Geographic clustering of testicular cancer incidence in the northern part of The Netherlands

Geographic variations in testicular cancer incidence may be caused by differences in environmental factors, genetic factors, or both. In the present study, geographic patterns of age-adjusted testicular cancer incidence rates (IRs) in 12 provinces in The Netherlands in the period 1989–1995 were analysed. In addition, the age-adjusted IR of testicular cancer by degree of urbanization was evaluated. Cancer incidence data were obtained from the Netherlands Cancer Registry. The overall annual age-adjusted IR of testicular cancer in The Netherlands in the period 1989–1995 was 4.4 per 100 000 men. The province Groningen in the north of the country showed the highest annual IR with 5.8 per 100 000 men, which was higher (P < 0.05) than the overall IR in The Netherlands (incidence rate ratio (IRR) 1.3, 95% confidence interval (CI) 1.1–1.6). The highest IR in Groningen was seen for both seminomas and non-seminomas. In addition, Groningen showed the highest age-specific IRs in all relevant younger age groups (15–29, 30–44 and 45–59 years), illustrating the consistency of data. The province Friesland, also situated in the northern part of the country, showed the second highest IR of testicular cancer with 5.3 cases per 100 000 men per year (IRR 1.2, 95% Cl 1.0–1.5, not significant). This mainly resulted from the high IR of seminoma in Friesland. Analysis of age-adjusted IRs of testicular cancer by degree of urbanization in The Netherlands showed no urban–rural differences at analysis of all histological types combined, or at separate analyses of seminomas and non-seminomas. Geographic clustering of testicular cancer seems to be present in the rural north of The Netherlands with some stable founder populations, which are likely to share a relatively high frequency of genes from common ancestors including genes possibly related to testicular cancer. Although this finding does not exclude the involvement of shared environmental factors in the aetiology of testicular cancer, it may also lend support to a genetic susceptibility to testicular cancer development. Testicular cancer cases in stable founder populations seem particularly suitable for searching for testicular cancer susceptibility genes because such genes are likely to be more frequent among affected men in such populations. © 1999 Cancer Research Campaig

SUBREGIONAL LOCALIZATION OF 20 SINGLE-COPY LOCI TO CHROMOSOME 6 BY FLUORESCENCE IN SITU HYBRIDIZATION

Although 338 genetic loci and 1 or more candidate tumor suppressor genes have been assigned to chromosome 6, the physical and genetic map of this chromosome is at a very preliminary stage. In this study, we have performed subregional localization of 20 single-copy DNA sequences previously assigned to chromosome 6 using the fluorescence in situ hybridization technique. One locus, D6S6, was localized at 6p12. Two loci, D6S160 and D6S32, were localized in proximal 6q, at 6q12 and 6q23.3, respectively. The remaining loci were clustered in two regions, 4 at 6q23.5-q25 (D6S33, D6S43, D6S85, MYB) and 13 at 6q26-q27 (D6S2, D6S21, D6S22, D6S25, D6S37, D6S39, D6S44, D6S48, D6S132, D6S133, D6S148, D6S170, D6S201). These data will aid in the eventual development of the physical map of chromosome 6

SUBREGIONAL MAPPING OF 8 SINGLE COPY LOCI TO CHROMOSOME 6 BY FLUORESCENCE IN SITU HYBRIDIZATION

We have subregionally mapped 8 independently derived probes which have been assigned to chromosome 6 (D6S61, D6S134, D6S149, D6S155, MACS, VIL2, IGF2R and PLG) by FISH. All the probes were mapped to the long arm of chromosome 6 except D6S61, which was assigned to the short arm at 6p25. The remaining probes were clustered at the 6q25-->q27 region except MACS which was mapped to 6q22.2

Complete sequence and polymorphism study of the human TYRP1 gene encoding tyrosinase-related protein 1

The complete 24,667 nucleotide sequence spanning the human TYRP1 gene has been determined from the inserts of two overlapping lambda clones. A LINE-1 repeat element is immediately adjacent to and may demarcate the immediate 5' promoter region of the gene. A search for polymorphism within the seven TYRP1 coding exons has been performed by an RNase mismatch detection procedure. Analysis of the TYRP1 gene in 100 Caucasian individuals of varying hair color has found no amino acid sequence variation nor revealed any hemizygous mutant allele in the hypopigmented phenotype of two 9p(-) syndrome patients