Please use this identifier to cite or link to this item: https://doi.org/10.1016/0304-3835(96)04289-9
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dc.titleDifferential expression of adenosine A1 receptors in colorectal cancer and related mucosa
dc.contributor.authorKhoo, H.-E.
dc.contributor.authorHo, C.-L.
dc.contributor.authorChhatwal, V.J.S.
dc.contributor.authorChan, S.T.F.
dc.contributor.authorNgoi, S.-S.
dc.contributor.authorMoochhala, S.M.
dc.date.accessioned2014-11-10T09:52:29Z
dc.date.available2014-11-10T09:52:29Z
dc.date.issued1996-08-23
dc.identifier.citationKhoo, H.-E., Ho, C.-L., Chhatwal, V.J.S., Chan, S.T.F., Ngoi, S.-S., Moochhala, S.M. (1996-08-23). Differential expression of adenosine A1 receptors in colorectal cancer and related mucosa. Cancer Letters 106 (1) : 17-21. ScholarBank@NUS Repository. https://doi.org/10.1016/0304-3835(96)04289-9
dc.identifier.issn03043835
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/107787
dc.description.abstractAdenosine A1 receptors (A1R) are known to inhibit while the A2 receptors (A2R) stimulate the G-protein cAMP second messenger system and may play a role in cell growth and carcinogenesis. Using a quantitative reverse transcription-polymerase chain reaction (RT-PCR) method, mRNA for A1R and A2R was measured in human colorectal adenocarcinomas and individual peritumoural colon tissues. There was differential expression of the mRNA for A1R with tumour tissues having significantly higher amounts compared to peritumoural normal tissues. The mRNA for A2R was not found to be differentially expressed. The increase in the inhibitory A1 receptor in tumour tissues may be in response to increased adenosine release from the hypoxic cells found in malignant tumour tissues, thus indicating a possible role for the adenosine A1 receptor in carcinogenesis.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/0304-3835(96)04289-9
dc.sourceScopus
dc.subjectAdenosine receptor
dc.subjectColorectal cancer
dc.subjectReverse transcription-polymerase chain reaction
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.contributor.departmentSURGERY
dc.description.doi10.1016/0304-3835(96)04289-9
dc.description.sourcetitleCancer Letters
dc.description.volume106
dc.description.issue1
dc.description.page17-21
dc.description.codenCALED
dc.identifier.isiutA1996VG54900003
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