Absence of nucleotide alteration in region of exon 34 of NOTCH1 and NOTCH2 receptor genes analysed in oral cancer samples: a preliminary observation
- Author:
Nor Nasyitah Ismail
;
Khairani Idah Mokhtar
- Publication Type:Journal Article
- Keywords:
oral cancer, NOTCH receptor, polymerase chain reaction.
- From:Archives of Orofacial Sciences
2010;5(1):17-23
- CountryMalaysia
- Language:English
-
Abstract:
Oral cancer is one of the common cancer cases identified in
the developing countries. Genetic mutation and overexpression of certain genes and proteins have been associated in the development of this
cancer. Notch signalling pathway is normally involved in controlling the development process of vertebrates and invertebrates; however, deregulation of this pathway was found to be responsible in the formation
of certain cancers including oral cancers. Activation of this pathway requires binding of the ligands to its receptors. Four NOTCH receptors (NOTCH 1, 2, 3 and 4) have been identified in mammals. Disruptions
within these molecules might interfere with the normal functions of Notch signalling pathway. Hence, this study was conducted to detect mutations of NOTCH1 and NOTCH2 receptor genes which might be occurring in the
oral cancer cases obtained from the local population. DNA extracted from fresh-frozen tissue biopsy of the tongue and buccal mucosa from 10 confirmed cases of oral cancer were subjected for polymerase chain
reaction (PCR) amplification using the specific sets of primers. The PCR products were sent for sequencing before final results were analysed. Due to time and cost limitation, only two out of four NOTCH receptor
genes; NOTCH1 and NOTCH2, were used in this analysis. The results revealed absence of nucleotide changes for both NOTCH receptor genes amplified from these oral cancer samples. More samples and further analysis looking into other regions in these genes are required to
conclude the involvement of NOTCH receptor genes mutation in causing oral cancer.
- Full text:W020150629325943821474.pdf
