Background: Glioblastoma multiforme (GBM) is a highly malignant glial tumor characterized by rapid growth and angiogenesis. Current frontline therapy consists of surgical resection, radiation, and chemotherapy; however, all patients will progress. Over the past decade, there have been increases in the quality and quantity of clinical data regarding the treatment of patients with GBM.
The management of complex oncology drugs in pharmacy and in medical benefits presents unique challenges for all parties who seek cost-effective, positive clinical outcomes for patients with cancer. New therapies are offering the exciting prospect of improved outcomes, prolonged life, and, in some cases, a cure for specific diseases. Targeted oncolytics and pharmacogenomics, which carry the promise of improved likelihood of successful treatment, have become welcome additions to the current standards of care.
Patients with HER2+ breast cancer who develop resistance to trastuzumab may soon have an alternative therapy, according to recent findings published in Clinical Cancer Research.
Use of hormone therapy for menopause is associated with reduced risks for esophageal, gastric, and colorectal cancers, according to results of a prospective study that were then combined with published studies in a meta-analysis. In this British study of women aged 50 to 64 years, researchers found no significant differences in risk by type of hormone therapy, duration of use, or between past and current users. The reduction in risk, however, was small in comparison to the increased risk of breast cancer that has been attributed to hormone therapy in this population.
Hsp90 inhibition has been found to be a successful therapeutic approach for combating diseases that use JAK/STAT signaling for tumor growth. In in vivo and in vitro models, researchers showed that the small molecule Hsp90 inhibitor ganetespib exhibited potent activity in tumor cells dependent specifically on JAK2 signaling. Specifically, ganetespib sustained depletion of JAK2 including active JAK2V617Fmutant, subsequently decreasing STAT activity and reducing STAT-target gene expression.
Results 1 - 10 of 21