bcl-2, the well known anti-apoptotic gene, cloned more than a decade ago, promotes cell viability without promoting cell proliferation. With few exceptions, high bcl-2 protein expression is associated with a favourable outcome in epithelial tumours. bcl-2 immunoreactivity in basal cell carcinomas (BCCs) is contradictory, with 67-100% immunopositivity being reported. Although BCCs are traditionally regarded as low-grade, indolent tumours, aggressive BCCs (A-BCCs) are mutilative, locally destructive tumours that often recur. bcl-2 protein expression as a predictor of BCC aggressiveness is poorly documented in the English-language literature. The bcl-2 protein immunoprofile of 50 clinically non-aggressive (NA-BCCs) and 25 clinically A-BCCs was investigated. Of the latter, 17 manifested with one, two or three recurrences. bcl-2 protein expression in each of the recurrences was also evaluated. bcl-2 expression was scored as follows: 0-5% positive cells=negative, 6-25%=1+, 26-50%=2+, 51-75%=3+, >75%=4+. "High" labeling encompassed 3+ or 4+ labeling while "low" labeling referred to 1 + or 2 + labeling. Although bcl-2 positivity was noted in all BCCs, low bcl-2 labeling was a statistically significant feature of A-BCCs (p < 0.01). High bcl-2 labeling of NA-BCCs was a reflection of the bcl-2 labeling of the dominant constituent nodular or superficial subtypes. Micronodular BCCs revealed 2+ or 3+ labeling. Initial and recurrent A-BCCs with a pure or predominantly infiltrative component, demonstrated 1+ or 2+ bcl-2 labeling. The differential bcl-2 expression in the various clinicopathological subtypes of BCCs suggests that, despite the common derivation of these tumours from a primitive basaloid stem cell and a limited potential for metastasis, they form a heterogeneous group of tumours that differ markedly in histologic and biological behaviour. While the superficial and nodular BCCs are indolent slow-growing tumours with high bcl-2 labeling, the aggressive BCCs are infiltrative, desmoplastic tumours with low bcl-2 labeling. In mixed tumours, heterogeneity of labeling is a distinctive feature and is contributed to in part by the labeling trends of the different histological subtypes. The micronodular BCC shows varied bcl-2 labeling but in combined tumours occupies a niche intermediate between the non-aggressive nodular and superficial and the aggressive infiltrative subtypes. The initial and subsequent biopsies of recurrent, adequately excised BCCs share a pure or mixed, predominantly infiltrative, stroma-rich histomorphology with low bcl-2 labeling, reflecting the immunoprofile of a more aggressive growth pattern.

Seventy three cases of Kaposi's sarcoma (KS) from the 3 histological subtypes (patch, plaque and nodular) were assessed for bcl-2 and p53 protein expression. The aim was to determine the level of expression of these proteins in KS and in the different subtypes. Commercially available antibodies to bcl-2 and p53 were applied after both microwave and pressure cooking antigen retrieval. Bcl-2 immunoexpression increased from the patch stage (36%) to the plaque stage (45%) to the nodular stage (70.83%). Better immunostaining for bcl-2 was obtained after pressure cooking. p53 on the other hand, was not expressed in the patch or plaque stages, but 54.16% of cases in the nodular stage were immunopositive. These results show a progression of immunoexpression of both bcl-2 and p53 from the early histological stages to the late tumor stage, implying that these proteins are upregulated late in the evolution of KS.

The inflammatory infiltrate at the epitheliomesenchymal interface, pseudoepitheliomatous hyperplasia, intra-epidermal accumulation and disintegration of neutrophils and histiocytes, and the associated release of lytic enzymes, play important contributory roles in TEE of GI. TEE of infectious agents is a poorly recognised mechanism of spread of infectious diseases and represents a public health hazard. In cutaneous vulval GI, TEE is highlighted as a hitherto unrecognised, potential method of spread of Calymmatobacterium granulomatis.