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Biomedical subjects

J C Murray

Publications and source records attributed to J C Murray.

At least 217 records · Page 12Linked to original sources
PubMed1989

Changing character of cervical cancer in young women.

To examine the hypothesis that the pattern of cervical cancer is changing data on women presenting with the disease over 34 years were studied retrospectively. During 1953-86, 2628 women with cervical cancer were referred to a large tertiary referral hospital in Sydney; 418 were aged 35 or less. During the period of review the proportion of young women with the disease increased from under 9% in the 1950s and 1960s to about 25% in the 1970s and 1980s; a similar but less pronounced trend was apparent for the whole of New South Wales in the 1970s and 1980s. The prevalence of less common morphological types of cervical cancer increased throughout the period, particularly in the young. Pelvic lymph node metastases were identified in younger patients with stage Ib and IIa tumours more commonly in the later years of the study, suggesting that the disease was becoming more severe. Overall rates of recurrence improved over time, but an apparent increase in early recurrences was observed in young patients with Ib and IIa tumours and without nodal disease. The results suggest that the clinical and pathological behaviour of cervical cancer changed over the period of review.

Adult↗
PubMed1989

Linkage localization of Börjeson-Forssman-Lehmann syndrome.

Börjeson-Forssman-Lehmann syndrome (BFLS) is a form of X-linked mental retardation (XLMR) with characteristic minor physical anomalies. It has no biochemical or cytogenetic markers. Heterozygous females may be entirely normal or may have mild-to-moderate manifestations. We studied 41 individuals from one family with BFLS for linkage on the X chromosome. The highest lod scores were 2.32 with DXS10 and 2.24 with DXS51, both at a theta = 0.0. A single recombinant was found between HPRT and BFLS. These results suggest that the BFLS locus is on the distal portion of Xq. Previously reported linkage studies in families with XLMR have not shown linkage with DXS10. This study suggests that one of the several X chromosome loci whose dysfunction is associated with mental retardation is located on distal Xq.

Abnormalities, Multiple↗
PubMed1989

Vascular markers for murine tumours.

Damage to the vasculature may represent an important component of several forms of cancer therapy. Methods for studying the structure and function of the vasculature of experimental mouse tumours are required. In this paper several relatively simple methods are described for the histological examination of the vascular structure of murine tumours. The methods have been applied to cryostat sections of two sarcomas and two carcinomas. Immunoperoxidase staining with polyclonal antibodies to laminin highlights the vascular basement membrane of sarcomas, but has limited use with carcinomas, while the monoclonal antibody MECA-20 is a good marker for the endothelial cells of all vessels in all four tumours tested. The presence of endothelial cells in normal tissues can also be demonstrated by the use of enzyme-histochemical techniques for alkaline phosphatase, 5'-nucleotidase and nucleotide diphosphatase (ADPase), but only one of these methods (ADPase) works consistently in tumours. The relative merits of these methods are discussed and in all cases related to the staining pattern obtained with normal mouse tissues. The significance of these methods for vascular targeting is also discussed.

Alkaline Phosphatase↗
PubMed1989

Mapping of the human complement factor I gene to 4q25.

A detailed genetic and physical map of human complement factor I (IF) using somatic cell hybrids, in situ hybridization, and genetic linkage is reported. The gene has been localized to band 4q25. The order GC-INP10-ADH3-EGF-IF-IL2-MNS is proposed for genes on 4q on the basis of genetic and physical mapping techniques. A BclI polymorphism found with the IF probe demonstrated a maternal origin for a de novo deletion of chromosome 4 that was used in physically mapping the gene. The genetic and physical distances around band 4q24 suggest that 1 cM is approximately 1.2 million bp of DNA. This work provides a useful addition to the map of 4q.

Chromosome Mapping↗
PubMed1989

Flavone acetic acid induces a coagulopathy in mice.

The effects of flavone acetic acid (FAA) on the coagulation properties of plasma from tumour-bearing and non-tumour-bearing mice have been investigated. The study was carried out primarily on CBA mice and the CaNT tumour, although substantiating data are included for two other tumours grown in the WH strain. FAA was injected at a range of single doses up to a maximum of 300 mg kg-1, and clotting properties of the plasma were measured in vitro at various times after FAA administration. Platelet numbers and the concentration of fibrin degradation products (FDP) in the plasma were also determined. Following a dose of 300 mg kg-1, the clotting times were significantly reduced at 15-30 min in both tumour-bearing and non-tumour-bearing mice of both strains. Detailed studies on coagulation in the CBA strain (+/- CaNT tumour) indicate that in tumour-bearing animals the initial decrease in clotting time is followed 4-6 h later by an increase in clotting time, thrombin time and FDP levels. Platelet counts of tumour-bearing mice also decreased significantly over this period. Similar experiments in non-tumour-bearing mice did not show these late effects. All the data from the coagulation tests on mice with CaNT tumours are consistent with the hypothesis that intravascular coagulation occurs following treatment with FAA, and that vascular occlusion in tumours, as a results of FAA-induced coagulopathy, may contribute to tumour regression.

Animals↗
PubMed1989

Loss of heterozygosity suggests tumor suppressor gene responsible for primary hepatocellular carcinoma.

Primary hepatocellular carcinoma (PHC), epidemiologically associated with chronic hepatitis B virus (HBV) infection, has historically been felt to be caused by the activation or introduction of an oncogene. However, transforming sequences from human PHC have not been reproducibly isolated. In this paper, evidence is presented that suggests PHC may result instead from the loss of an anti-oncogene. Seven of 12 human primary liver tumors tested against a panel of restriction fragment length polymorphisms (RFLPs) demonstrated loss of constitutional heterozygosity for markers on chromosome 4. Tumor and nontumor liver tissue were typed for 11 chromosome 4 RFLPs. In addition, at least one RFLP on nine other chromosomes (1, 2, 6, 7, 9, 11, 13, 14, and 17) was tested for allelic loss. Seven of nine tumors constitutionally heterozygous for chromosome 4q markers showed allele loss in tumor tissue. Six of the seven samples were jointly informative for both 4p and 4q markers. Five of the six demonstrated loss for only 4q RFLPs. In one individual, in which two samples were taken from distant locations within the same tumor, both samples showed loss of the same alleles. Among the other chromosomes informative for allele loss, one tumor showed changes on 13q. No other changes were observed in RFLPs located on the eight other chromosomes tested. These results indicate that an anti-oncogene may be located on 4q and suggest a mechanism for PHC and other cancers seroepidemiologically related to virus infection. Liver cancer caused by chronic HBV infection or other environmental agents may be linked through genetic events responsible for the loss of a tumor suppressor locus (anti-oncogene) located on chromosome 4.

Carcinoma, Hepatocellular↗
PubMed1989

Polymorphic human insulin-responsive glucose-transporter gene on chromosome 17p13.

Glucose uptake by heart, skeletal muscle, and adipose tissue is acutely regulated by insulin, which stimulates facilitative glucose transport, at least in part, by promoting the translocation of transporters from an intracellular pool to the plasma membrane. cDNAs encoding the major human insulin-responsive glucose transporter have been isolated and indicate that the insulin-responsive glucose transporter expressed by heart, skeletal muscle, and adipose tissue is a 509-amino acid protein having 65.3, 54.3, and 57.5% identity with the erythrocyte/HepG2, liver, and fetal muscle glucose transporters, respectively. The gene encoding the insulin-responsive glucose transporter (designated GLUT4) was mapped to the p11----p13 region of the short arm of human chromosome 17 by analyzing its segregation in a panel of reduced human-mouse somatic cell hybrids. In situ hybridization to prometaphase chromosomes indicated that GLUT4 was in band p13. A common two-allele restriction-fragment-length polymorphism (RFLP) was identified with Kpn I, and linkage of this RFLP to other polymorphic DNA markers in this region of chromosome 17 provides a set of probes that will be useful for examining the role of this gene in the pathogenesis of diabetes mellitus.

Chromosome Mapping↗
PubMed1989

Linkage analysis of neurofibromatosis type I, using chromosome 17 DNA markers.

The gene for von Recklinghausen neurofibromatosis type 1 (NF1) has recently been mapped to the pericentromeric region of human chromosome 17. To further localize the NF1 gene, linkage analysis using chromosome 17 DNA markers was performed on 11 multigeneration families with 175 individuals, 57 of whom were affected. The markers used were D17Z1 (p17H8), D17S58 (EW301), D17S54 (EW203), D17S57 (EW206), D17S73 (EW207), CRI-L946, HOX-2, and growth hormone. Tight linkage was found between NF1 and D17Z1, D17S58, and D17S57 with a recombination fraction of zero. One recombinant was detected between NF1 and D17S73, showing linkage with a 10% recombination fraction. No linkage was detected between NF1 and CRI-L946 or between HOX-2 and growth hormone. Our data are consistent with the proposed gene order pter D17S58-D17Z1-NF1-D17S57-D17S73 qter.

Chromosome Mapping↗
PubMed1989

Association of genetic variation of the transforming growth factor-alpha gene with cleft lip and palate.

Complex segregation analysis of pedigrees having nonsyndromic cleft lip with or without cleft palate (CL/P) (Chung et al. 1986; Marazita et al. 1986) has shown that a major-locus model best explains the observed recurrence of CL/P in Caucasian families. To identify this major gene, we compared the frequencies of 12 RFLPs at five loci-epidermal growth factor, transforming growth factor-alpha, epidermal growth factor receptor, glucocorticoid receptor, and estrogen receptor-in both a group of 80 subjects with nonsyndromic CL/P and 102 controls. These candidate genes were selected because studies in rodents had suggested their possible involvement in palatogenesis. A significant association was observed between two RFLPs at the transforming-growth-factor-alpha (TGFA) locus and the occurrence of clefting (P = .0047 and P = .0052). This suggests that either the TGFA gene itself or DNA sequences in an adjacent region contribute to the development of a portion of cases of CL/P in humans and provides an opportunity to begin to examine the molecular events underlying lip and palate formation.

Adolescent↗