Radiologic response assessment during anti-angiogenic therapy of malignant glioma: a case report

2010 ◽  
Vol 3 (S3) ◽  
pp. 28-29 ◽  
Author(s):  
M. Nowosielski ◽  
M. Hutterer ◽  
D. Putzer ◽  
G. Stockhammer ◽  
W. Recheis ◽  
...  
2020 ◽  
Vol 3 (68) ◽  
pp. 147
Author(s):  
Ioniţă Ducu ◽  
Roxana-Elena Bohîlţea ◽  
Dan Teleanu ◽  
Natalia Ţurcan ◽  
Monica Mihaela Cîrstoiu

2014 ◽  
Vol 2014 (1) ◽  
pp. 1-4 ◽  
Author(s):  
M. P. Christman ◽  
S. E. Turbett ◽  
S. Sengupta ◽  
K. U. Bakhadirov ◽  
C. A. Williamson ◽  
...  

2014 ◽  
Vol 2 (1) ◽  
Author(s):  
Linda Mahjoubi ◽  
Jennifer Marie-Louise ◽  
Harold Merle ◽  
Vincent Molinié

2008 ◽  
Vol 92 (2) ◽  
pp. 149-155 ◽  
Author(s):  
Andrew D. Norden ◽  
Jan Drappatz ◽  
Alona Muzikansky ◽  
Karly David ◽  
Mary Gerard ◽  
...  

2004 ◽  
Vol 13 (5) ◽  
pp. 395-400
Author(s):  
Kazuhiro TANAKA ◽  
Yoshio SAKAGAMI ◽  
Minoru SAITOH ◽  
Masahiro ASADA ◽  
Kazuhiro TERAMURA ◽  
...  

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. TPS3164-TPS3164
Author(s):  
Martin Kelly Nicholas ◽  
Matthias Holdhoff ◽  
Richard A. Peterson ◽  
Oana Cristina Danciu ◽  
Theodore M. Tarasow ◽  
...  

TPS3164 Background: The caspase family of cysteine proteases play key roles in the initiation and execution of apoptosis. The activation of procaspase-3 to caspase-3 is critical in both the intrinsic and extrinsic apoptotic cascades. Procaspase-3 levels are elevated in many cancers, including glioblastoma (GBM). As a result, caspase-3 levels are abnormally low in these tumors; thus they avoid apoptosis. PAC-1 is a small molecule that directly activates procaspase-3 and induces apoptosis of cancer cells. PAC-1 has activity against a wide range of cancer cell lines, and in animal models of cancer. PAC-1 crosses the blood brain barrier and has been shown to synergize with TMZ in both canine malignant glioma and meningioma that arise spontaneously. Methods: This Phase I dose escalation study uses a modified- Fibonacci 3+3 design to determine the MTD of PAC-1 when combined with TMZ in patients with recurrent malignant gliomas: anaplastic astrocytoma (AA) and GBM (open to enrollment). Here, we focus on component 2 of the study. Primary objectives: to establish MTD of PAC-1 when combined with a fixed dose of TMZ, tolerability, and toxicity using CTCAE v.4. Secondary and correlative objectives: pharmacokinetics, pharmacodynamics, preliminary anti-tumor activity correlation with procaspase-3 expression in tumor tissue, radiographic response using the Response Assessment in Neuro-Oncology (RANO) criteria, and neurocognitive function using a validated test battery. Inclusion criteria: diagnosis of recurrent high grade glioma (AA or GBM), ECOG PS 0-2, adequate organ function. Exclusion criteria: received prior cytotoxic therapy in the last 3-6 weeks (duration based on prior therapy) or uncontrolled chronic illness. Administration and design, Component 2: PAC-1, orally administered, is dosed at 375-650 mg daily (up to 3 dose levels) on days 1-21 of each 28-day cycle. A fixed dose of TMZ, (150 mg/m2), is administered orally, days 8 -12 of each cycle. The study is currently enrolling patients for Component 2. Clinical trial information: NCT02355535.


2010 ◽  
Vol 2010 ◽  
pp. 1-16 ◽  
Author(s):  
Ruman Rahman ◽  
Stuart Smith ◽  
Cheryl Rahman ◽  
Richard Grundy

Despite advances in surgery, radiation therapy, and chemotherapeutics, patients with malignant glioma have a dismal prognosis. The formations of aberrant tumour vasculature and glioma cell invasion are major obstacles for effective treatment. Angiogenesis is a key event in the progression of malignant gliomas, a process involving endothelial cell proliferation, migration, reorganization of extracellular matrix and tube formation. Such processes are regulated by the homeostatic balance between proangiogenic and antiangiogenic factors, most notably vascular endothelial growth factors (VEGFs) produced by glioma cells. Current strategies targeting VEGF-VEGF receptor signal transduction pathways, though effective in normalizing abnormal tumor vasculature, eventually result in tumor resistance whereby a highly infiltrative and invasive phenotype may be adopted. Here we review recent anti-angiogenic therapy for malignant glioma and highlight implantable devices and nano/microparticles as next-generation methods for chemotherapeutic delivery. Intrinsic and adaptive modes of glioma resistance to anti-angiogenic therapy will be discussed with particular focus on the glioma stem cell paradigm.


2011 ◽  
Vol 17 (3) ◽  
pp. 290-293 ◽  
Author(s):  
Yasunori Fujimoto ◽  
Naoya Hashimoto ◽  
Manabu Kinoshita ◽  
Yuko Miyazaki ◽  
Satoshi Tanaka ◽  
...  

10.5772/23021 ◽  
2011 ◽  
Author(s):  
Paula Province ◽  
Xiaosi Han ◽  
L. Burt ◽  
Hassan M.

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