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Drug Therapies

New cancer therapies have significantly improved survival outcomes, but have brought with them a wide range of oral toxicities, many of which are class-specific and otherwise new to the field of oncology, according to Nathaniel S. Treister, DMD, DMSc, Division Chief, Division of Oral Medicine and Dentistry, Brigham and Women’s Hospital, Boston, MA.
The key arguments supporting the use of combination therapy with checkpoint blockade immunotherapies as the standard of care for treating metastatic melanoma arise from the combination’s high disease control rates; rapid deep responses; improved response rates; longer progression-free survival (PFS); and good estimated overall survival (OS), approaching 70% at 3 years, said Steven J. O’Day, MD, Professor of Medical Oncology, John Wayne Cancer Institute at Providence Saint John’s Health Center, Santa Monica, CA, at the recent HemOnc Today Melanoma and Cutaneous Malignancies meeting.
Boston, MA-Rociletinib, a specially engineered third-generation EGFR inhibitor, is accumulating an impressive track record in early studies of non-small-cell lung cancer (NSCLC). The drug is specifically designed for use in patients with NSCLC and the T790M mutation, a heretofore patient population with unmet needs. T790M, the most common mutation associated with resistance to first-line EGFR-directed tyrosine kinase inhibitor (TKI) therapy, is present in 60% of patients with resistance to TKIs.
Antibody-drug conjugates (ADCs) offer a unique approach for the treatment of solid tumors and hematologic cancers. The idea is that a potent cytotoxic agent is linked to an antibody specifically targeted to tumor cells, and once the antibody binds to the tumor cell, the cytotoxic agent is unleashed inside the cells to attack the cancer.

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.

Chronic myelogenous leukemia (CML) is a hematologic malignancy initiated by a translocation event that results in the fusion of the breakpoint cluster region (BCR) of chromosome 22 with the Abelson leukemia oncogene (ABL) tyrosine kinase on chromosome 9 in bone marrow stem cells. This chromosomal abnormality is known as the Philadelphia (Ph) chromosome.1,2

The impact of chemotherapy-induced nausea and vomiting (CINV) for the patient with cancer cannot be overemphasized. Uncontrolled CINV has been cited as one of the greatest fears among people undergoing cancer treatments.1,2 Advances in antiemetic therapy in the past 20 years have improved patient experiences and outcomes. Despite this, the majority of patients with cancer will experience CINV during their chemotherapy treatments.1,3-6 In particular, nausea is less well controlled than vomiting.

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.


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