Aims-Loss of heterozygosity (LOH) at specific chromosomal regions strongly suggests the existence of tumour suppressor genes at the relevant segment. Frequent LOH on chromosome 5q has been reported in a wide variety of human tumours, including those of the lung. The aim of this study was to screen for LOH and to clarify the location of putative tumour suppressor genes on chromosome 5 implicated in the genesis and/or development of non-small cell lung carcinoma. Methods-Thirty three patients with advanced non-small cell lung carcinoma were screened for LOH with a panel of 21 microsatellite DNA markers spanning the entire chromosome 5, using semiautomated fluorochrome based methodology. Results-Twenty of the non-small cell lung carcinoma samples displayed LOH for one or more informative locus. LOH involving only 5q was found in 10 of 14 of the informative samples. Deletions involving 5p only were not present in the samples under study. There was no evidence of microsatellite instability in any of the analysed loci. These results indicate the presence of five distinct segments displaying high frequencies of deletion on chromosome 5, namely: 5q11.2-q12.2, 5q15 (D5S644 locus), 5q22.3-q23.1, 5q31.1, and 5q35.3. Eight of 14 samples had simultaneous interstitial deletions in at least two diVerent regions. Moreover, concomitant deletion of three and four distinct regions was displayed in three of 14 and two of 14, respectively, of the informative samples. Conclusion-Allelic deletion on chromosome 5 is a frequent event in patients with non-small cell lung carcinoma. These results suggest the involvement of these five regions, either independently or simultaneously, in both lung squamous cell carcinoma and lung adenocarcinoma. (J Clin Pathol: Mol Pathol 2000;53:184-187) Keywords: non-small cell lung carcinoma; chromosome 5; loss of heterozygosity Inactivation of tumour suppressor genes appears to be one of the genetic mechanisms involved in the development of solid tumours. This process includes mutation of one allele, followed by a deletion of the remaining one (loss of heterozygosity; LOH) or homozygous deletion of both alleles. Allelic deletions detected as LOH have proved useful for mapping regions of DNA that contain tumour suppressor genes.In non-small cell lung cancer the chromosomes most frequently aVected by LOH are 3p, 5q, 9p, 13q, and 17p.
Background: This study describes the possibility of implemen ng threedimensional prin ng technology to create a precise construc on of a planned bolus, based on computed tomography informa on stored in the Digital Imaging and Communica ons in Medicine (DICOM) format file. Materials and Methods: To create the bolus with a 3D printer, we converted data in the DICOM format to the stereolithography (STL) format. In addi on, we produced a paraffin bolus that, tradi onally, is manually placed directly on the pa ent. CT scans were acquired for both boluses, and the images were superimposed onto the pa ent CT scans that were used to design the bolus. The superimposi on of images was performed to compare the fit of the bolus printed on a 3D printer to that of the paraffin bolus made in the tradi onal way. In addi on, for both models, the dose distribu on was simulated. To quan fy the level of matching ML, special formula was used. The ML parameter had a value between 0 and 100%, where 100% indicated a perfect fit between the model and the 3D printed bolus. Results: We verified that 100% of the volume of the 3D printed bolus was located within the contour of the designed model. The ML of the bolus was 94%. For the classical paraffin bolus the ML was only 28%. Conclusion: A bolus printed on a threedimensional printer can faithfully reproduce the structure specified in the project plan. Compared to the classical paraffin bolus, the three-dimensional printed bolus more closely matched the planned model and possessed greater material uniformity.
Epidemiological studies have led to the suggestion that a genetic basis may exist in the individual variation in predisposition to cancer. Interindividual differences in human toxicological response to carcinogenic exposure have been attributed to heritable polymorphisms in metabolism, namely glutathione S-transferases (GSTs) coding for enzymes that are known to be detoxifiers of carcinogens. Within the human GST mu class, there is a specific isozyme that is frequently lacking. To check whether or not this association exists in the Portuguese population with lung cancer, we used polymerase chain reaction (PCR)-based genotyping to examine GSTM1 polymorphism (nulled and non-nulled) in 84 individuals as a control healthy population and a group of 98 lung cancer patients. In this study we were able to find a frequency of the GSTM1 phenotype among our healthy control subjects consistent with earlier genotyping studies in other Caucasoid populations. For the group of individuals with lung cancer as a whole, or in subsets of histological subtypes, our data for the Portuguese population did not show a positive correlation between the null allele and this neoplasm. In contrast, we found a slight increase in the frequency of the wild-type allele in our lung cancer group.
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