Ashit Baran Sarker

Epstein‐Barr virus infection in the neoplastic and nonneoplastic cells of lymphoid malignancies

The Epstein‐Barr virus (EBV) has been frequently detected in lymphoid malignancies. However, EBV infection in the nonneoplastic cells of lymphoid malignancies has not been extensively studied.

An Immunohistochemical and Ultrastructural Study of Case of Small‐cell Neuroendocrine Carcinoma in the Ampullary Region of the Duodenum

One case of small‐cell neuroendocrine carcinoma in the ampullary region of the duodenum is reported. The histological appearance of the tumor was identical to pulmonary small‐cell carcinoma. Neuroendocrine differentiation was demonstrated immunohistochemically by positive immunoreaction for neuron specific enolase, Leu 7 and chromogranin, and ultrastructurally by the presence of scanty dense core neurosecretory type granules. Small‐cell neuroendocrine carcinoma in the ampulla of Vater is extremely rare. To our knowledge, this is the sixth reported case.

Spindle cell hemagioendothelioma: A report of two cases

Two cases of spindle cell hemangioendothelioma (SCH) are reported. One of the patients was a 16 year old Japanese female, who had been suffering from Olliers disease (multiple enchondrornatosis) since 3 years of age and had developed multiple SCH in the right leg at the age of 11 years. Spindle cell hemangioendothelioma lesions coincided with the site of enchondromatosis and increased in number thereafter. This is the first report of Olliers disease complicated with multiple SCH. Another patient, a 33 year old Japanese female, who was a carrier of hepatitis B virus (HBV), developed solitary SCH in the lateral aspect of the right ankle where a lipoma was extirpated 10 years previously. Tumor cells of both cases were composed of four cell types: (i) spindle cells; (ii) epithelioid cells; (iii) vacuolated endothelial cells; and (iv) usual endothelial cells. Endothelia in the cavernous area and vacuolated cells reacted to Ulex europaeus agglutin 1 (UEA‐I), factor VIII‐related antigen and vimentin. Spindle cells and epithelioid cells reacted only to vimentin.

CD30 antigen in non‐Hodgkin's lymphoma

Expression of the CD30 antigen in lymphoid neoplasms and reactive lesions were examined immunohistologically using the monoclonal antibody BerH2. CD30 antigen was expressed in 17 of 18 patients with Hodgkins disease (HD), all of three anaplastic large cell lymphomas (ALCL), 11 of 52 T‐cell malignant lymphomas (TML) including ALCL, 13 of 153 B‐cell malignant lymphomas (BML) including ALCL, two of three malignant histiocytosis and one of four plasmacytomas, Although a single case of small cell lymphoma was positive, in cases of mixed cellular morphology, neoplastic cells of larger or more pleomorphic nuclei tended to be stained more extensively and intensively. This antigen is expressed in TML significantly more often than in BML (P 0.05). CD30 antigen was expressed less frequently at clinical stage I than those of stages II to IV. There was no significant relationship between CD30 antigen expression and that of proliferating cell nuclear antigen or CD43 antigen in non‐Hodgkins lymphomas (NHL). The CD30 antigen expression did not affect the prognosis of NHL overall, but in high grade TML, CD30 antigen‐positive individuals tended to have a more favorable prognosis than those that were negative. In reactive diseases, some plasma cells, immunoblasts, interdigitating cells, follicular center cells and histiocytes were stained positively, but not always, and with variable intensity. These results suggest that CD30 antigen is expressed In various cell lineages to some extent and may relate to cellular activation in some instances. When making the histopathologic diagnosis of HO or NHL including ALCL, CD30‐positive cell should be carefully interpreted. The authors believe that the name‘Ki‐1 lymphoma’or‘KM positive lymphoma’as a synonym of ALCL should therefore be abandoned.

Expression of vimentin and epithelial membrane antigen in human malignant lymphomas

Immunoreactivity with monoclonal antibodies against the intermediate filament protein, vimentin, and epithelial membrane antigen (EMA) was examined in 330 cases of lymphoma (317 non‐Hodgkins and 13 Hodgkins lymphomas), 12 reactive lymph nodes and mononuclear cells of the peripheral blood using either indirect immunoperox‐idase staining or the avidin‐biotin immunoperoxidase complex technique. The cell origin of each tumor was established using a panel of monoclonal antibodies against lymphocyte differentiation antigens. There were 41 T cell, 247 B cell and 29 undetermined lymphomas, and 13 cases of Hodgkins disease in the series. Vimentin was expressed in 24 T‐cell lymphomas (58.5%) and 60 B cell lymphomas (24.2%). This difference in frequency was statistically significant. Vimentin expression in follicular lymphomas was less frequent than in diffuse B‐cell lymphomas. In diffuse lymphomas, small and medium cell types were more reactive with anti‐vimentin than large cell types. Reed‐Sternberg cells (R‐S cells) in Hodgkins disease were positive for vimentin in 11 cases (84.6%). The frequency of EMA reactivity in lymphomas was low, particularly in T cell lymphomas. No positive cases were found among follicular lymphomas. In diffuse non Hodgkins lymphomas, EMA was expressed only in mixed and large cell types, but never in smaller ones. In conclusion, monoclonal antibodies against vimentin and EMA appear to be of limited usefulness for the diagnosis of non Hodgkins lymphomas, but anti vimentin antibody may be used as an adjunct to the diagnosis of R‐S cells in Hodgkins disease.

Bauhinia Purpurea (BPA) Binding to Normal and Neoplastic Thyroid Glands

Biotinylated bauhinia purpurea agglutinin (BPA) was studied, using the ABC method, in different thyroid gland conditions (26 follicular adenomas, 39 papillary carcinomas, 15 follicular carcinomas, and 10 normal thyroids), to determine whether specific lectin binding patterns were developed during malignant transformation that could enable the distinction of carcinoma from adenoma. In normal thyroids, BPA was very rarely and faintly reactive with follicular cells. In neoplastic conditions, BPA binding profiles for follicular adenoma were essentially identical to those of normal follicles, whereas BPA unequivocally reacted with follicular carcinoma and papillary carcinoma. BPA reacted more strongly with cells of papillary structures than with those forming solid nests and follicles. In papillary carcinoma, BPA binding was observed mostly in the apical surface and cytoplasm of carcinoma cells, whereas a diffuse cytoplasmic binding pattern was predominant in follicular carcinoma. Neuraminidase treatment had little or no effect on either normal or adenomatous follicular epithelium, whereas in follicular carcinoma, the number of positive cells and the staining intensity was increased. These findings suggest that BPA would be useful for the differential diagnosis of papillary and follicular carcinomas, and less consistently so, for differentiating follicular carcinoma from follicular adenoma. Peanut agglutinin with similar sugar specificity was not reactive with follicular cells either in normal or neoplastic glands.

Inflammatory pseudotumor of the urinary bladder with an aberrant expression of cytokeratin

A case of inflammatory pseudotumor of the urinary bladder in a 47 year old Japanese male patient is presented. Inflammatory pseudotumor of the urinary bladder is a benign but rare proliferative lesion of the submucosal stroma, easily mistaken for a malignant neoplasm. Based on the clinical diagnosis of bladder cancer by cystoscopy and magnetic resonance imaging (MRI), urologists started chemotherapy before results of the histological report were available which described inflammatory pseudotumor on the biopsy. Biopsied materials showed marked proliferation of irregularly bundled spindle ceils, varied in size and shape and separated in severe loose myxoid stroma with moderate infiltration of the inflammatory cells and capillary proliferations. At a glance, these findings resemble the sarcomatous pattern. However neither severe nuclear atypism nor atypical mitoses were present. Immunohistochemically, these spindle cells, which were positive for vimentin and α‐smooth muscle actin, showed a diffuse aberrant expression of cytokeratin. Some of them were positive for phosphotungstic acid hematoxylin. Electron microscopy revealed only the fibroblasts. No recurrence has been observed for 10 months. These findings indicate that inflammatory pseudotumor is a benign mesenchymal lesion that must be discriminated from true sarcoma to avoid subjecting the patient to unnecessary therapy. Only careful histological examination can enable a successful diagnosis.

Lectin Binding Patterns in Normal Liver, Chronic Active Hepatitis, Liver Cirrhosis, and Hepatocellular Carcinoma An Immunohistochemical and Immunoelectron Microscopic Study

We studied the binding patterns of 14 lectins in human normal and cirrhotic liver (LC) tissues and hepatocellular carcinomas (HCC) using the ABC method. Lectins were divided into 4 groups according to their binding patterns in normal tissues: (A) PHA, MPA, LcH, RCA I, and WGA, which bound to hepatocytes and all three types of sinusoidal cells; (B) BPA, GS‐I, PNA, and SBA, which bound to Kupffer cells and endothelia of interlobular arteries and veins and bile duct epithelia in the portal tract, but not to hepatocytes; (C) UEA‐I, which bound only to endothelia of interlobular arteries and veins and bile duct epithelia in the portal tract; (D) LBA, Lotus, LPA, and SJA, which showed no binding. Thus group B lectins may be useful markers of Kupffer cells. Only electron microscopic examination revealed the precise binding sites of lectins in sinusoidal cells and hepatocytes. Hepatocyte cell surface polarities demonstrated by lectin binding in LC and HCC were different from those in the normal liver. The binding pattern of PHA to LC hepatocytes changed from a membranous to both a membranous and a cytoplasmic pattern, and that of LcH to HCC cells changed to dot‐like staining in the cytoplasm. These changes of polarities in LC and HCC might be caused by changes in the distribution of lectin binding carbohydrates or by the altered glycosylation of glycoconjugates. Acta Pathol Jpn 42: 566–572, 1992.

Aberrant expression of the monocyte/macrophage phenotype in a human T cell line immortalized by HTLV‐I and an adult T cell leukemia/lymphoma cell line

An HTLV‐I‐immortalized human T cell line (JP‐2), a N‐methyl‐N′‐nitro‐N‐nitrosoguanidine‐treated JP‐2 line (JP‐2T), and an adult T cell leukemia cell line (ATL‐1T) were examined morphologically and phenotypically. All of these cell lines expressed some T cell markers, including CD4, and showed rearrangement of T cell receptor (TCR) genes, but they lacked CD3 and TCR antigens and expressed some myelomonocytic markers (CD68, HL‐21, CD15, CD16). JP‐2 cells grew in suspension, but JP‐2T and ATL‐1T cells, which mostly adhered to the surface of culture vessels, showed macrophage‐like morphological features and expressed more monocyte/macrophage markers (lysozyme, α1‐antitrypsin) and fibronectin. ATL‐1T cells transplanted into SCID mice lost the macrophage features. These results suggest that HTLV‐I infected T cells can express some macrophage features and that these cells may provide a model that will be useful in elucidating the phenotypic variability of T cell lymphomas.