Abstract
The effects of sorafenib--an oral multikinase inhibitor targeting the tumour and tumour vasculature--were evaluated in patients with advanced melanoma enrolled in a large multidisease Phase II randomised discontinuation trial (RDT). Enrolled patients received a 12-week run-in of sorafenib 400 mg twice daily (b.i.d.). Patients with changes in bi-dimensional tumour measurements <25% from baseline were then randomised to sorafenib or placebo for a further 12 weeks (ie to week 24). Patients with > or =25% tumour shrinkage after the run-in continued on open-label sorafenib, whereas those with > or =25% tumour growth discontinued treatment. This analysis focussed on secondary RDT end points: changes in bi-dimensional tumour measurements from baseline after 12 weeks and overall tumour responses (WHO criteria) at week 24, progression-free survival (PFS), safety and biomarkers (BRAF, KRAS and NRAS mutational status). Of 37 melanoma patients treated during the run-in phase, 34 were evaluable for response: one had > or =25% tumour shrinkage and remained on open-label sorafenib; six (16%) had <25% tumour growth and were randomised (placebo, n=3; sorafenib, n=3); and 27 had > or =25% tumour growth and discontinued. All three randomised sorafenib patients progressed by week 24; one remained on sorafenib for symptomatic relief. All three placebo patients progressed by week-24 and were re-started on sorafenib; one experienced disease re-stabilisation. Overall, the confirmed best responses for each of the 37 melanoma patients who received sorafenib were 19% stable disease (SD) (ie n=1 open-label; n=6 randomised), 62% (n=23) progressive disease (PD) and 19% (n=7) unevaluable. The overall median PFS was 11 weeks. The six randomised patients with SD had overall PFS values ranging from 16 to 34 weeks. The most common drug-related adverse events were dermatological (eg rash/desquamation, 51%; hand-foot skin reaction, 35%). There was no relationship between V600E BRAF status and disease stability. DNA was extracted from the biopsies of 17/22 patients. Six had V600E-positive tumours (n=4 had PD; n=1 had SD; n=1 unevaluable for response), and 11 had tumours containing wild-type BRAF (n=9 PD; n=1 SD; n=1 unevaluable for response). In conclusion, sorafenib is well tolerated but has little or no antitumour activity in advanced melanoma patients as a single agent at the dose evaluated (400 mg b.i.d.). Ongoing trials in advanced melanoma are evaluating sorafenib combination therapies.
MeSH Terms
Adult
Aged
Aged, 80 and over
Angiogenesis Inhibitors/therapeutic use,toxicity
Benzenesulfonates/therapeutic use,toxicity
DNA Primers
Female
Genes, ras
Humans
Male
Melanoma/blood supply,drug therapy,genetics,pathology
Middle Aged
Neoplasm Staging
Niacinamide/analogs & derivatives
Phenylurea Compounds
Polymerase Chain Reaction
Proto-Oncogene Proteins B-raf/genetics
Pyridines/therapeutic use,toxicity
Safety
Sorafenib
Chemicals
Angiogenesis Inhibitors
Benzenesulfonates
DNA Primers
Phenylurea Compounds
Pyridines
Niacinamide
Sorafenib
Proto-Oncogene Proteins B-raf
Authors & Affiliations
17 authors, click to expand affiliations / ORCID
Ahmad T
Flaherty K T
Gore M
Kaye S
Marais R
Gibbens I
Hackett S
James M
Schuchter L M
Nathanson K L
Xia C
Simantov R
Schwartz B
Poulin-Costello M
O'Dwyer P J
Ratain M J
References (19)
19 references, click to expand
-
BAY 43-9006 exhibits broad spectrum oral antitumor activity and targets the RAF/MEK/ERK pathway and receptor tyrosine kinases involved in tumor progression and angiogenesis.
Cancer Res. 2004 Oct 1;64(19):7099-109
PMID: 15466206
-
Differential impact of Raf-1 kinase activity on tumor cell resistance to paclitaxel and docetaxel.
Anticancer Drugs. 2000 Jul;11(6):439-43
PMID: 11001384
-
Guilty as charged: B-RAF is a human oncogene.
Cancer Cell. 2004 Oct;6(4):313-9
PMID: 15488754
-
The Raf inhibitor BAY 43-9006 (Sorafenib) induces caspase-independent apoptosis in melanoma cells.
Cancer Res. 2006 Feb 1;66(3):1611-9
PMID: 16452220
-
The role of Mcl-1 downregulation in the proapoptotic activity of the multikinase inhibitor BAY 43-9006.
Oncogene. 2005 Oct 20;24(46):6861-9
PMID: 16007148
-
Mutations of the BRAF gene in human cancer.
Nature. 2002 Jun 27;417(6892):949-54
PMID: 12068308
-
Clinical significance of BRAF mutations in metastatic melanoma.
J Transl Med. 2004 Dec 21;2(1):46
PMID: 15613230
-
Apoptosis induced by the kinase inhibitor BAY 43-9006 in human leukemia cells involves down-regulation of Mcl-1 through inhibition of translation.
J Biol Chem. 2005 Oct 21;280(42):35217-27
PMID: 16109713
-
Constitutive mitogen-activated protein kinase activation in melanoma is mediated by both BRAF mutations and autocrine growth factor stimulation.
Cancer Res. 2003 Feb 15;63(4):756-9
PMID: 12591721
-
Prognostic factors analysis of 17,600 melanoma patients: validation of the American Joint Committee on Cancer melanoma staging system.
J Clin Oncol. 2001 Aug 15;19(16):3622-34
PMID: 11504744
-
Phase II placebo-controlled randomized discontinuation trial of sorafenib in patients with metastatic renal cell carcinoma.
J Clin Oncol. 2006 Jun 1;24(16):2505-12
PMID: 16636341
-
Suppression of BRAF(V599E) in human melanoma abrogates transformation.
Cancer Res. 2003 Sep 1;63(17):5198-202
PMID: 14500344
-
Improving outcomes in advanced malignant melanoma: update on systemic therapy.
Drugs. 2005;65(6):733-43
PMID: 15819587
-
B-RAF is a therapeutic target in melanoma.
Oncogene. 2004 Aug 19;23(37):6292-8
PMID: 15208680
-
BRAF and RAS mutations in human lung cancer and melanoma.
Cancer Res. 2002 Dec 1;62(23):6997-7000
PMID: 12460918
-
Phase I clinical and pharmacokinetic study of the Novel Raf kinase and vascular endothelial growth factor receptor inhibitor BAY 43-9006 in patients with advanced refractory solid tumors.
J Clin Oncol. 2005 Feb 10;23(5):965-72
PMID: 15613696
-
Safety and pharmacokinetics of the dual action Raf kinase and vascular endothelial growth factor receptor inhibitor, BAY 43-9006, in patients with advanced, refractory solid tumors.
Clin Cancer Res. 2005 Aug 1;11(15):5472-80
PMID: 16061863
-
Phase I safety and pharmacokinetics of BAY 43-9006 administered for 21 days on/7 days off in patients with advanced, refractory solid tumours.
Br J Cancer. 2005 May 23;92(10):1855-61
PMID: 15870716
-
Metastatic melanoma: is biochemotherapy the future?
Med Oncol. 2005;22(2):101-11
PMID: 15965272