No abstract

We examined the clinicopathologic features of 11 surgically resected hepatocellular carcinomas (HCCs) less than 3 cm in diameter with marked inflammatory cell infiltration (LHCCs). In comparison with the other 152 HCCs without such an infiltration (controls), there were no significant differences in male/female ratio, age, serum ␣-fetoprotein levels, and laboratory and imaging findings. All the 11 LHCC cases were hepatitis B surface antigen (HBsAg) negative and hepatitis C virus antibody positive. Among the 152 controls, 116 cases were also HBsAg negative and HCVAb positive and were referred to as HCV-only controls. The clinical features were not significantly different between the LHCC and the HCV-only controls. The LHCC group tended to have higher numbers of lymphocytes and monocytes in pre-and post-operative peripheral blood, but there were no significant group differences. Recurrence rate was 9.1% in the LHCC group, 47.7% in the controls and 47.5% in the HCV-only controls (P F .01). Five-year survival rate was 100% in the LHCC group, 65.1% in the controls and 68.1% in the HCV-only controls (P Ͻ .01). Histologically, remarkable inflammatory cell infiltration, mostly lymphocytic, was observed in the cancerous tissue of the LHCC group. Varying degrees of piecemeal necrosis of cancer nests produced by infiltrating lymphocytes were observed in all the 11 cases. Lymph follicle formation was also found in 10 of 11 cases (90.9%). Liver cirrhosis was associated in 6 LHCC cases (54.5%), in 117 control cases (77.0%), and in 91 HCV-only controls (78.4%). Tumor invasion into the portal vein in the vicinity of the tumor was found in 1 LHCC case (9.1%), in 54 controls (35.5%), and in 34 HCV-only controls (29.3%). Immunohistochemically, most of the infiltrating lymphocytes, other than those in the lymph follicle, were identified as T lymphocyte, and CD8 ؉ T lymphocyte was more predominant than CD4 ؉ T lymphocyte. Better prognosis of the LHCC group could attribute to the anti-tumor effect induced by cellular immunity of CD8 ؉ and CD4 ؉ T lymphocytes, and partly by humoral immunity of B cells which formed lymph follicles. (HEPATOLOGY 1998;27:407-414.)When tumor tissues are associated with tumor-infiltrating lymphocytes at a high density or with sinus histiocytosis in its regional lymph node at a high intensity, good postoperative survival rates for cancers have been reported in various organs. [1][2][3][4][5][6] As a mechanism of the good survival, involvement of anti-tumor effect via cellular immunity mainly of T lymphocyte and via humoral immunity of B lymphocyte, or of cytokines produced by the cancer cell itself, has been considered. [2][3][4][5][6][7][8][9][10][11] Meanwhile, as a result of the remarkable advance and popularization of various diagnostic imaging methods, the number of hepatocellular carcinoma (HCC) detected has been increasing and has been successfully resected. [15][16][17] Occasionally, HCCs with marked lymphocyte infiltration have been found among the resected tumors, 18-23 but their clinicopathologic ...

Recently, it has been shown that approximately 80% of Merkel cell carcinomas harbor a novel polyomavirus named Merkel cell polyomavirus, thought to be a carcinogenic agent. However, it is not fully elucidated whether Merkel cell carcinomas differ with regard to the presence or absence of Merkel cell polyomavirus. To address this, we investigated morphologic differences between Merkel cell polyomavirus-positive and -negative Merkel cell carcinomas by morphometry. Using polymerase chain reaction and real-time quantitative polymerase chain reaction, Merkel cell polyomavirus was detected in 20 (77%) of 26 Merkel cell carcinoma cases, including 4 Merkel cell carcinomas combined with squamous cell carcinomas. Interestingly, Merkel cell polyomavirus was detected only in ordinary (pure) Merkel cell carcinomas; none of the 4 combined Merkel cell carcinomas + squamous cell carcinomas was positive for Merkel cell polyomavirus (P = .001). Morphometric analyses revealed that Merkel cell polyomavirus-negative Merkel cell carcinomas had more irregular nuclei (P < .001) and more abundant cytoplasm (P = .001) than Merkel cell polyomavirus-positive Merkel cell carcinomas, which had uniform round nuclei and scant cytoplasm. Reliability of the morphometry was confirmed using intraobserver and interobserver reliability tests. These results demonstrated statistically significant differences in tumor cell morphology between Merkel cell polyomavirus-positive and -negative Merkel cell carcinomas and reconfirmed the absence of Merkel cell polyomavirus in combined tumors. Furthermore, the results strongly suggest fundamental biological differences between Merkel cell polyomavirus-positive and -negative Merkel cell carcinomas, supporting that Merkel cell polyomavirus plays an important role in the pathogenesis of Merkel cell polyomavirus-positive Merkel cell carcinoma.

No abstract

Classical trichoblastic fibroma or small nodular type trichoblastoma (Ackerman) is a rare tumour. This tumour, trichoepithelioma and basal cell carcinoma (BCC) have some overlapping histopathological features. There are only a few reports on immunohistochemical studies in large series of these three neoplasms. We investigated immunostaining patterns of 10 different anticytokeratin (CK) antibodies and several other markers in these neoplasms, comparing them with the patterns in normal adult and fetal skin. In trichoblastic fibroma (three cases), CK1/5/10/14, CK7, CK8/18, CK10/11, CK14, CK17 and CK19 were expressed in the basaloid nests, and CK6 and involucrin were detected in the inner layers of keratinous cysts. Trichoepithelioma (seven cases) expressed CK1/5/10/14, CK8/18, CK14, CK17 and CK19 in the basaloid nests, and CK6, CK10, CK10/11 and involucrin were positive in the keratinous cysts. However, no CK7 expression was observed. Solid and keratotic types of BCC (29 cases) expressed CK1/5/10/14, CK7, CK8/18, CK14, CK17 and CK19 in the basaloid nests. The keratinous cysts in BCC were stained with anti-CK6, CK10, CK10/11 and involucrin antibodies. Coupled with the expression of CK8/18, CK17 and CK19 in the outer root sheath of the adult hair follicle, these three neoplasms shared a keratin phenotype characteristic of the outer root sheath. Judging from our immunohistochemical results, trichoblastic fibroma and BCC cannot be differentiated by their patterns of CK expression. The expression of CK7, which is noted in fetal hair follicles, trichoblastic fibroma and BCC, suggests the presence of subpopulations that retain fetal phenotypic characteristics in these two neoplasms. Although the current concept regards trichoepithelioma and trichoblastic fibroma as a single tumour group, the lack of CK7 expression in trichoepithelioma supports the notion that the two are different.