2011 Fiscal Year Final Research Report
Therapy for advanced renal cancer via ER stress modulation
| Project/Area Number |
21791533
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
INAMOTO Teruo 大阪医科大学, 医学部, 助教 (20330087)
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| Project Period (FY) |
2009 – 2011
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| Keywords | sunitinib / IL-2 |
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| Research Abstract |
Modulation of growth factor signaling ; The epidermal growth factor receptor is expressed in a variety of human malignancies, including head and neck, breast, colorectal, lung, prostate, kidney, ovary, brain, pancreas, and bladder cancers. Epidermal growth factor receptor(EGFR) is a potential target for the treatment of urologic malignancies but a clinical response is expected in a small proportion. To come up with potential markers of response to EGFR tagetted therapy in cell lines, cell lines were investigated for anti-growth response to EGFR-therapy. E-cadherin was silenced by small interfering RNA in two sensitive cell lines, and the effect on the response to drugs was tested. Expression of intact ErbB4, E-cadherin, and b-catenin and loss of expression of platelet-derived growth factor receptor were associated with response to drug sensitivity. E-cadherin seems to play a central role in modulation of EGFR response.
Nuclear receptor signaling ; The peroxisome proliferator-activated receptor(PPAR) is a group of transcription factors that regulates cell growth, fatty acid regulation, and immune surveillance. Evidence is certainly accumulating for presence of PPAR in bladder cancer tissues. It is reported that PPAR agonist specifically increases natural killer T-lymphocytes specific markers. In addition to the close association between immune system and PPAR activation, PPAR agonists such as rosiglitazone to BCG regimens may have potent antitumor effects since bladder cancer cell lines demonstrates dose dependent inhibition of cancer cell growth in the presence of the PPAR agonist. Given these findings, along with previous findings, translational usage of molecular targets in clinical settings is awaited.
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[Journal Article] Conversion of prostate cancer from hormone independency to dependency due to AMACR inhibition : involvement of increased AR expression and decreased IGF1 expression2009
Author(s)
Takahara K, Azuma H, Sakamoto T, Kiyama S, Inamoto T, Ibuki N, Nishida T, Nomi H, Ubai T, Segawa N, Katsuoka Y
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Journal Title
Anticancer Res
Volume: 29(7)
Pages: 2497-505
URL
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[Presentation] Receptor heterodimerization : a new mechanism for platelet-derived growth factor-induced resistance to anti-epidermal growth factor receptor therapy in bladder cancer2009
Author(s)
Black P, Brown G, McConkey D, Kassouf W, Inamoto T, Arora A, Gallagher D, Munsell M, Bar-Eli M, Dinney C, and Adam L
Organizer
Can Urol Assoc
Place of Presentation
サンディエゴ(USA)
Year and Date
20090600
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[Presentation] Donor-specific tolerance induced by treatment with Superagonistic CD28 antibody in rat renal allografts2009
Author(s)
Azuma, H. Nomi, H., Ubai, T., Inamoto, T., Ibuki, N., Koyama, K., Isaka, Y., Takahara, S., Katsuoka, Y.
Organizer
The American Urological Association(AUA)'s Annual Meeting
Place of Presentation
シカゴ(USA)
Year and Date
20090400
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