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1.
Ann Oncol ; 28(7): 1436-1447, 2017 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-28379322

RESUMO

In recent years, the number of approved and investigational agents that can be safely administered for the treatment of lymphoma patients for a prolonged period of time has substantially increased. Many of these novel agents are evaluated in early-phase clinical trials in patients with a wide range of malignancies, including solid tumors and lymphoma. Furthermore, with the advances in genome sequencing, new "basket" clinical trial designs have emerged that select patients based on the presence of specific genetic alterations across different types of solid tumors and lymphoma. The standard response criteria currently in use for lymphoma are the Lugano Criteria which are based on [18F]2-fluoro-2-deoxy-D-glucose positron emission tomography or bidimensional tumor measurements on computerized tomography scans. These differ from the RECIST criteria used in solid tumors, which use unidimensional measurements. The RECIL group hypothesized that single-dimension measurement could be used to assess response to therapy in lymphoma patients, producing results similar to the standard criteria. We tested this hypothesis by analyzing 47 828 imaging measurements from 2983 individual adult and pediatric lymphoma patients enrolled on 10 multicenter clinical trials and developed new lymphoma response criteria (RECIL 2017). We demonstrate that assessment of tumor burden in lymphoma clinical trials can use the sum of longest diameters of a maximum of three target lesions. Furthermore, we introduced a new provisional category of a minor response. We also clarified response assessment in patients receiving novel immune therapy and targeted agents that generate unique imaging situations.


Assuntos
Antineoplásicos/uso terapêutico , Linfoma não Hodgkin/diagnóstico por imagem , Linfoma não Hodgkin/tratamento farmacológico , Tomografia por Emissão de Pósitrons/normas , Critérios de Avaliação de Resposta em Tumores Sólidos , Tomografia Computadorizada por Raios X/normas , Antineoplásicos/efeitos adversos , Consenso , Meios de Contraste/administração & dosagem , Progressão da Doença , Intervalo Livre de Doença , Determinação de Ponto Final , Fluordesoxiglucose F18/administração & dosagem , Humanos , Linfoma não Hodgkin/mortalidade , Linfoma não Hodgkin/patologia , Estadiamento de Neoplasias , Valor Preditivo dos Testes , Fatores de Tempo , Resultado do Tratamento , Carga Tumoral
2.
Oncogene ; 28(31): 2773-83, 2009 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-19525976

RESUMO

To address the biological heterogeneity of lung cancer, we studied 199 lung adenocarcinomas by integrating genome-wide data on copy number alterations and gene expression with full annotation for major known somatic mutations in this cancer. This showed non-random patterns of copy number alterations significantly linked to EGFR and KRAS mutation status and to distinct clinical outcomes, and led to the discovery of a striking association of EGFR mutations with underexpression of DUSP4, a gene within a broad region of frequent single-copy loss on 8p. DUSP4 is involved in negative feedback control of EGFR signaling, and we provide functional validation for its role as a growth suppressor in EGFR-mutant lung adenocarcinoma. DUSP4 loss also associates with p16/CDKN2A deletion and defines a distinct clinical subset of lung cancer patients. Another novel observation is that of a reciprocal relationship between EGFR and LKB1 mutations. These results highlight the power of integrated genomics to identify candidate driver genes within recurrent broad regions of copy number alteration and to delineate distinct oncogenetic pathways in genetically complex common epithelial cancers.


Assuntos
Adenocarcinoma/genética , Fosfatases de Especificidade Dupla/genética , Receptores ErbB/genética , Perfilação da Expressão Gênica , Neoplasias Pulmonares/genética , Fosfatases da Proteína Quinase Ativada por Mitógeno/genética , Mutação , Adenocarcinoma/patologia , Linhagem Celular Tumoral , Proliferação de Células , Aberrações Cromossômicas , Análise por Conglomerados , Inibidor p16 de Quinase Dependente de Ciclina/genética , Feminino , Dosagem de Genes , Regulação Neoplásica da Expressão Gênica , Genes ras/genética , Estudo de Associação Genômica Ampla , Humanos , Hibridização in Situ Fluorescente , Estimativa de Kaplan-Meier , Neoplasias Pulmonares/patologia , Masculino , Hibridização de Ácido Nucleico , Interferência de RNA
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