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PMID: 16880785 Published · ppublish English Clinical Trial, Phase II Journal Article Randomized Controlled Trial

Sorafenib in advanced melanoma: a Phase II randomised discontinuation trial analysis.

British journal of cancer ·Vol. 95 ·No. 5 ·2006-09-04 ·Pages 581-6

Eisen T, Ahmad T, Flaherty KT, Gore M, Kaye S, Marais R, Gibbens I, Hackett S, James M, Schuchter LM, Nathanson KL, Xia C, Simantov R, Schwartz B, Poulin-Costello M, O'Dwyer PJ, Ratain MJ

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
Eisen T
Royal Marsden Hospital, Downs Road, Surrey SMT 5PT, UK. [email protected]
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
  1. 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
  2. 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
  3. Guilty as charged: B-RAF is a human oncogene.
    Cancer Cell. 2004 Oct;6(4):313-9 PMID: 15488754
  4. 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
  5. 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
  6. Mutations of the BRAF gene in human cancer.
    Nature. 2002 Jun 27;417(6892):949-54 PMID: 12068308
  7. Clinical significance of BRAF mutations in metastatic melanoma.
    J Transl Med. 2004 Dec 21;2(1):46 PMID: 15613230
  8. 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
  9. 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
  10. 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
  11. 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
  12. Suppression of BRAF(V599E) in human melanoma abrogates transformation.
    Cancer Res. 2003 Sep 1;63(17):5198-202 PMID: 14500344
  13. Improving outcomes in advanced malignant melanoma: update on systemic therapy.
    Drugs. 2005;65(6):733-43 PMID: 15819587
  14. B-RAF is a therapeutic target in melanoma.
    Oncogene. 2004 Aug 19;23(37):6292-8 PMID: 15208680
  15. BRAF and RAS mutations in human lung cancer and melanoma.
    Cancer Res. 2002 Dec 1;62(23):6997-7000 PMID: 12460918
  16. 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
  17. 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
  18. 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
  19. Metastatic melanoma: is biochemotherapy the future?
    Med Oncol. 2005;22(2):101-11 PMID: 15965272
Article Info
Journal
British journal of cancer
Abbr.
Br J Cancer
ISSN
0007-0920
Published
2006-09-04
Epub
2006-00-01
Pages
581-6
Language
English
Region
England
NLM ID
0370635
PMCID
PMC2360687
Subset
IM
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