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1.
Cancer Epidemiol Biomarkers Prev ; 32(11): 1552-1557, 2023 11 01.
Artículo en Inglés | MEDLINE | ID: mdl-37410096

RESUMEN

BACKGROUND: While cigarette smoking has declined among the U.S. general population, sale and use of non-cigarette alternative tobacco products (ATP; e.g., e-cigarettes, cigars) and dual use of cigarettes/ATPs are rising. Little is known about ATP use patterns in cancer survivors enrolled in clinical trials. We investigated prevalence of tobacco product use, and factors associated with past 30-day use, among patients with cancer in national trials. METHODS: Cancer survivors (N = 756) enrolled in 9 ECOG-ACRIN clinical trials (2017-2021) completed a modified Cancer Patient Tobacco Use Questionnaire (C-TUQ) which assessed baseline cigarette and ATP use since cancer diagnosis and in the past 30 days. RESULTS: Patients were on average 59 years old, 70% male, and the mean time since cancer diagnosis was 26 months. Since diagnosis, cigarettes (21%) were the most common tobacco product used, followed by smokeless tobacco use (5%), cigars (4%), and e-cigarettes (2%). In the past 30 days, 12% of patients reported smoking cigarettes, 4% cigars, 4% using smokeless tobacco, and 2% e-cigarettes. Since cancer diagnosis, 5.5% of the sample reported multiple tobacco product use, and 3.0% reported multiple product use in the past 30 days. Males (vs. females; OR 4.33; P = 0 < 0.01) and individuals not living with another person who smokes (vs. living with; OR, 8.07; P = 0 < 0.01) were more likely to use ATPs only versus cigarettes only in the past 30 days. CONCLUSIONS: Among patients with cancer, cigarettes were the most prevalent tobacco product reported. IMPACT: Regardless, ATPs and multiple tobacco product use should be routinely assessed in cancer care settings.


Asunto(s)
Supervivientes de Cáncer , Sistemas Electrónicos de Liberación de Nicotina , Neoplasias , Productos de Tabaco , Tabaco sin Humo , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Adenosina Trifosfato , Azatioprina , Neoplasias/epidemiología , Uso de Tabaco/epidemiología , Estados Unidos/epidemiología , Ensayos Clínicos como Asunto
2.
Cancer J ; 22(3): 182-9, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-27341596

RESUMEN

Colorectal cancer is commonly diagnosed throughout the world, and treatment options have greatly expanded over the last 2 decades. Targeting angiogenesis has been a major focus of study in a variety of malignancy types. Targeting angiogenesis has been achieved by several mechanisms in colorectal cancer, including use of antiangiogenic small molecule tyrosine kinase inhibitors (TKIs). There have been many attempts and failures to prove efficacy of TKIs in the treatment of colorectal cancer including sorafenib, sunitinib, vatalanib, and tivozanib. Regorafenib was the first TKI to demonstrate efficacy and is an orally active inhibitor of angiogenic (including the vascular endothelial growth factor receptors 1, 2, and 3), stromal, and oncogenic receptor tyrosine kinases. There are ongoing investigations of both regorafenib and ninetanib; however, there remains a critical need to better understand novel combinations with TKIs that could prove more efficacious than available options.


Asunto(s)
Inhibidores de la Angiogénesis/uso terapéutico , Antineoplásicos/uso terapéutico , Neoplasias Colorrectales/tratamiento farmacológico , Neoplasias Colorrectales/patología , Terapia Molecular Dirigida , Neovascularización Patológica/tratamiento farmacológico , Inhibidores de Proteínas Quinasas/uso terapéutico , Inhibidores de la Angiogénesis/farmacología , Antineoplásicos/farmacología , Ensayos Clínicos como Asunto , Neoplasias Colorrectales/metabolismo , Neoplasias Colorrectales/mortalidad , Descubrimiento de Drogas , Humanos , Estadificación de Neoplasias , Neovascularización Patológica/metabolismo , Compuestos de Fenilurea/farmacología , Compuestos de Fenilurea/uso terapéutico , Inhibidores de Proteínas Quinasas/farmacología , Piridinas/farmacología , Piridinas/uso terapéutico , Resultado del Tratamiento , Factores de Crecimiento Endotelial Vascular/antagonistas & inhibidores , Factores de Crecimiento Endotelial Vascular/genética , Factores de Crecimiento Endotelial Vascular/metabolismo
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