Biomedical subjects
Publications and source records attributed to L Bowles.
Patients and relatives often assume nurses have a higher level of knowledge than they actually possess. In the search for a professional body of knowledge, nurses may underestimate the valuable lessons patients can teach them. The nursing press may exacerbate the theory-practice gap by underrepresenting the experiences of patients, careers and relatives.
As yet, there is no reported study of chromosome allele loss in fibrolamellar carcinoma (FLC), a distinct, rare variant of hepatocellular carcinoma (HCC). We searched for evidence of allele loss in FLC using 18 DNA probes for 10 chromosomes and compared the pattern of loss with our series of HCC. Two of the probes, lambda MS32 (1q42-43) and cMS621 (5p) showed allele losses in one tumour, while other probes showed no loss. The frequency of allele loss in FLC was much lower than in HCC, which may be associated with their different prognoses.
Little is known of the molecular-genetic changes in carcinoma of the pancreas (CaP). In order to investigate the allele loss, or loss of heterozygosity (LOH), in CaP, we studied 13 patients with exocrine CaP and two with endocrine CaP using restriction fragment length polymorphism analysis. Twenty probes assigned to chromosomes 1, 5, 7, 9, 11, 12, 13, 14, 16, 17 and 18 were used. The frequency of LOH, or fractional allele loss (FAL), was found in two endocrine tumours to be 0.333 and 0.455 respectively; and FAL in 13 oxocrine tumours ranged from 0 to 0.25. Allele loss was shown in both exocrine and endocrine tumours by the probes Lambda MS1 at 1p33-35, and pMS51 at 11q13. Probes for other chromosomes have as yet shown no consistent LOH. In conclusion, the study showed LOH on chromosomes 1 and 11 in both exocrine and endocrine CaP.
DNA restriction fragment length polymorphism analysis was carried out on a primary and recurrent hepatocellular carcinoma in a hepatitis B virus negative patient. For the primary tumour, allele losses were found on the short arm of chromosome 17 (probe: p144-D6, 17p13) and the long arm of chromosome 5 with the probe Lambda MS8 (5q35-qter); other probes showed either no allele loss or a non-informative pattern. The recurrent cancer also showed allele loss with p144-D6, but not with Lambda MS8. In addition, the recurrent tumour had allele losses with Lambda MS43 (12q24.3-qter), pYNZ22 (17p13), and DNA rearrangement revealed by the probe Lambda MS32 (1q42-43), a pattern not seen in the primary lesion. These results indicate that the second hepatocellular carcinoma was of independent clonality and probably represents a de novo neoplasm rather than a recurrence.
Suppressor gene loci involved in the development of hepatocellular carcinoma (HCC) have not been fully identified. The aim of this study was to look for consistent allele loss, or loss of heterozygosity (LOH), in HCC which might represent such gene loci. We have prepared DNA from tumour and non-tumour material from 16 patients with HCC (nine with and seven without liver cirrhosis). Tumour DNA was compared with non-tumour DNA by Southern analysis performed with a panel of 22 probes recognising restriction fragment length polymorphisms assigned to chromosomes 1, 4, 5, 7, 9, 11, 12, 13, 14, 16, 17, 18 and 20. Non-tumour DNA from five of the seven patients with HCC without cirrhosis was heterozygous with the probe Lambda MS8 (5q35-qter), and in all five there was LOH in tumour DNA. Probes for other regions of chromosome 5 have as yet shown no LOH in this group of patients. Cirrhotic HCC patients exhibited LOH on chromosomes 1q and 5p but not in the region 5q35-qter. Both groups of HCC showed LOH on chromosome 17p13. Screening with other probes has not shown any consistent LOH in either group as yet. A comparison of LOH on chromosome 5 in seven patients with colorectal metastasis in the liver showed a different pattern, which suggests that the proposed tumour suppressor gene locus for HCC without cirrhosis on chromosome 5 appears to be distinct from the familial adenomatous polyposis coli gene.
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