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We have used selected ion flow tube mass spectrometry (SIFT-MS) to determine the concentration of formaldehyde in the headspace of urine from patients suffering from bladder and prostate cancer and from several healthy subjects as controls. We address the potential problems associated with the use of ion chemistry to quantify formaldehyde in the presence of the relatively large number densities of water molecules and show that formaldehyde can be quantified in urine headspace using analysis by SIFT-MS. These studies show that formaldehyde is clearly elevated in the headspace of the urine from the cancer patients as compared with urine from the healthy controls. Thus, with further improvements in the methodology and the sensitivity of our SIFT-MS technique, formaldehyde quantification in urine headspace using this new analytical method could be a valuable non-invasive indicator of the presence of early-stage tumours in the body.

We describe the use of our selected ion flow tube mass spectrometric technique (SIFT-MS) for the analysis of the headspace above urine. Ammonia, nitric oxide, acetone, ethanol and methanol are identified as the dominant species. As expected, the ammonia is increased in the headspace by making the urine alkaline and the nitric oxide is increased by making the urine acidic. Nitric oxide is abnormally high in the headspace of acidified bacterially infected urine and nitrous acid is also detected. The potential clinical implications of analyses of urine by SIFT-MS are alluded to.

Recent studies have shown that loss of heterozygosity (LOH) on chromosome 10q is a frequent event in a number of tumour types including colorectal cancers. Because previous studies have used markers located mainly distally on chromosome 10, we have examined 114 sporadic colorectal adenocarcinomas for LOH using a panel of 9 highly polymorphic microsatellite markers spanning the long arm of chromosome 10. Using microdissected tumour material, LOH of one or more chromosome 10q markers was a frequent event (75 of 114; 66%). The highest frequency of loss (42 of 96; 44%) was observed at the marker D10S1790 located at 10q21.1. The mean age of presentation, of patients with LOH of D10S1790 was significantly (p ‫؍‬ 0.0006) lower (67.1 years) compared to patients with retention of this marker (73.5 years). When we compared frequency of loss at this marker in patients presenting before 70 years of age (68%) to those above 70 years (23%) we observed a significant difference Key words: chromosome 10q; LOH; sporadic colorectal adenocarcinoma; TSG; tumor progressionColorectal adenocarcinoma is the second most common cause of cancer related death in the Western world. The majority of colorectal cancers are considered sporadic and present in the 7th and 8th decades of life, whereas hereditary colorectal adenocarcinoma accounts for approximately 10% of all cases and usually presents before the age of 50 years. 1 The initiation and progression of sporadic colorectal tumors has been described as a multi-step etiology involving the progressive loss of tumour suppressor function and concomitant inappropriate oncogene activation resulting in the deregulation of controlled cellular proliferation. 2 Frequent loss of heterozygosity (LOH) has been shown in regions harboring known tumour suppressor genes including 5q21(APC), 17p13(p53) and 18q21(DCC) involved in the development of sporadic colorectal adenocarcinoma. 2 Studies have shown frequent LOH on chromosome 10q in several tumour types including malignant gliomas, 3 malignant melanomas, 4 prostate, 5,6 endometrial, 7 breast 8,9 and bladder cancer. 10 Early studies of this chromosome, however, showed infrequent loss in colorectal cancer. 11 A subsequent allelotyping study 12 of sporadic colorectal adenocarcinomas showed that LOH on chromosome 10q was an infrequent event, however, this study only investigated a single locus (10q25-26). More recently Frayling et al. 13 using a more centromeric marker (D10S220) showed frequent LOH (37%) in sporadic colorectal adenocarcinomas on 10q11-21 suggesting the presence of a tumour suppressor gene (TSG) in this region. The presence of a TSG in this region is supported by findings in other tumour types including renal, 14 chondrosarcomas 15 and malignant glioma 3 that have shown frequent LOH at 10q11-21.Recently a TSG called PTEN, MMAC1 or TEP1 16 -18 has been localized to the chromosomal loci 10q23.3, loss and concomitant mutation in the retained PTEN allele have been shown in glioblastomas, 19 malignant melanoma, 20,21 squamous cell lung carcino...

We have used selected ion flow tube mass spectrometry (SIFT-MS) to determine the concentration of formaldehyde in the headspace of urine from patients suffering from bladder and prostate cancer and from several healthy subjects as controls. We address the potential problems associated with the use of ion chemistry to quantify formaldehyde in the presence of the relatively large number densities of water molecules and show that formaldehyde can be quantified in urine headspace using analysis by SIFT-MS. These studies show that formaldehyde is clearly elevated in the headspace of the urine from the cancer patients as compared with urine from the healthy controls. Thus, with further improvements in the methodology and the sensitivity of our SIFT-MS technique, formaldehyde quantification in urine headspace using this new analytical method could be a valuable non-invasive indicator of the presence of early-stage tumours in the body.

No abstract

The objective of this study was to determine whether the association between GSTM1 null/GSTTI null and survival in ovarian cancer is mediated by the influence of these genes on p53 expression. In 81 women with pure invasive ovarian cancer, GSTM1 null and GSTT1 null genotypes were identified using polymerase chain reaction and p53 expression was assessed using immunohistochemistry. The association of these factors with survival was examined using Cox's proportional hazards regression models. Performance status (P < 0.001), operative stage (P = 0.004), residual disease (P = 0.001), histologic subtype (P = 0.05), tumor grade (P = 0.007), and the combined GSTMI null/GSTTl null genotype (P = 0.023) were all individually associated with survival. p53 expression was not associated with survival (P = 0.45). In a multivariate analysis, the effects of GSTM1 null/GSTT1 null on survival were lost when residual disease and tumor grade were included. The effects of p53 expression on survival were unchanged when residual disease, tumor grade, operative stage, and performance score were included. GSTM1 null/GSTT1null did not influence the effects of p53 expression on survival and vice versa. The GSTM1 null/GSTT1 null genotype was associated with response to primary chemotherapy (P = 0.007) but p53 expression was not. We conclude that the association of GSTM1 null/GSTTl null with survival appears to be mediated through different mechanisms to p53 expression in ovarian cancer and in addition, may be a better predictor of outcome.