Characterization of the tissue light penetration in prostate photodynamic therapy (PDT) is important to plan the arrangement and weighting of light sources so that sufficient light fluence is delivered to the treatment volume. The optical properties (absorption [μ a ], transport scattering [ ] and effective attenuation [μ eff ] coefficients) of 13 patients with locally recurrent prostate cancer were measured in situ using interstitial isotropic detectors. Measurements were made at 732 nm before and after motexafin lutetium (MLu)-mediated PDT in four quadrants. Optical properties were derived by applying the diffusion theory to the fluence rates measured at several distances (0.5-5 cm) from a point source. μ a and varied between 0.07 and 1.62 cm −1 (mean 0.37 ± 0.24 cm −1 ) and 1.1 and 44 cm −1 (mean 14 ± 11 cm −1 ), respectively. μ a was proportional to the concentration of MLu measured by an ex vivo fluorescence assay. We have observed, on average, a reduction of the MLu concentration after PDT, presumably due to the PDT consumption of MLu. μ eff varied between 0.91 and 6.7 cm −1 (mean 2.9 ± 0.7 cm −1 ), corresponding to an optical penetration depth (δ = 1/μ eff ) of 0.1-1.1 cm (mean 0.4 ± 0.1 cm). The mean penetration depth at 732 nm in human prostate is at least two times smaller than that found in normal canine prostates, which can be explained by a four times increase of the mean value of in human prostates. The mean light fluence rate per unit source strength at 0.5 cm from a point source was 1.5 ± 1.1 cm −2 , excluding situations when bleeding occurs. The total number of measurements was N = 121 for all mean quantities listed above. This study showed significant inter-and intraprostatic differences in the optical properties, suggesting that a real-time dosimetry measurement and feedback system for monitoring light fluences during treatment should be considered for future PDT studies. ¶ Posted on the website on 9 November 2004.
LOH analysis suggests that multiple tumor suppressor genes play a role in the development of human TCC. The human homolog of the Drosophila PTCH was recently cloned and mapped to the BCNS locus on 9q22.3, a chromosomal region commonly deleted in TCCs. We ®rst examined the steady state mRNA transcription of the PTCH, SMOH and GLI3 genes of the HH signal transduction pathway in TCC cell lines and normal urothelium. Normal urothelium and TCC cell lines express these three genes within the PTCH signal transduction pathway. We then screened for PTCH mutations in`hot spot' exons 6, 8, 13 and 16 by PCR/ SSCP analysis of genomic DNAs from 54 TCC tumor samples and control autologous peripheral blood lymphocytes. DNA sequence analysis con®rmed TCCspeci®c mutations in two of 54 patients (3.7%). These mutations resulted a single amino acid substitution and two frame shifts. One tumor had PTCH mutations in exon 16 as well as exon 13 and one tumor had a mutation in exon 13 alone. Both TCC tumors that contained PTCH mutations had a loss of heterozygosity at 9q. Although the PTCH protein has an unknown function in urothelial cells, the detection of the PTCH, SMOH and GLI3 transcripts in normal urothelium and TCC cell lines and rare PTCH mutations in tumor samples suggest that the HH pathway may have a role in controlling the proliferation of urothelial cells and that PTCH mutations may contribute to the development of a subset of TCCs.
A panel of 18 superficial or invasive transitional cell carcinomas (TCCs) was analyzed for chromosome 9 deletions by performing a high-density loss of heterozygosity (LOH) analysis. Twenty-five microsatellite loci were assayed by the polymerase chain reaction (PCR) and 7 restriction fragment length polymorphism (RFLP) loci were analyzed by Southern blotting. Concordant results were obtained with these methods, including direct comparisons at 2 loci. Chromosome 9 LOH was observed in 13 (72%) of 18 informative cases, including 10 superficial lesions. In contrast, LOH on chromosomes 10, 15, 20 and 21 was < or = 8%. Evidence for missing copies of chromosome 9 was observed in 7 of 13 LOH cases. Comparison of cases with subchromosomal LOH implicated the region between the D9S55 locus on 9p12 and the argininosuccinate synthetase (ASS) locus on 9q34.1 as the location of a tumor suppressor gene relevant to TCC.
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