This shows you the differences between two versions of the page.
ggranger [2010/06/19 06:30] mlabadm |
ggranger [2010/06/19 06:41] (current) mlabadm |
||
---|---|---|---|
Line 86: | Line 86: | ||
Taken together, the results presented here show that the interaction between known pathways and well-studied cellular processes might work at levels not yet explored. Even though interactions are probably not direct, the network shows how sets of genes which have been independently studied in the context of cancer might collaborate for a given phenotype. | Taken together, the results presented here show that the interaction between known pathways and well-studied cellular processes might work at levels not yet explored. Even though interactions are probably not direct, the network shows how sets of genes which have been independently studied in the context of cancer might collaborate for a given phenotype. | ||
- | References: | + | **References:** |
American Cancer Society. Cancer Facts and Figures 2008. | American Cancer Society. Cancer Facts and Figures 2008. | ||
Line 96: | Line 96: | ||
Ji J., Liu R., Tong T., Song Y., Jin S., Wu M., Zhan Q. Gadd45a regulates β-catenin distribution and maintains cell–cell adhesion/contactGadd45a induces β-catenin distribution. Oncogene. 26:6396-6405, 2007 | Ji J., Liu R., Tong T., Song Y., Jin S., Wu M., Zhan Q. Gadd45a regulates β-catenin distribution and maintains cell–cell adhesion/contactGadd45a induces β-catenin distribution. Oncogene. 26:6396-6405, 2007 | ||
- | Krishnamoorthy B., Narayanan K., Miyamoto S., Balakrishnan A. Epithelial Cells Release Proinflammatory Cytokines and Undergo c-Myc-Induced Apoptosis on Exposure to Filarial Parasitic Sheath Protein-Bc12 Mediates Rescue by Activating c-H-Ras. In Vitro Cellular & Developmental Biology. Animal. 36: 532-538, 2000. | + | Krishnamoorthy B., Narayanan K., Miyamoto S., Balakrishnan A. Epithelial cells release proinflammatory cytokines and undergo c-Myc-induced apoptosis on exposure to filarial parasitic sheath protein-Bc12 mediates rescue by activating c-H-Ras. In Vitro Cellular & Developmental Biology. Animal. 36: 532-538, 2000. |
Lorenzi M.V., Horii Y., Yamanaka R., Sakaguchi K., Miki T. FRAG1, a gene that potently activates fibroblast growth factor receptor by C-terminal fusion through chromosomal rearrangement. PNAS. 93: 8956-8961, 1996. | Lorenzi M.V., Horii Y., Yamanaka R., Sakaguchi K., Miki T. FRAG1, a gene that potently activates fibroblast growth factor receptor by C-terminal fusion through chromosomal rearrangement. PNAS. 93: 8956-8961, 1996. | ||
Line 106: | Line 106: | ||
Resnitzky D. and Kimchi A. Deregulated c-myc expression abrogates the interferon- and interleukin 6-mediated G0/G1 cell cycle arrest but not other inhibitory responses in M1 myeloblastic cells. Cell Growth & Differentiation. 2: 33-41. | Resnitzky D. and Kimchi A. Deregulated c-myc expression abrogates the interferon- and interleukin 6-mediated G0/G1 cell cycle arrest but not other inhibitory responses in M1 myeloblastic cells. Cell Growth & Differentiation. 2: 33-41. | ||
- | Shchors K., Shchors E., Rostker F., Lawlor E.R., Brown-Swigart L., Evan G.I. The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1β. Genes Dev. 20: 2527–2538, 2006. | + | Shchors K., Shchors E., Rostker F., Lawlor E.R., Brown-Swigart L., Evan G.I. The Myc-dependent angiogenic switch in tumors is mediated by interleukin 1. Genes Dev. 20: 2527–2538, 2006. |
Weinstein I.B. and Joe A.K. Mechanisms of disease: Oncogene addiction—a rationale for molecular targeting in cancer therapy. Nature Clinical Practice Oncology. 3:448–457, 2006. | Weinstein I.B. and Joe A.K. Mechanisms of disease: Oncogene addiction—a rationale for molecular targeting in cancer therapy. Nature Clinical Practice Oncology. 3:448–457, 2006. |