Therapeutic potential of tranilast, an anti-allergy drug, in proliferative disorders.
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[1] G. Prud’homme,et al. Tranilast treatment decreases cell growth, migration and inhibits colony formation of human breast cancer cells. , 2011, Experimental and molecular pathology.
[2] T. Nemoto,et al. Successful treatment of desmoid tumor of the chest wall with tranilast: a case report , 2010, Journal of medical case reports.
[3] Y. Glinka,et al. Breast Cancer Stem-Like Cells Are Inhibited by a Non-Toxic Aryl Hydrocarbon Receptor Agonist , 2010, PloS one.
[4] Satoshi Kobayashi,et al. Tranilast modulates fibrosis, epithelial‐mesenchymal transition and peritubular capillary injury in unilateral ureteral obstruction rats , 2010, Pathology.
[5] K. Izumi,et al. Preliminary results of tranilast treatment for patients with advanced castration-resistant prostate cancer. , 2010, Anticancer research.
[6] G. Prud’homme,et al. Tranilast inhibits cell proliferation and migration and promotes apoptosis in murine breast cancer , 2010, Anti-cancer drugs.
[7] A. Naiki‐Ito,et al. Tranilast suppresses prostate cancer growth and osteoclast differentiation in vivo and in vitro , 2010, The Prostate.
[8] Russell S. Thomas,et al. Activation of the aryl-hydrocarbon receptor inhibits invasive and metastatic features of human breast cancer cells and promotes breast cancer cell differentiation. , 2010, Molecular endocrinology.
[9] K. Miyazaki,et al. Tranilast strongly sensitizes pancreatic cancer cells to gemcitabine via decreasing protein expression of ribonucleotide reductase 1. , 2009, International journal of oncology.
[10] S. Safe,et al. The aryl hydrocarbon receptor as a target for estrogen receptor-negative breast cancer chemotherapy. , 2009, Endocrine-related cancer.
[11] E. Keller,et al. Tranilast inhibits hormone refractory prostate cancer cell proliferation and suppresses transforming growth factor β1‐associated osteoblastic changes , 2009, The Prostate.
[12] G. Prud’homme,et al. Tranilast inhibits the growth and metastasis of mammary carcinoma , 2009, Anti-cancer drugs.
[13] Mutsuo Takahashi,et al. Tranilast, an anti-allergic drug, down-regulates the growth of cultured neurofibroma cells derived from neurofibromatosis type 1. , 2009, The Tohoku journal of experimental medicine.
[14] N. Kerkvliet. AHR-mediated immunomodulation: the role of altered gene transcription. , 2009, Biochemical pharmacology.
[15] David Padua,et al. Roles of TGFβ in metastasis , 2009, Cell Research.
[16] T. Onozuka,et al. Vulval syringoma successfully treated with tranilast , 2005, The British journal of dermatology.
[17] 清水 俊行. Suppression of matrix metalloproteinase production in nasal fibroblasts by tranilast, an antiallergic agent, in vitro , 2005 .
[18] M. Yashiro,et al. Tranilast (N-3,4-dimethoxycinamoyl anthranilic acid): a novel inhibitor of invasion-stimulating interaction between gastric cancer cells and orthotopic fibroblasts. , 2003, Anticancer research.
[19] S. Kawashiri,et al. Effects of fibroblast growth inhibitor on proliferation and metastasis of oral squamous cell carcinoma. , 2003, Oral oncology.
[20] T. Nikaido,et al. Tranilast inhibits the proliferation of uterine leiomyoma cells in vitro through G1 arrest associated with the induction of p21(waf1) and p53. , 2002, The Journal of clinical endocrinology and metabolism.
[21] E. Uchida,et al. Anti-tumor effect of N-[3,4-dimethoxycinnamoyl]-anthranilic acid (tranilast) on experimental pancreatic cancer. , 2002, Journal of Nippon Medical School = Nippon Ika Daigaku zasshi.
[22] J. Dichgans,et al. N‐[3,4‐dimethoxycinnamoyl]‐anthranilic acid (tranilast) inhibits transforming growth factor‐β release and reduces migration and invasiveness of human malignant glioma cells , 2001, International journal of cancer.
[23] H. Miyata,et al. Tranilast : A new application in the cardiovascular field as an antiproliferative drug , 1998 .
[24] L. Nie,et al. Inhibition of proliferation of MCF-7 breast cancer cells by a blocker of Ca(2+)-permeable channel. , 1997, Cell calcium.
[25] Y. Chung,et al. Tranilast (N-(3,4-dimethoxycinnamoyl) anthranilic acid) down-regulates the growth of scirrhous gastric cancer. , 1997, Anticancer research.
[26] 茂木 定之. Treatment of keloid and hypertrophic scars by iontophoretic transdermal delivery of tranilast , 1997 .
[27] N. Katoh,et al. Solitary Mastocytoma Treated with Tranilast , 1996, The Journal of dermatology.
[28] T. Nishikawa,et al. Tranilast, a selective inhibitor of collagen synthesis in human skin fibroblasts. , 1994, Journal of biochemistry.
[29] K. Ichikawa,et al. Inhibitory action of tranilast, an anti-allergic drug, on the release of cytokines and PGE2 from human monocytes-macrophages. , 1993, Japanese Journal of Pharmacology.
[30] K. Yoshikawa,et al. Clinical Evaluation of Tranilast for Keloid and Hypertrophic Scar , 1992 .
[31] M. Nakazawa,et al. Study of the mechanism of inhibitory action of tranilast on chemical mediator release. , 1988, Japanese journal of pharmacology.
[32] M. Isaji,et al. Selective inhibition of collagen accumulation by N-(3,4-dimethoxycinnamoyl)anthranilic acid (N-5') in granulation tissue. , 1987, Biochemical pharmacology.
[33] A. Koda,et al. The inhibition mechanism of histamine release by N-(3,4-dimethoxycinnamoyl) anthranilic acid. , 1985, International archives of allergy and applied immunology.
[34] H. Azuma,et al. PHARMACOLOGICAL PROPERTIES OF N‐(3′,4′‐DIMETHOXYCINNAMOYL) ANTHRANILIC ACID (N‐5′), A NEW ANTI‐ATOPIC AGENT , 1976, British journal of pharmacology.
[35] Y. Yanagihara,et al. Inhibition of hypersensitivity reactions by a new drug, N(3',4'-dimethoxycinnamoyl) anthranilic acid (N-5'). , 1976, The Journal of allergy and clinical immunology.