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Molecular Cancer Therapeutics
Molecular Cancer Therapeutics
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Spotlight on Clinical Response

BRAF and NRAS mutations in melanoma: potential relationships to clinical response to HSP90 inhibitors

Udai Banerji, Annette Affolter, Ian Judson, Richard Marais and Paul Workman
Udai Banerji
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Annette Affolter
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Ian Judson
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Richard Marais
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Paul Workman
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DOI: 10.1158/1535-7163.MCT-08-0145 Published April 2008
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    Figure 1.

    Representative traces of mutation status. A, patient 28 WTBRAF exon 15, codon 600: valine (GTG, arrow). B, patient 27 V600EBRAF exon 15, codon 600, showing a valine → glutamic acid substitution (GTG to GAG, arrow). C, patient 25 WTNRAS exon 2, codon 13 (GGT, arrow). D, patient 20 G13DNRAS exon 2, codon 13 showing a glycine → aspartic acid substitution (GGT to GAT, arrow).

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    BRAF and NRAS mutations in melanoma specimens: relationship with time to progression

    Patient no.BRAFNRASTime to progression while on 17-AAG (mo)
    20WTG13D49
    24V600EWT2
    25V600EWT1.5
    26WTWT1.5
    27V600EWT15
    28WTWT1
    • NOTE: Six patients with metastatic malignant melanoma were treated with 17-AAG at doses of 320 to 450 mg/m2/wk. The time to progression on treatment along with BRAF and NRAS mutation status are summarized.

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Molecular Cancer Therapeutics: 7 (4)
April 2008
Volume 7, Issue 4
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BRAF and NRAS mutations in melanoma: potential relationships to clinical response to HSP90 inhibitors
Udai Banerji, Annette Affolter, Ian Judson, Richard Marais and Paul Workman
Mol Cancer Ther April 1 2008 (7) (4) 737-739; DOI: 10.1158/1535-7163.MCT-08-0145

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BRAF and NRAS mutations in melanoma: potential relationships to clinical response to HSP90 inhibitors
Udai Banerji, Annette Affolter, Ian Judson, Richard Marais and Paul Workman
Mol Cancer Ther April 1 2008 (7) (4) 737-739; DOI: 10.1158/1535-7163.MCT-08-0145
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Molecular Cancer Therapeutics
eISSN: 1538-8514
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