RESUMO
INTRODUCTION: Treatment advances in metastatic renal cell carcinoma (mRCC) have improved overall survival (OS) in mRCC patients over the last two decades. This single center retrospective analysis assesses if the purported survival benefits are also applicable in elderly mRCC patients. METHODS: 401 patients with mRCC treated at Hannover Medical School from 01/2003-05/2016 were identified and evaluated by chart review. Treatment periods were defined as 01.01.2003-31.12.2009 (P1) and 01.01.2010-31.05.2016 (P2). Age groups were defined according to WHO classes (≤ 60 years: younger, > 60-75 years: elderly and > 75 years: old). Descriptive statistics, Kaplan-Meier analysis and logistic regression were performed. RESULTS: Median OS improved from 35.1 months in P1 to 59.1 months in P2. Sub-division into the respective age groups revealed median survival of 38.1 (95%-CI: 28.6-47.6) months in younger patients, 42.9 (95%-CI: 29.5-56.3) months among elderly patients and 27.3 (95%-CI: 12.8-41.8) months among old patients. Risk reduction for death between periods was most evident among old patients (young: HR 0.71 (95%-CI: 0.45-1.13, p = 0.2); elderly: HR 0.62 (95%-CI: 0.40-0.97, p = 0.04); old: HR 0.43 (95%-CI: 0.18-1.05, p = 0.06)). Age ≥ 75 years was an independent risk factor for death in P1 but not in P2. CONCLUSION: Improved OS in the targeted treatment period was confirmed. Surprisingly elderly and old patients seem to profit the most form expansion of therapeutic armamentarium, within the TKI-dominated observation period.
Assuntos
Carcinoma de Células Renais , Neoplasias Renais , Idoso , Carcinoma de Células Renais/tratamento farmacológico , Carcinoma de Células Renais/patologia , Pré-Escolar , Intervalo Livre de Doença , Humanos , Neoplasias Renais/tratamento farmacológico , Neoplasias Renais/patologia , Pessoa de Meia-Idade , Inibidores de Proteínas Quinases/uso terapêutico , Estudos Retrospectivos , Resultado do TratamentoAssuntos
Sarcoma Histiocítico/patologia , Linfo-Histiocitose Hemofagocítica/diagnóstico , Linfoma Folicular/patologia , Antígenos CD/análise , Antígenos de Neoplasias/análise , Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Biomarcadores Tumorais , Medula Óssea/patologia , Cromossomos Humanos Par 14/genética , Cromossomos Humanos Par 14/ultraestrutura , Cromossomos Humanos Par 18/genética , Cromossomos Humanos Par 18/ultraestrutura , Ciclofosfamida/administração & dosagem , Dexametasona/administração & dosagem , Diagnóstico Diferencial , Progressão da Doença , Doxorrubicina/administração & dosagem , Etoposídeo/administração & dosagem , Feminino , Sarcoma Histiocítico/diagnóstico , Sarcoma Histiocítico/tratamento farmacológico , Sarcoma Histiocítico/genética , Humanos , Linfonodos/patologia , Linfoma Folicular/tratamento farmacológico , Linfoma Folicular/genética , Pessoa de Meia-Idade , Prednisolona/administração & dosagem , Rituximab/administração & dosagem , Translocação Genética , Vincristina/administração & dosagemRESUMO
The influence of amorphous carbon on FePt catalyst particles under chemical vapor deposition conditions typically applied for CNT growth is examined through two routes. In the first, FePt catalyst particles supported on alumina are exposed to a well-established cyclohexane thermal CVD reaction at various temperatures. At higher temperatures where self-pyrolysis leads to copious amorphous carbon and carbon tar formation, carbon nanotubes are still able to form. In the second route, an amorphous carbon film is first deposited over the catalyst particles prior to the CVD reaction. Even for reactions where further amorphous carbon is deposited due to self-pyrolysis, graphitization is still demonstrated. Our findings reveal that the presence of amorphous carbon does not prevent catalytic hydrocarbon decomposition and graphitization processes. We also show an additional catalytic reaction to be present, catalytic hydrogenation, a process in which carbon in contact with the catalyst surface reacts with H(2) to form CH(4).