Interobserver variability of histopathological prognostic parameters in cutaneous malignant melanoma: impact on patient management.

Clinical management of primary cutaneous melanomas is based on histopathological staging of the tumour. The aim of this study was to investigate, in a non-selected population in clinical practice, the agreement rate between general pathologists and pathologists experienced in melanoma in terms of the evaluation of histopathological prognostic parameters in cutaneous malignant melanomas, and to what extent the putative variability affected clinical management. A total of 234 cases of invasive cutaneous malignant melanoma were included in the study from the Stockholm-Gotland Healthcare Region in Sweden. Overall interobserver variability between a general pathologist and an expert review was 68.8-84.8%. Approximately 15.5% of melanomas ≤1 mm were re-classified either as melanoma in situ or melanomas >1 mm after review. In conclusion, review by a pathologist experienced in melanoma resulted in a change in recommendations about surgical excision margins and/or sentinel node biopsy in subgroups of T1 melanomas.

Differences in the peritumoural inflammatory skin infiltrate between squamous cell carcinomas in organ transplant recipients and immunocompetent patients.

Organ transplant recipients (OTR) have a greatly increased risk (up to 100 times) of developing squamous cell carcinomas (SCC) in the skin. This is attributed specifically to chronic immunosuppression, causing dysfunctional viral defence and tumour protection. To investigate the possible link between increasing risk of SCCs and type of inflammation in these tumour-prone patients, we analysed the peritumoural infiltrates with regard to cell types and densities. Seven SCCs from immunosuppressed OTR and 14 SCCs from immunocompetent patients were immun-histochemically stained for CD3, CD4, CD8, CD56, CD20, CD138, CD14, CD68, CD1a. Cell counts were performed with the aid of computer-based image analysis of > 100,000 cells. When comparing the percentage distributions, significant differences were detected (outlined as median values (min-max)): T cells (CD3+): OTR 57% (35-78), controls 68% (48-80), p = 0.036; plasma cells (CD138+): OTR 2% (0.7-7), controls 0.2% (0-1.2), p = 0.001; mono-cytes (CD14+): OTR 3.2% (1.1-5.6), controls 9.3% (2.2-17.2), p = 0.014. Surprisingly, no differences in cell densities, i.e. cells/mm2 tumour section area, were detected between the 2 groups. In conclusion, we found that the peritumoural infiltrates in immunosuppressed compared with immunocompetent patients differ in cellular composition, inferring a more tumour-submissive environment in OTR. However, cellular densities were equal, suggesting deviating cellular functionality in OTR.

Changes in tissue prostatic acidic phosphatase during endocrine treatment of patients with prostatic carcinoma.

OBJECTIVE: We have previously developed methods for the quantification of different macromolecules in aspiration biopsy material and described the changes in prostate-specific antigen (T-PSA) during cancer treatment. We have now studied the changes in tissue prostatic acidic phosphatase (T-PAP) in 58 endocrine-treated patients with prostatic carcinoma and compared these data with cancer development data and tissue PSA (T-PSA) levels. MATERIAL AND METHODS: PAP and PSA were quantified in aspiration biopsies taken before treatment and after 6 and 12 months of treatment. Patients were followed until death or for >98 months. RESULTS: Pretreatment T-PSA was more strongly associated with survival than T-PAP. Both T-PSA and T-PAP decreased in responders during treatment. In non-responders, T-PSA and T-PAP increased after 12 months in 17/18 and 7/13 patients, respectively. Estrogen-treated responders had significantly higher T-PSA, but not T-PAP, treatment values than those treated with orchidectomy or gonadotropin-releasing hormone. CONCLUSIONS: The inferiority of serum PAP compared to PSA for monitoring cancer treatment may reflect its less pronounced changes at the tissue level, indicating different in vivo regulation of the two markers. Estrogen stimulation of PSA synthesis in vivo may underlie the higher PSA levels observed during estrogen treatment.