dc.contributor.author | Wakhisi, J | |
dc.date.accessioned | 2013-06-10T15:31:01Z | |
dc.date.available | 2013-06-10T15:31:01Z | |
dc.date.issued | 2001-07 | |
dc.identifier.citation | East Afr Med J. 2001 Jul;78(7 Suppl):S48-9 | en |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/pubmed/11957250 | |
dc.identifier.uri | http://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/31064 | |
dc.description.abstract | Genetic 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.iso | en | en |
dc.title | Lessons learned from colorectal model of tumourigenesis. | en |
dc.type | Article | en |
local.publisher | Department of biochemistry | en |