Inside life of melanoma cell signaling, molecular insights, and therapeutic targets

Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and m...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Sosman, Jeffrey A. [verfasserIn] Margolin, Kim A. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Schlagwörter:	Melanoma Clin Oncol Sorafenib BRAF Mutation Axitinib

Übergeordnetes Werk:	Enthalten in: Current oncology reports - Philadelphia, Pa. : Current Science, Inc., 1999, 11(2009), 5 vom: 11. Aug., Seite 405-411
Übergeordnetes Werk:	volume:11 ; year:2009 ; number:5 ; day:11 ; month:08 ; pages:405-411

Links:	Volltext

DOI / URN:	10.1007/s11912-009-0054-y

Katalog-ID:	SPR02298562X

Internformat


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520			\|a Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma.
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matchkey_str	article:15346269:2009----::nieiefeaoaelinlnmlclrnihs
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allfields	10.1007/s11912-009-0054-y doi (DE-627)SPR02298562X (SPR)s11912-009-0054-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sosman, Jeffrey A. verfasserin aut Inside life of melanoma cell signaling, molecular insights, and therapeutic targets 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma. Melanoma (dpeaa)DE-He213 Clin Oncol (dpeaa)DE-He213 Sorafenib (dpeaa)DE-He213 BRAF Mutation (dpeaa)DE-He213 Axitinib (dpeaa)DE-He213 Margolin, Kim A. verfasserin aut Enthalten in Current oncology reports Philadelphia, Pa. : Current Science, Inc., 1999 11(2009), 5 vom: 11. Aug., Seite 405-411 (DE-627)332626490 (DE-600)2054295-1 1534-6269 nnns volume:11 year:2009 number:5 day:11 month:08 pages:405-411 https://dx.doi.org/10.1007/s11912-009-0054-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 11 2009 5 11 08 405-411
spelling	10.1007/s11912-009-0054-y doi (DE-627)SPR02298562X (SPR)s11912-009-0054-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sosman, Jeffrey A. verfasserin aut Inside life of melanoma cell signaling, molecular insights, and therapeutic targets 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma. Melanoma (dpeaa)DE-He213 Clin Oncol (dpeaa)DE-He213 Sorafenib (dpeaa)DE-He213 BRAF Mutation (dpeaa)DE-He213 Axitinib (dpeaa)DE-He213 Margolin, Kim A. verfasserin aut Enthalten in Current oncology reports Philadelphia, Pa. : Current Science, Inc., 1999 11(2009), 5 vom: 11. Aug., Seite 405-411 (DE-627)332626490 (DE-600)2054295-1 1534-6269 nnns volume:11 year:2009 number:5 day:11 month:08 pages:405-411 https://dx.doi.org/10.1007/s11912-009-0054-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 11 2009 5 11 08 405-411
allfields_unstemmed	10.1007/s11912-009-0054-y doi (DE-627)SPR02298562X (SPR)s11912-009-0054-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sosman, Jeffrey A. verfasserin aut Inside life of melanoma cell signaling, molecular insights, and therapeutic targets 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma. Melanoma (dpeaa)DE-He213 Clin Oncol (dpeaa)DE-He213 Sorafenib (dpeaa)DE-He213 BRAF Mutation (dpeaa)DE-He213 Axitinib (dpeaa)DE-He213 Margolin, Kim A. verfasserin aut Enthalten in Current oncology reports Philadelphia, Pa. : Current Science, Inc., 1999 11(2009), 5 vom: 11. Aug., Seite 405-411 (DE-627)332626490 (DE-600)2054295-1 1534-6269 nnns volume:11 year:2009 number:5 day:11 month:08 pages:405-411 https://dx.doi.org/10.1007/s11912-009-0054-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 11 2009 5 11 08 405-411
allfieldsGer	10.1007/s11912-009-0054-y doi (DE-627)SPR02298562X (SPR)s11912-009-0054-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sosman, Jeffrey A. verfasserin aut Inside life of melanoma cell signaling, molecular insights, and therapeutic targets 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma. Melanoma (dpeaa)DE-He213 Clin Oncol (dpeaa)DE-He213 Sorafenib (dpeaa)DE-He213 BRAF Mutation (dpeaa)DE-He213 Axitinib (dpeaa)DE-He213 Margolin, Kim A. verfasserin aut Enthalten in Current oncology reports Philadelphia, Pa. : Current Science, Inc., 1999 11(2009), 5 vom: 11. Aug., Seite 405-411 (DE-627)332626490 (DE-600)2054295-1 1534-6269 nnns volume:11 year:2009 number:5 day:11 month:08 pages:405-411 https://dx.doi.org/10.1007/s11912-009-0054-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 11 2009 5 11 08 405-411
allfieldsSound	10.1007/s11912-009-0054-y doi (DE-627)SPR02298562X (SPR)s11912-009-0054-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.81 bkl Sosman, Jeffrey A. verfasserin aut Inside life of melanoma cell signaling, molecular insights, and therapeutic targets 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma. Melanoma (dpeaa)DE-He213 Clin Oncol (dpeaa)DE-He213 Sorafenib (dpeaa)DE-He213 BRAF Mutation (dpeaa)DE-He213 Axitinib (dpeaa)DE-He213 Margolin, Kim A. verfasserin aut Enthalten in Current oncology reports Philadelphia, Pa. : Current Science, Inc., 1999 11(2009), 5 vom: 11. Aug., Seite 405-411 (DE-627)332626490 (DE-600)2054295-1 1534-6269 nnns volume:11 year:2009 number:5 day:11 month:08 pages:405-411 https://dx.doi.org/10.1007/s11912-009-0054-y lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.81 ASE AR 11 2009 5 11 08 405-411
language	English
source	Enthalten in Current oncology reports 11(2009), 5 vom: 11. Aug., Seite 405-411 volume:11 year:2009 number:5 day:11 month:08 pages:405-411
sourceStr	Enthalten in Current oncology reports 11(2009), 5 vom: 11. Aug., Seite 405-411 volume:11 year:2009 number:5 day:11 month:08 pages:405-411
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Melanoma Clin Oncol Sorafenib BRAF Mutation Axitinib
dewey-raw	610
isfreeaccess_bool	false
container_title	Current oncology reports
authorswithroles_txt_mv	Sosman, Jeffrey A. @@aut@@ Margolin, Kim A. @@aut@@
publishDateDaySort_date	2009-08-11T00:00:00Z
hierarchy_top_id	332626490
dewey-sort	3610
id	SPR02298562X
language_de	englisch
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author	Sosman, Jeffrey A.
spellingShingle	Sosman, Jeffrey A. ddc 610 bkl 44.81 misc Melanoma misc Clin Oncol misc Sorafenib misc BRAF Mutation misc Axitinib Inside life of melanoma cell signaling, molecular insights, and therapeutic targets
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topic_title	610 ASE 44.81 bkl Inside life of melanoma cell signaling, molecular insights, and therapeutic targets Melanoma (dpeaa)DE-He213 Clin Oncol (dpeaa)DE-He213 Sorafenib (dpeaa)DE-He213 BRAF Mutation (dpeaa)DE-He213 Axitinib (dpeaa)DE-He213
topic	ddc 610 bkl 44.81 misc Melanoma misc Clin Oncol misc Sorafenib misc BRAF Mutation misc Axitinib
topic_unstemmed	ddc 610 bkl 44.81 misc Melanoma misc Clin Oncol misc Sorafenib misc BRAF Mutation misc Axitinib
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title	Inside life of melanoma cell signaling, molecular insights, and therapeutic targets
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title_full	Inside life of melanoma cell signaling, molecular insights, and therapeutic targets
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title_sort	inside life of melanoma cell signaling, molecular insights, and therapeutic targets
title_auth	Inside life of melanoma cell signaling, molecular insights, and therapeutic targets
abstract	Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma.
abstractGer	Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma.
abstract_unstemmed	Abstract Melanoma is one of the fastest growing tumor types in the United States. Immunotherapy and chemotherapy benefit only a few patients with metastatic disease. Therapy targeting a signaling pathway critical to the cancer’s growth can provide dramatic benefit in several other malignancies and may be a valuable strategy for advanced melanoma, if drugs with a favorable therapeutic index are effective against essential molecular pathways. One such target is the V600E “gain-of-function” BRAF mutation found in 60% of melanomas; other mutations or molecular alterations cooperate with V600E BRAF, particularly those that cause loss of function of PTEN, upstream of Akt and mammalian target of rapamycin. Rapid development of new agents, a better understanding of the target pathways and mechanisms of resistance, and carefully designed strategies to optimize combinations and sequences of these agents, potentially with chemotherapy or immunotherapy, may ultimately have the potential to overcome the previously insurmountable obstacle of therapy resistance in melanoma.
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title_short	Inside life of melanoma cell signaling, molecular insights, and therapeutic targets
url	https://dx.doi.org/10.1007/s11912-009-0054-y
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author2	Margolin, Kim A.
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doi_str	10.1007/s11912-009-0054-y
up_date	2024-07-03T16:08:32.071Z
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