Phase I study of low-dose metronomic temozolomide for recurrent malignant gliomas
暂无分享,去创建一个
[1] J. Wolchok,et al. Anticancer immunotherapy by CTLA-4 blockade: obligatory contribution of IL-2 receptors and negative prognostic impact of soluble CD25 , 2015, Cell Research.
[2] F. Végran,et al. Dacarbazine-mediated upregulation of NKG2D ligands on tumor cells activates NK and CD8 T cells and restrains melanoma growth. , 2013, The Journal of investigative dermatology.
[3] L. Deangelis,et al. Phase II trial of continuous low-dose temozolomide for patients with recurrent malignant glioma. , 2013, Neuro-oncology.
[4] P. Gutin,et al. NovoTTF-100A versus physician's choice chemotherapy in recurrent glioblastoma: a randomised phase III trial of a novel treatment modality. , 2012, European journal of cancer.
[5] S. Ansell,et al. Soluble IL-2Rα facilitates IL-2-mediated immune responses and predicts reduced survival in follicular B-cell non-Hodgkin lymphoma. , 2011, Blood.
[6] A. Koch,et al. Continuous low-dose temozolomide and celecoxib in recurrent glioblastoma , 2010, Journal of Neuro-Oncology.
[7] David C. Alsop,et al. Perfusion MRI of brain tumours: a comparative study of pseudo-continuous arterial spin labelling and dynamic susceptibility contrast imaging , 2010, Neuroradiology.
[8] Jung-Il Lee,et al. Phase II trial of low-dose continuous (metronomic) treatment of temozolomide for recurrent glioblastoma. , 2010, Neuro-oncology.
[9] T. Mikkelsen,et al. Bevacizumab alone and in combination with irinotecan in recurrent glioblastoma. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[10] Masahiro Inoue,et al. Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis. , 2009, Cancer cell.
[11] F. Ghiringhelli,et al. Treg depletion with a low-dose metronomic temozolomide regimen in a rat glioma model , 2009, Cancer Immunology, Immunotherapy.
[12] John A Butman,et al. Phase II trial of single-agent bevacizumab followed by bevacizumab plus irinotecan at tumor progression in recurrent glioblastoma. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[13] D. Alsop,et al. Continuous flow‐driven inversion for arterial spin labeling using pulsed radio frequency and gradient fields , 2008, Magnetic resonance in medicine.
[14] 本吉 康英. Different mechanisms for anti-tumor effects of low- and high-dose cyclophosphamide , 2008 .
[15] I. Jonassen,et al. Angiogenesis-independent tumor growth mediated by stem-like cancer cells , 2006, Proceedings of the National Academy of Sciences.
[16] K. Eguchi,et al. Different mechanisms for anti-tumor effects of low- and high-dose cyclophosphamide. , 2006, Oncology reports.
[17] E. Wong. Tumor growth, invasion, and angiogenesis in malignant gliomas , 2006, Journal of Neuro-Oncology.
[18] R. Kerbel,et al. Optimal biologic dose of metronomic chemotherapy regimens is associated with maximum antiangiogenic activity. , 2005, Blood.
[19] Kevin J. Tracey,et al. High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal , 2005, Nature Reviews Immunology.
[20] S. Murakami. Soluble interleukin-2 receptor in cancer. , 2004, Frontiers in bioscience : a journal and virtual library.
[21] William C. Parks,et al. Matrix metalloproteinases as modulators of inflammation and innate immunity , 2004, Nature Reviews Immunology.
[22] D. Hicklin,et al. A Comparative Analysis of Low-Dose Metronomic Cyclophosphamide Reveals Absent or Low-Grade Toxicity on Tissues Highly Sensitive to the Toxic Effects of Maximum Tolerated Dose Regimens , 2004, Cancer Research.
[23] Robert S. Kerbel,et al. The anti-angiogenic basis of metronomic chemotherapy , 2004, Nature Reviews Cancer.
[24] B. Chauffert,et al. CD4+CD25+ regulatory T cells suppress tumor immunity but are sensitive to cyclophosphamide which allows immunotherapy of established tumors to be curative , 2004, European journal of immunology.
[25] Peter Bohlen,et al. Antitumor effects in mice of low-dose (metronomic) cyclophosphamide administered continuously through the drinking water. , 2002, Cancer research.
[26] R. Schilsky,et al. First-line oral capecitabine therapy in metastatic colorectal cancer: a favorable safety profile compared with intravenous 5-fluorouracil/leucovorin. , 2002, Annals of oncology : official journal of the European Society for Medical Oncology.
[27] A. Buzdar,et al. Multicenter, Phase II study of capecitabine in taxane‐pretreated metastatic breast carcinoma patients , 2001, Cancer.
[28] M P Carol,et al. MR-spectroscopy guided target delineation for high-grade gliomas. , 2001, International journal of radiation oncology, biology, physics.
[29] D. Osoba,et al. A phase II study of temozolomide vs. procarbazine in patients with glioblastoma multiforme at first relapse , 2000, British Journal of Cancer.
[30] Susan M. Chang,et al. Multicenter phase II trial of temozolomide in patients with anaplastic astrocytoma or anaplastic oligoastrocytoma at first relapse. Temodal Brain Tumor Group. , 1999, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[31] M J Gleason,et al. Outcomes and prognostic factors in recurrent glioma patients enrolled onto phase II clinical trials. , 1999, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[32] E. Shevach,et al. CD4+CD25+ Immunoregulatory T Cells Suppress Polyclonal T Cell Activation In Vitro by Inhibiting Interleukin 2 Production , 1998, The Journal of experimental medicine.
[33] M. Klempner,et al. Specific matrix metalloproteinase profiles in the cerebrospinal fluid correlated with the presence of malignant astrocytomas, brain metastases, and carcinomatous meningitis , 1998, Cancer.
[34] P. Forsyth,et al. Phase II study of prolonged oral therapy with etoposide (VP16) for patients with recurrent malignant glioma , 1996, Journal of Neuro-Oncology.
[35] C. Quarterman,et al. Phase I trial of temozolomide (CCRG 81045: M&B 39831: NSC 362856). , 1992, British Journal of Cancer.
[36] T. Cascino,et al. Response criteria for phase II studies of supratentorial malignant glioma. , 1990, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[37] R. North. Cyclophosphamide-facilitated adoptive immunotherapy of an established tumor depends on elimination of tumor-induced suppressor T cells , 1982, The Journal of experimental medicine.
[38] E. Kaplan,et al. Nonparametric Estimation from Incomplete Observations , 1958 .
[39] T. Cloughesy,et al. Regional and Voxel‐Wise Comparisons of Blood Flow Measurements Between Dynamic Susceptibility Contrast Magnetic Resonance Imaging (DSC‐MRI) and Arterial Spin Labeling (ASL) in Brain Tumors , 2014, Journal of neuroimaging : official journal of the American Society of Neuroimaging.
[40] A. Heimberger,et al. The role of tregs in glioma-mediated immunosuppression: potential target for intervention. , 2010, Neurosurgery clinics of North America.
[41] G. A. Rouleau,et al. Patterns of relapse and prognosis after bevacizumab failure in recurrent glioblastoma , 2009 .
[42] J. Uhm. Temozolomide Rechallenge in Recurrent Malignant Glioma by Using a Continuous Temozolomide Schedule: The “Rescue” Approach , 2009 .
[43] A. Teramoto,et al. The expression of matrix metalloproteinase-2 and-9 in human gliomas of different pathological grades , 2006, Brain Tumor Pathology.
[44] D. Carney. The pharmacology of intravenous and oral etoposide , 1991, Cancer.
[45] D. Alsop,et al. Cerebrospinal Fluid Research Cerebrospinal Fluid Matrix Metalloproteinase-9 Increases during Treatment of Recurrent Malignant Gliomas , 2022 .