|1.||Hellerqvist, C G: 4 articles (12/2001 - 09/2000)|
|2.||Wamil, B D: 4 articles (12/2001 - 09/2000)|
|3.||Wada, Tsutomu: 3 articles (07/2012 - 04/2011)|
|4.||Yan, H P: 3 articles (12/2001 - 10/2000)|
|5.||Hirahara, Noriyuki: 2 articles (07/2012 - 09/2011)|
|6.||Fujieda, Ayako: 2 articles (07/2012 - 09/2011)|
|7.||Fujioka, Masaki: 2 articles (07/2012 - 09/2011)|
|8.||Edamatsu, Takeo: 2 articles (07/2012 - 09/2011)|
|9.||Yakes, F M: 2 articles (12/2001 - 10/2000)|
|10.||Carter, C E: 2 articles (10/2000 - 09/2000)|
10/15/2000 - "CM101 induced loss of tumor immunoprivilege through changes in the expression of leukocyte p53, tumor Fas and fasL coupled with neovascularitis and leukocyte infiltration, constitutes a plausible molecular pathway for tumor reduction observed in cancer patients."
10/15/2000 - "Collectively, these data suggest that CM101 up-regulates p53 in tumor-infiltrating leukocytes, initiating a loss of tumor immunoprivilege and consequently rendering the tumor sensitive to Fas/fasL-mediated apoptosis. "
10/15/2000 - "To further our understanding of the mechanism of action of CM101 as an antitumor agent, we examined the role of the inflammatory response in inducing tumor apoptosis in a normal mouse and tumor-bearing mouse model. "
10/15/2000 - "CM101 treatment overrides tumor-induced immunoprivilege leading to apoptosis."
08/01/1999 - "Time-activity curves showed no difference in tumor flow at the times measured in the experimental group injected with CM-101 or when compared to saline solutions in either the peripheral or central portions of the tumor. "
10/27/1998 - "Electrophysiologic measurements on isolated central nervous system and neurons in culture showed that CM101 protected axons from Wallerian degeneration; reversed gamma-aminobutyrate-mediated depolarization occurring in traumatized neurons; and improved recovery of neuronal conductivity of isolated central nervous system in culture."
01/01/1997 - "In vivo studies in mice have demonstrated that CM101 induced inflammatory responses in neoplastic tumor neovasculature causing inhibition of tumor growth and tumor cell necrosis. "
01/01/1993 - "In nude mice bearing human tumor xenografts, intravenously administered GBS toxin caused tumor necrosis and hemorrhagic lesions, and substantially inhibited the rate of growth of the tumors. "
01/01/1993 - "In BALB/c mice bearing Madison lung tumors, GBS toxin induced an inflammatory response resulting in marked changes in tumor morphology, including vasodilation, endothelial and tumor cell necrosis, invasion of lymphocytes and macrophages, and capillary thrombosis. "
10/15/2000 - "Data from refractory cancer patients in a Phase I clinical trial with CM101 indicated a similar mechanism of tumor-targeted inflammation. "
01/01/1997 - "GBS toxin, named CM101 in the clinic, was hypothesized, on the basis of our previous in vivo studies, to induce inflammation in pulmonary neovasculature in neonates by cross-linking of embryonic receptors still expressed after birth and in tumor neovasculature in adults. "
|5.||Bronchopulmonary Sequestration (Pulmonary Sequestration)
|2.||streptococcal polysaccharide type III group B
|5.||Messenger RNA (mRNA)
|6.||Fas Ligand Protein (Fas Ligand)
|7.||Interleukin-12 (IL 12)
|9.||Thromboxane A2 (A2, Thromboxane)
|10.||Sodium Chloride (Saline Solution)
|1.||Heterologous Transplantation (Xenotransplantation)