Titulo:
Genotipo complejo en un paciente con GIST.
.
Sumario:
Se presenta el caso de un hombre de 35 años diagnosticado de un tumor del estroma gastrointestinal (GIST) localizado en el yeyuno proximal y estratificado como de alto riesgo, en quien se resecó el primario sin evidencia de recaída, hasta documentar múltiples lesiones hepáticas, por lo que inició imatinib (Glivec®) 400 mg/día. Después de encontrar progresión, se aumentaron las dosis del inhibidor sin respuesta, por lo que inició sunitinib (Sutent®) 50 mg/día con el mismo resultado. Posteriormente, se realizó una reevaluación del histotipo y genotipificación, encontrando positividad para la mutación del exón 9 del gen KIT. A partir de noviembre del 2009, se administró sorafenib (Nexavar®) 400 mg cada 12 horas, logrando una respuesta metabóli... Ver más
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Henry Becerra - 2012
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Genotipo complejo en un paciente con GIST. Complex genotype in a GIST patient. Se presenta el caso de un hombre de 35 años diagnosticado de un tumor del estroma gastrointestinal (GIST) localizado en el yeyuno proximal y estratificado como de alto riesgo, en quien se resecó el primario sin evidencia de recaída, hasta documentar múltiples lesiones hepáticas, por lo que inició imatinib (Glivec®) 400 mg/día. Después de encontrar progresión, se aumentaron las dosis del inhibidor sin respuesta, por lo que inició sunitinib (Sutent®) 50 mg/día con el mismo resultado. Posteriormente, se realizó una reevaluación del histotipo y genotipificación, encontrando positividad para la mutación del exón 9 del gen KIT. A partir de noviembre del 2009, se administró sorafenib (Nexavar®) 400 mg cada 12 horas, logrando una respuesta metabólica superior al 50% (evaluada por tomografía por emisión de positrones –PET/TAC–) y parcial siguiendo los criterios descritos por Choi y colaboradores. Durante el tratamiento de tercera línea, se efectuó una nueva biopsia del tumor, que demostró un genotipo complejo, incluyendo la mutación V600E del BRAF, y manteniendo el beneficio clínico con la intervención descrita hasta julio del 2011; en el momento, el paciente continúa vivo. A continuación, se plantea un análisis de los mecanismos moleculares que explican la resistencia a los inhibidores de tirosina-quinasa y las implicaciones sobre la terapéutica del GIST. The case of a 35-year-old man is presented; he was diagnosed as having a gastrointestinal stromal tumour (GIST) which was located in the proximal jejunum and stratified as being high risk. The primary GIST was resected without evidence of relapse until multiple hepatic lesions were documented so that treatment with 400 mg/day imatinib (Glivec®) was begun. After progression was found, the inhibitor dose was increased without response, meaning that 50 mg/day sunitinib (Sutent®) was begun with the same result. The histotype and genotyping were thus re-evaluated, positivity for KIT gene exon 9 mutation being found; 400 mg BID sorafenib (Nexavar®) was administered from November 2009 onwards, achieving a 50% metabolic response (evaluated by PET/CAT) and partial response following the criteria described by Choi and coworkers. A new biopsy of the tumour was made during third-line treatment, demonstrating a complex genotype including the BRAF V600E mutation. Clinical benefit was maintained with the aforementioned intervention until July 2011; the patient was still alive at this point. A detailed analysis of the molecular mechanisms explaining resistance to tyrosine kinase inhibitors and the implications concerning GIST therapy was then proposed. Becerra, Henry Cardona, Andrés Felipe Acevedo, Andrés Vargas, Carlos Carranza, Hernán Otero, Jorge Álvarez, Johanna Aguirre, Diego Serrano, Silvia Zuluaga, Alirio GIST BRAF cKIT patología molecular sorafenib resistencia GIST BRAF cKIT molecular pathology sorafenib resistance 1 1 Núm. 1 , Año 2012 : Abril Artículo de revista Journal article 2012-04-01T00:00:00Z 2012-04-01T00:00:00Z 2012-04-01 application/pdf Asociación Colombiana de Hematología y Oncología (ACHO) Revista Colombiana de Hematología y Oncología 2256-2877 2256-2915 https://revista.acho.info/index.php/acho/article/view/291 10.51643/22562915.291 https://doi.org/10.51643/22562915.291 spa https://creativecommons.org/licenses/by-nc-sa/4.0 Henry Becerra - 2012 Esta obra está bajo una licencia internacional Creative Commons Atribución-NoComercial-CompartirIgual 4.0. 70 77 Rossi CR, Mocellin S, Mancarelli R, Foletto M, Pilati P, Nitti D, et al. Gastrointestinal stromal tumours: from a surgical to a molecular approach. Int J Cancer. 2003;107(2):171-6. Duffaud F, Blay JY. Gastrointestinal stromal tumors: biology and treatment. Oncology. 2003;65(3):187-97. Thuneberg L. Interstitial cells of Cajal: intestinal pacemaker cells? Adv Anat Embryo Cell Biol. 1982;71:1-130. Chan JK. Mesenchymal tumours of the gastrointestinal tract: a paradise for acronyms (STUMP, GIST, GANT, and now GIPACT). Implications of c-kit in genesis, and yet another of many emerging roles of the interstitial cell of Cajal in the pathogenesis of gastrointestinal disease? Adv Anat Pathol. 1999;6(1):19-40. Vargas C, Cardona AF, Carranza H, Otero JM, Reveiz L, Ospina E, et al. Tumores del estroma gastrointestinal (GIST): experiencia en dos instituciones hospitalarias de Bogotá D.C., Colombia (estudio del ONCOLGroup). Rev Col Gastroenterol. 2008;23(3):213-23. Oliveros R, Quintero AP, Sánchez R, Mesa JA. Tumores estromales gastrointestinales (GIST) en el Instituto Nacional de Cancerología (INC) 2000-2008. Rev Col Cancerol. 2011;15(4):1-34. Nickl NJ. Gastrointestinal stromal tumors: new progress, new questions. Curr Opin Gastroenterol. 2004;20(5):482-7. Joensuu H, Roberts P, Sarlomo-Rikala M, Andersson LC, Tervahartiala P, Tuveson D, et al. Effect of the tyrosine kinase inhibitor STI571 in a patient with a metastatic gastrointestinal stromal tumor. N Engl J Med. 2001;344(14):1052-6. Joensuu H. Second line therapies for the treatment of gastrointestinal stromal tumor. Curr Opin Oncol. 2007;19(4):353- 8. Rajagopalan H, Bardelli A, Lengauer C, Kinzler KW, Vogelstein B, Velculescu VE. Tumorigenesis: RAF/RAS oncogenes and mismatch-repair status. Nature. 2002;418(6901):934. Miranda C, Nucifora M, Molinari M, Conca E, Anania MC, Bordoni A, et al. KRAS and BRAF mutations predict primary resistance to imatinib in gastrointestinal stromal tumors. Clin Cancer Res. 2012;18(6):1769-76. Miettinen M, Lasota J. Gastrointestinal stromal tumors: pathology and prognosis at different sites. Semin Diagn Pathol. 2006;23(2):70-83. Liegl-Atzwanger B, Fletcher JA, Fletcher CD. Gastrointestinal stromal tumors. Virchows Arch. 2010;456(2):111-27. Fletcher CD, Berman JJ, Corless C, Gorstein F, Lasota J, Longley BJ, et al. Diagnosis of gastrointestinal stromal tumors: a consensus approach. Hum Pathol. 2002;33(5):459-65. Fernández JA, Sánchez Canovas M, Parrilla P. Controversias en el tratamiento de los tumores del estroma gastrointestinal (GIST) primarios. Cir Esp. 2010;88:69-80. Scarpa M, Bertin M, Ruffolo C, Polese L, D’Amico DF, Angriman I. A systematic review on the clinical diagnosis of gastrointestinal stromal tumors. J Surg Oncol. 2008;98(5):384-92. van de Rijn M, Hendrickson MR, Rouse RV. CD34 expression by gastrointestinal tract stromal tumors. Human Pathol. 1994:25(8):766-71. Downs-Kelly E, Rubi BP. Gastrointestinal stromal tumors: molecular mechanisms and targeted therapies. Patholog Res Int. 2011;4:1-7. Daniels M, Lurkin I, Pauli R, Erbstösser E, Hildebrandt U, Hellwig K, et al. Spectrum of KIT/PDGFRA/BRAF mutations and Phosphatidylinositol-3-Kinase pathway gene alterations in gastrointestinal stromal tumors (GIST). Cancer Lett. 2011;312(1):43-54. Longley BJ, Reguera MJ, Ma Y. Classes of c-KIT activating mutations: proposed mechanisms of action and implications for disease classification and therapy. Leuk Res. 2001;25(7):571-6. Medeiros F, Corless CL, Duensing A, Hornick JL, Oliveira AM, Heinrich MC, et al. KIT-negative gastrointestinal stromal tumors. Am J Surg Pathol. 2004;28(7):889-94. Agaram NP, Wong GC, Guo T, Maki RG, Singer S, Dematteo RP, et al. Novel V600E BRAF mutations in imatinib-naive and imatinib-resistant gastrointestinal stromal tumors. Genes Chromosomes Cancer. 2008;47(10):853-9. Davies H, Bignell GR, Cox C, Stephens P, Edkins S, Clegg S, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417(6892):949-54. Brose MS, Volpe P, Feldman M, Kumar M, Rishi I, Gerrero R, et al. BRAF and RAS mutations in human lung cancer and melanoma. Cancer Res. 2002;62(23):6997-7000. Tiacci E, Trifonov V, Schiavoni G, Holmes A, Kern W, Martelli MP, et al. BRAF mutations in hairy-cell leukemia. N Engl J Med. 2011;364(24):2305-15. Michaloglou C, Vredeveld LC, Mooi WJ, Peeper DS. BRAF (E600) in benign and malignant human tumours. Oncogene. 2008;27(7):877-95. Curtin JA, Fridlyand J, Kageshita T, Patel HN, Busam KJ, Kutzner H, et al. Distinct sets of genetic alterations in melanoma. N Engl J Med. 2005;353(20):2135-47. Antonescu CR, Besmer P, Guo T, Arkun K, Hom G, Koryotowski B, et al. Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation. Clin Cancer Res. 2005;11(11):4182-90. Solit DB, Garraway LA, Pratilas CA, Sawai A, Getz G, Basso A, et al. BRAF mutation predicts sensitivity to MEK inhibition. Nature. 2006;439(7074):358-62. Rossi F, Ehlers I, Agosti V, Socci ND, Viale A, Sommer G, et al. Oncogenic Kit signaling and therapeutic intervention in a mouse model of gastrointestinal stromal tumor. Proc Natl Acad Sci USA. 2006;103(34):12843-8. Chapman PB, Hauschild A, Robert C, Haanen JB, Ascierto P, Larkin J, et al. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med. 2011;364(26):2507-16. Nimeiri HS, Maki RG, Kasza K, D’Adamo D, Chow W, et al. Activity of sorafenib (SOR) in patients (pts) with imatinib (IM) and sunitinib (SU)-resistant (RES) gastrointestinal tumors (GIST): A phase II trial of the University of Chicago Phase II Consortium. J Clin Oncol. 2008;26:abstr 10502. Kindler HL, Campbell NP, Wroblewski K, Maki RG, D’Adamo DR, Chow WA, et al. Sorafenib in patients with imatinib and sunitinib resistant gastrointestinal stromal tumors (GIST): Final results of a University of Chicago Phase II Consortium trial. J Clin Oncol. 2011;29:abstr 10009. Cauchi C, Somaiah N, Engstrom P, Litwin S, López M, Lee L, et al. Evaluation of nilotinib (N) in advanced GIST previously treated with imatinibmesylate (IM) and sunitinib (S). J Clin Oncol. 2010;28:15s, abstr 10090. Guo T, Agaram NP, Wong GC, Hom G, D’Adamo D, Maki RG, et al. Sorafenib inhibits the imatinib-resistant KITT670I gatekeeper mutation in gastrointestinal stromal tumor. Clin Cancer Res. 2007;13(16):4874-81. Italiano A, Cioffi A, Maki RG, Schöffski P, Rutkowski P, Le Cesne A, et al. Patterns of care, prognosis, and survival of patients with metastatic gastrointestinal stromal tumors (GIST) refractory to first-line imatinib and second-line sunitinib. J Clin Oncol. 2011;29:abstr 10044. Agaram NP, Laquaglia MP, Ustun B, Guo T, Wong GC, Socci ND, et al. Molecular characterization of pediatric gastrointestinal stromal tumors. Clin Cancer Res. 2008;14(10):3204-15. Pierotti MA, Tamborini E, Negri T, Pricl S, Pilotti S. Targeted therapy in GIST: in silico modeling for prediction of resistance. Nat Rev Clin Oncol. 2011;8(3):161-70. https://revista.acho.info/index.php/acho/article/download/291/261 info:eu-repo/semantics/article http://purl.org/coar/resource_type/c_6501 info:eu-repo/semantics/publishedVersion http://purl.org/coar/version/c_970fb48d4fbd8a85 info:eu-repo/semantics/openAccess http://purl.org/coar/access_right/c_abf2 Text Publication |
| institution |
ASOCIACION COLOMBIANA DE HEMATOLOGIA Y ONCOLOGIA |
| thumbnail |
https://nuevo.metarevistas.org/ASOCIACIONCOLOMBIANADEHEMATOLOGIAYONCOLOGIA/logo.png |
| country_str |
Colombia |
| collection |
Revista Colombiana de Hematología y Oncología |
| title |
Genotipo complejo en un paciente con GIST. |
| spellingShingle |
Genotipo complejo en un paciente con GIST. Becerra, Henry Cardona, Andrés Felipe Acevedo, Andrés Vargas, Carlos Carranza, Hernán Otero, Jorge Álvarez, Johanna Aguirre, Diego Serrano, Silvia Zuluaga, Alirio GIST BRAF cKIT patología molecular sorafenib resistencia GIST BRAF cKIT molecular pathology sorafenib resistance |
| title_short |
Genotipo complejo en un paciente con GIST. |
| title_full |
Genotipo complejo en un paciente con GIST. |
| title_fullStr |
Genotipo complejo en un paciente con GIST. |
| title_full_unstemmed |
Genotipo complejo en un paciente con GIST. |
| title_sort |
genotipo complejo en un paciente con gist. |
| title_eng |
Complex genotype in a GIST patient. |
| description |
Se presenta el caso de un hombre de 35 años diagnosticado de un tumor del estroma gastrointestinal (GIST) localizado en el yeyuno proximal y estratificado como de alto riesgo, en quien se resecó el primario sin evidencia de recaída, hasta documentar múltiples lesiones hepáticas, por lo que inició imatinib (Glivec®) 400 mg/día. Después de encontrar progresión, se aumentaron las dosis del inhibidor sin respuesta, por lo que inició sunitinib (Sutent®) 50 mg/día con el mismo resultado. Posteriormente, se realizó una reevaluación del histotipo y genotipificación, encontrando positividad para la mutación del exón 9 del gen KIT. A partir de noviembre del 2009, se administró sorafenib (Nexavar®) 400 mg cada 12 horas, logrando una respuesta metabólica superior al 50% (evaluada por tomografía por emisión de positrones –PET/TAC–) y parcial siguiendo los criterios descritos por Choi y colaboradores. Durante el tratamiento de tercera línea, se efectuó una nueva biopsia del tumor, que demostró un genotipo complejo, incluyendo la mutación V600E del BRAF, y manteniendo el beneficio clínico con la intervención descrita hasta julio del 2011; en el momento, el paciente continúa vivo. A continuación, se plantea un análisis de los mecanismos moleculares que explican la resistencia a los inhibidores de tirosina-quinasa y las implicaciones sobre la terapéutica del GIST.
|
| description_eng |
The case of a 35-year-old man is presented; he was diagnosed as having a gastrointestinal stromal tumour (GIST) which was located in the proximal jejunum and stratified as being high risk. The primary GIST was resected without evidence of relapse until multiple hepatic lesions were documented so that treatment with 400 mg/day imatinib (Glivec®) was begun. After progression was found, the inhibitor dose was increased without response, meaning that 50 mg/day sunitinib (Sutent®) was begun with the same result. The histotype and genotyping were thus re-evaluated, positivity for KIT gene exon 9 mutation being found; 400 mg BID sorafenib (Nexavar®) was administered from November 2009 onwards, achieving a 50% metabolic response (evaluated by PET/CAT) and partial response following the criteria described by Choi and coworkers. A new biopsy of the tumour was made during third-line treatment, demonstrating a complex genotype including the BRAF V600E mutation. Clinical benefit was maintained with the aforementioned intervention until July 2011; the patient was still alive at this point. A detailed analysis of the molecular mechanisms explaining resistance to tyrosine kinase inhibitors and the implications concerning GIST therapy was then proposed.
|
| author |
Becerra, Henry Cardona, Andrés Felipe Acevedo, Andrés Vargas, Carlos Carranza, Hernán Otero, Jorge Álvarez, Johanna Aguirre, Diego Serrano, Silvia Zuluaga, Alirio |
| author_facet |
Becerra, Henry Cardona, Andrés Felipe Acevedo, Andrés Vargas, Carlos Carranza, Hernán Otero, Jorge Álvarez, Johanna Aguirre, Diego Serrano, Silvia Zuluaga, Alirio |
| topicspa_str_mv |
GIST BRAF cKIT patología molecular sorafenib resistencia |
| topic |
GIST BRAF cKIT patología molecular sorafenib resistencia GIST BRAF cKIT molecular pathology sorafenib resistance |
| topic_facet |
GIST BRAF cKIT patología molecular sorafenib resistencia GIST BRAF cKIT molecular pathology sorafenib resistance |
| citationvolume |
1 |
| citationissue |
1 |
| citationedition |
Núm. 1 , Año 2012 : Abril |
| publisher |
Asociación Colombiana de Hematología y Oncología (ACHO) |
| ispartofjournal |
Revista Colombiana de Hematología y Oncología |
| source |
https://revista.acho.info/index.php/acho/article/view/291 |
| language |
spa |
| format |
Article |
| rights |
https://creativecommons.org/licenses/by-nc-sa/4.0 Henry Becerra - 2012 Esta obra está bajo una licencia internacional Creative Commons Atribución-NoComercial-CompartirIgual 4.0. info:eu-repo/semantics/openAccess http://purl.org/coar/access_right/c_abf2 |
| references |
Rossi CR, Mocellin S, Mancarelli R, Foletto M, Pilati P, Nitti D, et al. Gastrointestinal stromal tumours: from a surgical to a molecular approach. Int J Cancer. 2003;107(2):171-6. Duffaud F, Blay JY. Gastrointestinal stromal tumors: biology and treatment. Oncology. 2003;65(3):187-97. Thuneberg L. Interstitial cells of Cajal: intestinal pacemaker cells? Adv Anat Embryo Cell Biol. 1982;71:1-130. Chan JK. Mesenchymal tumours of the gastrointestinal tract: a paradise for acronyms (STUMP, GIST, GANT, and now GIPACT). Implications of c-kit in genesis, and yet another of many emerging roles of the interstitial cell of Cajal in the pathogenesis of gastrointestinal disease? Adv Anat Pathol. 1999;6(1):19-40. Vargas C, Cardona AF, Carranza H, Otero JM, Reveiz L, Ospina E, et al. Tumores del estroma gastrointestinal (GIST): experiencia en dos instituciones hospitalarias de Bogotá D.C., Colombia (estudio del ONCOLGroup). Rev Col Gastroenterol. 2008;23(3):213-23. Oliveros R, Quintero AP, Sánchez R, Mesa JA. Tumores estromales gastrointestinales (GIST) en el Instituto Nacional de Cancerología (INC) 2000-2008. Rev Col Cancerol. 2011;15(4):1-34. Nickl NJ. Gastrointestinal stromal tumors: new progress, new questions. Curr Opin Gastroenterol. 2004;20(5):482-7. Joensuu H, Roberts P, Sarlomo-Rikala M, Andersson LC, Tervahartiala P, Tuveson D, et al. Effect of the tyrosine kinase inhibitor STI571 in a patient with a metastatic gastrointestinal stromal tumor. N Engl J Med. 2001;344(14):1052-6. Joensuu H. Second line therapies for the treatment of gastrointestinal stromal tumor. Curr Opin Oncol. 2007;19(4):353- 8. Rajagopalan H, Bardelli A, Lengauer C, Kinzler KW, Vogelstein B, Velculescu VE. Tumorigenesis: RAF/RAS oncogenes and mismatch-repair status. Nature. 2002;418(6901):934. Miranda C, Nucifora M, Molinari M, Conca E, Anania MC, Bordoni A, et al. KRAS and BRAF mutations predict primary resistance to imatinib in gastrointestinal stromal tumors. Clin Cancer Res. 2012;18(6):1769-76. Miettinen M, Lasota J. Gastrointestinal stromal tumors: pathology and prognosis at different sites. Semin Diagn Pathol. 2006;23(2):70-83. Liegl-Atzwanger B, Fletcher JA, Fletcher CD. Gastrointestinal stromal tumors. Virchows Arch. 2010;456(2):111-27. Fletcher CD, Berman JJ, Corless C, Gorstein F, Lasota J, Longley BJ, et al. Diagnosis of gastrointestinal stromal tumors: a consensus approach. Hum Pathol. 2002;33(5):459-65. Fernández JA, Sánchez Canovas M, Parrilla P. Controversias en el tratamiento de los tumores del estroma gastrointestinal (GIST) primarios. Cir Esp. 2010;88:69-80. Scarpa M, Bertin M, Ruffolo C, Polese L, D’Amico DF, Angriman I. A systematic review on the clinical diagnosis of gastrointestinal stromal tumors. J Surg Oncol. 2008;98(5):384-92. van de Rijn M, Hendrickson MR, Rouse RV. CD34 expression by gastrointestinal tract stromal tumors. Human Pathol. 1994:25(8):766-71. Downs-Kelly E, Rubi BP. Gastrointestinal stromal tumors: molecular mechanisms and targeted therapies. Patholog Res Int. 2011;4:1-7. Daniels M, Lurkin I, Pauli R, Erbstösser E, Hildebrandt U, Hellwig K, et al. Spectrum of KIT/PDGFRA/BRAF mutations and Phosphatidylinositol-3-Kinase pathway gene alterations in gastrointestinal stromal tumors (GIST). Cancer Lett. 2011;312(1):43-54. Longley BJ, Reguera MJ, Ma Y. Classes of c-KIT activating mutations: proposed mechanisms of action and implications for disease classification and therapy. Leuk Res. 2001;25(7):571-6. Medeiros F, Corless CL, Duensing A, Hornick JL, Oliveira AM, Heinrich MC, et al. KIT-negative gastrointestinal stromal tumors. Am J Surg Pathol. 2004;28(7):889-94. Agaram NP, Wong GC, Guo T, Maki RG, Singer S, Dematteo RP, et al. Novel V600E BRAF mutations in imatinib-naive and imatinib-resistant gastrointestinal stromal tumors. Genes Chromosomes Cancer. 2008;47(10):853-9. Davies H, Bignell GR, Cox C, Stephens P, Edkins S, Clegg S, et al. Mutations of the BRAF gene in human cancer. Nature. 2002;417(6892):949-54. Brose MS, Volpe P, Feldman M, Kumar M, Rishi I, Gerrero R, et al. BRAF and RAS mutations in human lung cancer and melanoma. Cancer Res. 2002;62(23):6997-7000. Tiacci E, Trifonov V, Schiavoni G, Holmes A, Kern W, Martelli MP, et al. BRAF mutations in hairy-cell leukemia. N Engl J Med. 2011;364(24):2305-15. Michaloglou C, Vredeveld LC, Mooi WJ, Peeper DS. BRAF (E600) in benign and malignant human tumours. Oncogene. 2008;27(7):877-95. Curtin JA, Fridlyand J, Kageshita T, Patel HN, Busam KJ, Kutzner H, et al. Distinct sets of genetic alterations in melanoma. N Engl J Med. 2005;353(20):2135-47. Antonescu CR, Besmer P, Guo T, Arkun K, Hom G, Koryotowski B, et al. Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation. Clin Cancer Res. 2005;11(11):4182-90. Solit DB, Garraway LA, Pratilas CA, Sawai A, Getz G, Basso A, et al. BRAF mutation predicts sensitivity to MEK inhibition. Nature. 2006;439(7074):358-62. Rossi F, Ehlers I, Agosti V, Socci ND, Viale A, Sommer G, et al. Oncogenic Kit signaling and therapeutic intervention in a mouse model of gastrointestinal stromal tumor. Proc Natl Acad Sci USA. 2006;103(34):12843-8. Chapman PB, Hauschild A, Robert C, Haanen JB, Ascierto P, Larkin J, et al. Improved survival with vemurafenib in melanoma with BRAF V600E mutation. N Engl J Med. 2011;364(26):2507-16. Nimeiri HS, Maki RG, Kasza K, D’Adamo D, Chow W, et al. Activity of sorafenib (SOR) in patients (pts) with imatinib (IM) and sunitinib (SU)-resistant (RES) gastrointestinal tumors (GIST): A phase II trial of the University of Chicago Phase II Consortium. J Clin Oncol. 2008;26:abstr 10502. Kindler HL, Campbell NP, Wroblewski K, Maki RG, D’Adamo DR, Chow WA, et al. Sorafenib in patients with imatinib and sunitinib resistant gastrointestinal stromal tumors (GIST): Final results of a University of Chicago Phase II Consortium trial. J Clin Oncol. 2011;29:abstr 10009. Cauchi C, Somaiah N, Engstrom P, Litwin S, López M, Lee L, et al. Evaluation of nilotinib (N) in advanced GIST previously treated with imatinibmesylate (IM) and sunitinib (S). J Clin Oncol. 2010;28:15s, abstr 10090. Guo T, Agaram NP, Wong GC, Hom G, D’Adamo D, Maki RG, et al. Sorafenib inhibits the imatinib-resistant KITT670I gatekeeper mutation in gastrointestinal stromal tumor. Clin Cancer Res. 2007;13(16):4874-81. Italiano A, Cioffi A, Maki RG, Schöffski P, Rutkowski P, Le Cesne A, et al. Patterns of care, prognosis, and survival of patients with metastatic gastrointestinal stromal tumors (GIST) refractory to first-line imatinib and second-line sunitinib. J Clin Oncol. 2011;29:abstr 10044. Agaram NP, Laquaglia MP, Ustun B, Guo T, Wong GC, Socci ND, et al. Molecular characterization of pediatric gastrointestinal stromal tumors. Clin Cancer Res. 2008;14(10):3204-15. Pierotti MA, Tamborini E, Negri T, Pricl S, Pilotti S. Targeted therapy in GIST: in silico modeling for prediction of resistance. Nat Rev Clin Oncol. 2011;8(3):161-70. |
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