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Billions of dollars are spent each year to fund research as scientists continue to identify the causes of cancer and to develop strategies for prevention, detection, treatments, and cures. The following statistics allow a glimpse into the immense field of cancer research funding.
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The 2012 American Society for Rad­iation Oncology (ASTRO) Annual Meeting, held in Boston, Massachusetts, coincided with Super­storm Sandy. Despite the havoc wreaked by the storm, Boston was largely spared, although ASTRO canceled Monday afternoon’s Plenary Session when public transportation was shut down. Below are some highlights from the meeting, including some news stories from the Plenary Session, which was available online.
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In a phase 3 head-to-head comparison trial, the anaplastic lymphoma kinase (ALK) inhibitor crizotinib proved more effective than standard chemo­therapy with pemetrexed or doce­taxel as a second-line treatment for non–small cell lung cancer (NSCLC) patients with the ALK genetic abnormality.
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Anticoagulation prophylaxis is effective in preventing both symptomatic and asymptomatic catheter-related deep vein thrombosis in ambulatory cancer patients with locally advanced or metastatic solid tumors, French investigators reported at the European Society for Medical Oncology (ESMO) 2012 Congress, held in Vienna, Austria.1
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Carfilzomib (Kyprolis, Onyx Pharmaceuticals, South San Francisco, CA) is a proteasome inhibitor that recently received accelerated FDA approval as single-agent treatment for relapsed or refractory multiple myeloma (RRMM),1 as well as designation as a “Preferred Regimen” for salvage therapy according to the National Comprehensive Cancer Network (NCCN) guidelines.2 Carfilzomib differs structurally and mechanistically from bortezomib; it functions by irreversibly inhibiting chymotrypsin-like activity of the constitutive proteasome and the immunoproteasome and offers a novel treatment option for patients with advanced MM.3

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Carfilzomib (Kyprolis, Onyx Pharmaceuticals, Inc, South San Francisco, CA) is a selective proteasome inhibitor that irreversibly binds to active sites within the proteolytic core of the 26S proteasome, resulting in inhibition of proteasome activity. Preclinical studies have shown carfilzomib inhibits tumor growth and promotes tumor cell death, with sustained proteasome inhibition for more than 48 hours when using a consecutive-day dosing regimen.1-4

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The recent FDA approval of single-agent carfilzomib (Kyprolis) adds to the armamentarium of agents for the treatment of relapsed and refractory multiple myeloma. Carfilzomib was approved based on an open-label, single-arm study of single-agent carfilzomib after the failure of at least 2 previous therapies. Within the inclusion criteria, the subjects were required to have failed bortezomib. Although bortezomib and carfilz­omib are both proteasome inhibitors, carfilzomib selectively and irreversibly binds to its target, which results in sustained proteasome inhibition that is absent of off-target effects relative to bortezomib.1,2
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ES has received 5 prior lines of therapy, with progression of disease documented on her most recent therapy with a rise in SPEP from 1.3 to 2.2 g/dL and in UPEP from 556 to 1342 mg/24 hours. The current clinical considerations include anemia, renal insufficiency, and PN grade 1 with pain.

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Carfilzomib (Kyprolis, Onyx Pharmaceuticals, South San Francisco, CA) is a proteasome inhibitor that recently received accelerated FDA approval as single-agent treatment for relapsed or refractory multiple myeloma (RRMM),1 as well as designation as a “Preferred Regimen” for salvage therapy according to the National Comprehensive Cancer Network (NCCN) guidelines.2 Carfilzomib differs structurally and mechanistically from bortezomib; it functions by irreversibly inhibiting chymotrypsin-like activity of the constitutive proteasome and the immunoproteasome and offers a novel treatment option for patients with advanced MM.3

Read More ›

The recent FDA approval of single-agent carfilzomib (Kyprolis) adds to the armamentarium of agents for the treatment of relapsed and refractory multiple myeloma. Carfilzomib was approved based on an open-label, single-arm study of single-agent carfilzomib after the failure of at least 2 previous therapies. Within the inclusion criteria, the subjects were required to have failed bortezomib. Although bortezomib and carfilz­omib are both proteasome inhibitors, carfilzomib selectively and irreversibly binds to its target, which results in sustained proteasome inhibition that is absent of off-target effects relative to bortezomib.1,2
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