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dc.contributor.authorWakhisi, J
dc.date.accessioned2013-06-10T15:31:01Z
dc.date.available2013-06-10T15:31:01Z
dc.date.issued2001-07
dc.identifier.citationEast Afr Med J. 2001 Jul;78(7 Suppl):S48-9en
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/11957250
dc.identifier.urihttp://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/31064
dc.description.abstractGenetic analytical techniques were carried out to identify mutations in adenomatous polyposis coli (APC) gene and K-ras oncogene in colorectal tumourigenesis. These two genes are said to be early mutation genes among other mutation genes that constitute the model for colorectal tumourigenesis. To do this analysis, DNA was isolated from colorectal formalin fixed paraffin-embedded tumour tissue sections. The sections were deparaffinised, digested in proteinase-K, followed by DNA isolation. The DNA was amplified by Polymerase Chain Reaction (PCR), screened by using Denaturing Gradient Gel Electrophoresis (DGGE) or Single Strand Conformation Polymorphism (SSCP) and then sequenced. These results lend support to the fact that colorectal cancer and indeed cancer in general develops through a multi-step process; also that accumulation of genetic mutations underlie the development of neoplasia. We are in the process of extending this study to cancer of oesophagus to see if a similar or parallel model of carcinogenesis holds and in what sequence it is.en
dc.language.isoenen
dc.titleLessons learned from colorectal model of tumourigenesis.en
dc.typeArticleen
local.publisherDepartment of biochemistryen


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