|Vandetanib for the treatment of patients with locally advanced or metastatic hereditary medullary thyroid cancer.|
|PMID: 20065189 Owner: NLM Status: MEDLINE|
|PURPOSE There is no effective therapy for patients with distant metastasis of medullary thyroid carcinoma (MTC). Activating mutations in the RET proto-oncogene cause hereditary MTC, which provides a strong therapeutic rationale for targeting RET kinase activity. This open-label, phase II study assessed the efficacy of vandetanib, a selective oral inhibitor of RET, vascular endothelial growth factor receptor, and epidermal growth factor receptor signaling, in patients with advanced hereditary MTC. METHODS Patients with unresectable locally advanced or metastatic hereditary MTC received initial treatment with once-daily oral vandetanib 300 mg. The dose was adjusted additionally in some patients on the basis of observed toxicity until disease progression or any other withdrawal criterion was met. The primary assessment was objective tumor response (by RECIST [Response Evaluation Criteria in Solid Tumors]). Results Thirty patients received initial treatment with vandetanib 300 mg/d. On the basis of investigator assessments, 20% of patients (ie, six of 30 patients) experienced a confirmed partial response (median duration of response at data cutoff, 10.2 months). An additional 53% of patients (ie, 16 of 30 patients) experienced stable disease at >/= 24 weeks, which yielded a disease control rate of 73% (ie, 22 of 30 patients). In 24 patients, serum calcitonin levels showed a 50% or greater decrease from baseline that was maintained for at least 4 weeks; 16 patients showed a similar reduction in serum carcinoembryonic antigen levels. The most common adverse events were diarrhea (70%), rash (67%), fatigue (63%), and nausea (63%). CONCLUSION In this study, vandetanib demonstrated durable objective partial responses and disease control with a manageable adverse event profile. These results demonstrate that vandetanib may provide an effective therapeutic option in patients with advanced hereditary MTC, a rare disease for which there has been no effective therapy.|
|Samuel A Wells; Jessica E Gosnell; Robert F Gagel; Jeffrey Moley; David Pfister; Julie A Sosa; Michael Skinner; Annetta Krebs; James Vasselli; Martin Schlumberger|
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|Type: Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't Date: 2010-01-11|
|Title: Journal of clinical oncology : official journal of the American Society of Clinical Oncology Volume: 28 ISSN: 1527-7755 ISO Abbreviation: J. Clin. Oncol. Publication Date: 2010 Feb|
|Created Date: 2010-02-09 Completed Date: 2010-03-04 Revised Date: 2012-06-04|
Medline Journal Info:
|Nlm Unique ID: 8309333 Medline TA: J Clin Oncol Country: United States|
|Languages: eng Pagination: 767-72 Citation Subset: IM|
|Dept of Surgery, Washington University School of Medicine, Box 8109, 660 S Euclid Ave, St Louis, MO 63110, USA. email@example.com|
|APA/MLA Format Download EndNote Download BibTex|
Antineoplastic Agents / administration & dosage*, adverse effects
Calcitonin / blood
Carcinoembryonic Antigen / blood
Carcinoma, Medullary / drug therapy*, genetics, metabolism, mortality, secondary
Drug Administration Schedule
Genetic Predisposition to Disease
Piperidines / administration & dosage*, adverse effects
Protein Kinase Inhibitors / administration & dosage*, adverse effects
Proto-Oncogene Proteins c-ret / antagonists & inhibitors*, genetics
Quinazolines / administration & dosage*, adverse effects
Thyroid Neoplasms / drug therapy*, genetics, metabolism, mortality, pathology
Tumor Markers, Biological / blood
|0/Antineoplastic Agents; 0/Carcinoembryonic Antigen; 0/N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0/Piperidines; 0/Protein Kinase Inhibitors; 0/Quinazolines; 0/Tumor Markers, Biological; 9007-12-9/Calcitonin; EC 220.127.116.11/Proto-Oncogene Proteins c-ret; EC 18.104.22.168/RET protein, human|
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