The lancet oncology
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The lancet oncology · Jan 2013
Randomized Controlled Trial Multicenter StudyTivantinib for second-line treatment of advanced hepatocellular carcinoma: a randomised, placebo-controlled phase 2 study.
Tivantinib (ARQ 197), a selective oral inhibitor of MET, has shown promising antitumour activity in hepatocellular carcinoma as monotherapy and in combination with sorafenib. We aimed to assess efficacy and safety of tivantinib for second-line treatment of advanced hepatocellular carcinoma. ⋯ ArQule, Daiichi Sankyo (Daiichi Sankyo Group).
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The lancet oncology · Jan 2013
Randomized Controlled Trial Multicenter StudySelumetinib plus docetaxel for KRAS-mutant advanced non-small-cell lung cancer: a randomised, multicentre, placebo-controlled, phase 2 study.
No targeted therapies are available for KRAS-mutant non-small-cell lung cancer (NSCLC). Selumetinib is an inhibitor of MEK1/MEK2, downstream of KRAS, with preclinical evidence of synergistic activity with docetaxel in KRAS-mutant cancers. We did a prospective, randomised, phase 2 trial to assess selumetinib plus docetaxel in previously treated patients with advanced KRAS-mutant NSCLC. ⋯ AstraZeneca.
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The lancet oncology · Jan 2013
Randomized Controlled Trial Multicenter StudyAdjuvant lapatinib for women with early-stage HER2-positive breast cancer: a randomised, controlled, phase 3 trial.
Worldwide, many patients with HER2-positive early stage breast cancer do not receive trastuzumab-the standard adjuvant treatment. We investigated the efficacy and safety of adjuvant lapatinib for patients with trastuzumab-naive HER2-positive early-stage breast cancer, started at any time after diagnosis. ⋯ GlaxoSmithKline.
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The RAF inhibitors vemurafenib and dabrafenib are emerging as the standard of care for Val600 BRAF-mutant metastatic melanoma. These drugs have shown clinical benefit over the standard care (dacarbazine); however, they are associated with frequent cutaneous adverse events, which can be concerning to the patient and their physician. Herein, we review the range of cutaneous disorders that seem to be induced by RAF inhibitors, including cutaneous squamous-cell carcinoma, hyperkeratotic lesions, Grover's disease, keratosis pilaris-like reactions, and photosensitivity. These disorders often affect patients' quality of life; therefore, dermatological assessment and timely management is essential to ensure that patients continue to use RAF inhibitors.
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Glial tumours in children have distinct patterns of epigenetic alteration, chromosomal structure, and gene and protein expression that differentiate them from their histological counterparts in adults. Understanding paediatric gliomas at the molecular level provides important prognostic and therapeutic insights, such as which genetic alterations confer a favourable response to adjuvant therapy, or which signalling pathways might be amenable to specific molecularly targeted agents. For clinicians, the ultimate goal is to individualise therapeutic regimens on the basis of the molecular fingerprint of a particular tumour and the prognosis conferred by this profile. In this Review, we examine a series of studies of molecular and genomic analysis of glial tumours in children, and discuss the many clinical insights that these molecular features provide.