Resistance to cancer treatments in renal cell carcinomas: Discovering novel apoptotic pathways

Rajandram, R ., Pat, B., Li, J., Percy, C. J., Vesey, D., Johnson, D. W. and Gobe, G. C. (2006). Resistance to cancer treatments in renal cell carcinomas: Discovering novel apoptotic pathways. In: Abstracts of the 42nd Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology. Australian and New Zealand Society of Nephrology Annual Scientific Meeting, Melbourne, Australia, (A42-A42). 14-18 August 2006. doi:10.1111/j.1440-1797.2006.00656.x


Author Rajandram, R .
Pat, B.
Li, J.
Percy, C. J.
Vesey, D.
Johnson, D. W.
Gobe, G. C.
Title of paper Resistance to cancer treatments in renal cell carcinomas: Discovering novel apoptotic pathways
Conference name Australian and New Zealand Society of Nephrology Annual Scientific Meeting
Conference location Melbourne, Australia
Conference dates 14-18 August 2006
Proceedings title Abstracts of the 42nd Annual Scientific Meeting of the Australian and New Zealand Society of Nephrology   Check publisher's open access policy
Journal name Nephrology   Check publisher's open access policy
Place of Publication Richmond, Vic., Australia
Publisher Wiley-Blackwell Publishing Asia
Publication Year 2006
Sub-type Published abstract
DOI 10.1111/j.1440-1797.2006.00656.x
ISSN 1320-5358
1440-1797
Volume 11
Issue S2
Start page A42
End page A42
Total pages 1
Language eng
Formatted Abstract/Summary
 Purpose: Renal cell carcinomas (RCCs) are resistant to cancer therapies in part by a lack of induced apoptosis. This project aimed to identify an RCC cell line in which apoptosis could be induced to such a level that the altered pathways might be analysed, and then use microarray to describe apoptosis-regulating genes that were significantly different in the apoptotic RCC versus its control. Methods: Two RCC cell lines (ACHN and SN12K-1) were treated with IFN-α (500 IU/mL), radiotherapy (20 Gy) or dual therapy of these treatments. Controls had ‘sham’ treatment. Apoptosis was quantified at 24 and 48 hrs. ACHN treated with dual therapy for 24 hrs had a moderate but significant increase in apoptosis over controls (4.91 ± 0.44% v. 1.44 ± 0.15%) (p < 0.05) and were used further for microarray assay. Microarrays (N = 3; 112 apoptosis-related genes) were done using RNA extracted from treated and control ACHN and analysed for alterations of minimum 2-fold in transcripts.  Results/Conclusions: 40 genes had upregulated and one had down-regulated 2-fold transcripts in treated cells. Bcl-2, Bax and p53 were significantly up-regulated in the array and subsequent protein analysis (Western immunoblots) showed close correlation with alterations in RNA transcript. A search of the literature revealed three gene families were novel in treated RCCs: the TNF receptor-associated factor, caspase recruitment domain, and cell death-inducing DFF-45 effector domain families. These may be worthy of further study as their modulation may attain a better level of apoptosis in treated RCCs. Their value as biomarkers needs further study.
Subjects 11 Medical and Health Sciences
1112 Oncology and Carcinogenesis
Keyword Renal
Carcinomas
Cancer therapy
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status UQ
Additional Notes DOI is for abstracts published on pages A1–A51 - Abstract 2525

Document type: Conference Paper
Collection: School of Medicine Publications
 
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Created: Tue, 02 Feb 2010, 09:30:37 EST by Ms May Balasaize on behalf of Faculty Of Health Sciences