Genetic basis for the increased expression of vacuolar H+ translocating ATPase genes upon imatinib treatment in human lymphoblastoid cells
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- 作者：Hemant Kulkarni (1)
Harald H. H. G?ring (1)
Joanne E. Curran (1)
Vincent Diego (1)
Thomas D. Dyer (1)
Shelley Cole (1)
Ken R. Walder (2)
Greg R. Collier (3)
John Blangero (1)
Melanie A. Carless (1) - 关键词：Chronic myeloid leukemia ; Metastasis ; Imatinib ; Microarray
- 刊名：Cancer Chemotherapy and Pharmacology
- 出版年：2013
- 出版时间：April 2013
- 年：2013
- 卷：71
- 期：4
- 页码：1095-1100
- 全文大小：295KB
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Harald H. H. G?ring (1)
Joanne E. Curran (1)
Vincent Diego (1)
Thomas D. Dyer (1)
Shelley Cole (1)
Ken R. Walder (2)
Greg R. Collier (3)
John Blangero (1)
Melanie A. Carless (1)
1. Department of Genetics, Texas Biomedical Research Institute, San Antonio, TX, 78227, USA
2. Deakin University, Geelong, VIC, Australia
3. Barwon Biotechnology, Geelong, VIC, Australia - ISSN：1432-0843
文摘
Purpose The role of v-ATPases in cancer biology is being increasingly recognized. Yeast studies indicate that the tyrosine kinase inhibitor imatinib may interact with the v-ATPase genes and alter the course of cancer progression. Data from humans in this regard are lacking. Methods We constructed 55 lymphoblastoid cell lines from pedigreed, cancer-free human subjects and treated them with IC20 concentration of imatinib mesylate. Using these cell lines, we (i) estimated the heritability and differential expression of 19 genes encoding several subunits of the v-ATPase protein in response to imatinib treatment; (ii) estimated the genetic similarity among these genes; and (iii) conducted a high-density scan to find cis-regulating genetic variation associated with differential expression of these genes. Results We found that the imatinib response of the genes encoding v-ATPase subunits is significantly heritable and can be clustered to identify novel drug targets in imatinib therapy. Further, five of these genes were significantly cis-regulated and together represented nearly half-log fold change in response to imatinib (p?=?0.0107) that was homogenous (p?=?0.2598). Conclusions Our results proffer support to the growing view that personalized regimens using proton pump inhibitors or v-ATPase inhibitors may improve outcomes of imatinib therapy in various cancers.