was started. He showed rapid recovery of symptoms and marked regression of pulmonary infiltration in his chest X-ray. Lymphocyte stimulation test was positive to flomoxef, which was compatible with the diagnosis of drug-induced pneumonitis. To our knowledge, there has been no previous case of pulmonary hypersensitivity to flomoxef reported in Japan.