This population-based study shows that, because of the benign biological behavior of pilocytic astrocytomas and advances in microneurosurgery, the survival rates for patients with these tumors are excellent, regardless of postoperative radiotherapy.

No abstract

CTAs may be useful in the determination of suspected malignancy in cutaneous melanomas. The low incidence of particular CTAs can be overcome by increasing the number of CTAs analysed.

Melanoma-associated antigens are at the center of many immunotherapeutic trials in melanoma. Little is known about the impact of antigen expression on the natural course of disease. We stained 110 cases of primary melanoma with a median follow-up of 13 years (range 10-18 years) for melanoma-associated antigens gp100, MelanA/MART-1, MAGE-3, tyrosinase, and for HLA class I molecules. Of 91 cases evaluated, we found immunoreactivity for gp100, MelanA/MART-1, and tyrosinase in 88%, 80%, and 87% of primary tumors, respectively, for MAGE-3 in 37% and for HLA class I in 86% of primary tumors. Loss, that is, heterogeneous expression within primary tumors, was most pronounced for gp100 (73% of primary tumors) and least for MAGE-3 (27% of primary tumors). MelanA/MART-1 and tyrosinase expression loss was 58% and 59% of primary tumors, respectively. There was a high rate of expression loss for HLA class I (74%). Univariate and multivariate statistical analysis of expression in primary tumors and loss of melanoma antigens as well as HLA class I in individual primary tumors showed no significant correlation to overall survival. Loss of gp100 and loss of tyrosinase expression showed a negative survival trend over homogeneous expression of these antigens, although not reaching statistical significance (P = 0.08 and P = 0.09, respectively). We conclude that loss of melanoma antigen expression as well as HLA class I expression is a frequent observation in primary melanoma. However, no statistically significant correlation between loss of these antigens in individual primary tumors and negative impact on overall survival was found in our cohort.

In the prospective clinical long-term study of 246 patients with chronic pancreatitis, 26 patients (24 men) developed 27 histologically proved malignant tumors (11%). Four additional patients with neoplasia were excluded (papilloma, two; Bowen's disease of the tonsils, one; and seminoma, one, occurring 8 years before onset of pancreatitis). In six patients pancreatic cancer was diagnosed (2.4%), which indicates a slightly increased risk over the general population. Interestingly, 21 patients developed extrapancreatic cancer (8.5%), including a very high incidence that has not been noted previously. The cancers were located in the oral cavity (in six), larynx (three), bronchus (eight), and gastrointestinal tract (four). The data suggest a causal relationship between chronic pancreatitis and cancer. As possible factors, smoking, alcohol abuse, diabetes, malnutrition, immune deficiency, and high dietary fat intake are discussed. There is, however, no definite evidence for any single known factor.