Ophthalmology (Eye & Ear Hospital) - Research Publications
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ItemAcute hemorrhagic conjunctivitis due to enterovirus 70 in India.(Centers for Disease Control and Prevention (CDC), 1999)An outbreak of acute hemorrhagic conjunctivitis occurred in Delhi, India, during August and September 1996. The etiologic agent was confirmed as enterovirus type 70 by a modified centrifugation-enhanced culture method followed by immunofluorescence and neutralization tests. After nearly a decade, this virus is reemerging as a cause of acute hemorrhagic conjunctivitis in India.
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ItemLOSS OF HETEROZYGOSITY AT 11P13 IN WILMS-TUMORS DOES NOT NECESSARILY INVOLVE MUTATIONS IN THE WT1 GENE(STOCKTON PRESS, 1993-06)Loss of heterozygosity (LOH) in tumour cells is generally accepted as 'exposing' recessive cancer genes. The short arm of chromosome 11 shows consistent LOH in Wilms' tumours along its entire length. Occasionally, however, only the 11p13 and/or the 11p15 regions are involved. Deletions of the 11p13 region consistently predisposes to Wilms' tumorigenesis. We have analysed the recently cloned WT1 gene from the 11p13 region exon-by-exon in five tumours previously shown to have undergone LOH for the 11p13 region, using single strand conformation polymorphism analysis (SSCP) and PCR sequencing. Our analysis using SSCP failed to identify any band shifts in the WT1 gene from these tumours. In addition we also sequenced the zinc finger region of WT1, which is the part of the gene most frequently showing mutations. Only the normal sequence was found in all of these tumours. These results demonstrate that LOH in Wilms' tumours is not always related to mutations in the WT1 genes and argues strongly that another gene, probably in the 11p15 region, may be more important in Wilms' tumorigenesis.
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ItemMOLECULAR-GENETIC ANALYSIS OF CHROMOSOME 11P IN FAMILIAL WILMS-TUMOR(STOCKTON PRESS, 1994-06)In the family reported here, a mother and both of her children developed a Wilms tumour, and all three tumours were of the relatively rare monomorphous epithelial histopathological subtype. Using restriction fragment length polymorphism analysis, both sibs were shown to inherit the same maternal allele from the 11p13 region but different maternal alleles from the 11p15 region. Using a combination of single-strand conformation polymorphism (SSCP) and polymerase chain reaction (PCR) sequencing techniques, no mutations were identified in the WT1 tumour-suppressor gene from the 11p13 region, but a novel polymorphism was identified in exon 1. mRNA expression studies using the insulin-like growth factor II (IGF-II) gene, located in 11p15, showed that there was no relaxation of imprinting at this locus. There was also no evidence of loss of heterozygosity on the long arm of chromosome 16. These findings indicate that the WT1 and IGF-II genes, together with the long arm of chromosome 16, are not directly implicated in tumorigenesis in this Wilms family, but that a recombination event has occurred on the short arm of chromosome 11.