Identification of a region of frequent loss of heterozygosity at 11q24 in colorectal cancer.

Loss of heterozygosity (LOH) at 11q23-qter occurs frequently in ovarian and other cancers, but for colorectal cancer, the evidence is conflicting. Seven polymorphic loci were analyzed between D11S897 and D11S969 in 50 colorectal tumors. Two distinct LOH regions were detected, suggesting possible sites for tumor-suppressor genes involved in colorectal neoplasia: a large centromeric region between D11S897 and D11S925, and a telomeric 4.9-Mb region between D11S912 and D11S969. There was no correlation with clinicopathological features. This analysis describes a region of LOH in the region 11q23.3-24.3 for the first time in colorectal cancer and provides complementary evidence for the ongoing effort to identify the gene(s) involved.

In vivo semiconductor dosimetry as part of routine quality assurance.

This paper describes the initial physics testing necessary before diodes can be used for in vivo dosimetry as well as the development of a protocol for clinical use in head and neck treatment and the preliminary results acquired. 50 patients were entered into the pilot study. A total of 300 treatment set-ups were measured (184 entrance doses and 116 exit doses). Wedged and unwedged components of each field were measured separately, making the total number of entrance doses 284 and total number of exit doses 207. There was no significant systematic deviation in the measured entrance dose compared with the expected (mean +0.4%, SD 2.7%). Discrepancies between the observed and expected entrance doses of greater than 5% were recorded in 6% (16/284) of measurements. The mean of the measured exit doses was 2.4% lower than expected (SD 4.8%). Discrepancies between the observed and expected exist doses of greater than 5% were recorded in 32% (67/207) of measurements. Possible causes for these discrepancies are discussed. Overall analysis of the data for individual patients suggest that in one patient out of the 50 there may have been a delivered target volume dose discrepancy of greater than 5% (+6.5%). The significance of the results and the implications for routine use are discussed.

Hypertrophy of proximal tubular epithelial cells induced by low pH in vitro is independent of ammoniagenesis.

Metabolic acidosis can lead to tubular hypertrophy in vivo. This is thought to arise from stimulation of renal production of ammonia, a known hypertrophic agent. To examine this effect in vitro, confluent opossum (OK) proximal tubular epithelial cells were cultured at acidic pH (7.21 +/- 0.02) or at control pH (7.37 +/- 0.01) for 4 days. Protein content was 9% higher at acidic pH whereas DNA content was unaffected. The resulting increase in mean cell size (protein/DNA ratio) was 10% but correlated inversely with the mass of cells in control wells, varying from +48% at low cell mass to -14% at high cell mass. In contrast, low pH decreased 3H-thymidine incorporation by 9%. However, ammonia production was unaffected. These changes in protein/DNA ratio and 3H-thymidine incorporation cannot therefore be attributed to acid-induced ammoniagenesis and imply that low pH exerts a more direct effect on tubular cell growth than previously envisaged.

Idiopathic epidural lipomatosis as a cause of pain and neurological symptoms attributed initially to radiation damage.

Epidural lipomatosis is a rare condition in which overgrowth of extradural fat can lead to back pain, spinal cord compression and radiculopathy. A 51-year-old man developed back pain and reduced mobility following a standard course of radiotherapy for a Stage I seminoma. His symptoms and radiological appearances were initially attributed to radiation fibrosis. Further investigations and operative intervention revealed epidural lipomatosis. The excess lipomatous tissue was removed with complete resolution of his symptoms.