Prevention of Carcinogen-Induced Oral Cancer by Sulforaphane
Bauman JE, Zang Y, Sen M, Li C, Wang L, Egner PA, Fahey JW, Normolle DP, Grandis JR, Kensler TW, Johnson DE
Cancer prevention research (Philadelphia, Pa.) · 85 citas
Cómo se estudió
- Diseño
- Ensayo clínico controlado (indexado por PubMed)
- Estudiado en
- Personas, más trabajo en animales o laboratorio
- Resultado principal
- Eventos clínicos como enfermedad o muerte
- Consumo medido con
- Biomarcadores de consumo
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Institutes of Health
- Universidad u hospital
- Cancer Institute, University of Pittsburgh
- Gobierno
- National Cancer Institute
- Gobierno
- NIH
- Gobierno
- NCI NIH HHS
- Organización sin fines de lucro
- Lewis B. and Dorothy Cullman Foundation and also used UPCI
- Subvenciones
- National Cancer Institute (P50 CA097190); National Cancer Institute (R35 CA197222); National Cancer Institute (R01 CA190610); National Cancer Institute (P30 CA 047904); National Institutes of Health (P30CA47904); National Institutes of Health (P50-CA097190); National Institutes of Health (R01CA190610 and R35CA197222)
Según 6 financiadores declarados.
Publicación
- Publicado
- 2016-06-23 · Cancer Prev Res (Phila) · vol. 9 · número 7 · págs. 547–557
- Editorial
- American Association for Cancer Research
- Citado
- 120 citas · más que el 96% de estudios similares · 4.9× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 57 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · IL-33, ST2, and ILC Pathways · Bioactive Compounds and Antitumor Agents
- Palabras clave
- Sulforaphane, Carcinogen, Glucoraphanin, Cruciferous vegetables, Pharmacology, Cancer research, Cancer, Chemistry, Head and neck squamous-cell carcinoma, Medicine, Internal medicine, Biology, Head and neck cancer, Biochemistry, Glucosinolate, Brassica
- MeSH
- cell line, animals, mice, inbred c57bl, humans, mice, brassica, mouth neoplasms, isothiocyanates, sulfoxides, plant extracts, antineoplastic agents, phytogenic, carcinogens, pilot projects, cross-over studies, nf-e2-related factor 2
11 autores
- Julie E. Bauman🇺🇸University of Pittsburgh; UPMC Hillman Cancer Center
- Yan Zang🇺🇸University of Pittsburgh
- Malabika Sen🇺🇸University of Pittsburgh
- Changyou Li🇺🇸University of Pittsburgh
- Lin Wang🇺🇸University of Pittsburgh
- Patricia A. Egner🇺🇸Johns Hopkins University
- Jed W. Fahey🇺🇸Johns Hopkins University; Johns Hopkins Medicine
- Daniel Paul Normolle🇺🇸University of Pittsburgh; UPMC Hillman Cancer Center
- Jennifer Rubin Grandis🇺🇸University of California, San Francisco
- Thomas W. Kensler🇺🇸Johns Hopkins University; University of Pittsburgh; Johns Hopkins Medicine; UPMC Hillman Cancer Center
- Daniel E. Johnson🇺🇸 · autor de correspondenciaUniversity of Pittsburgh
Resumen
El texto original del estudio, en el idioma en que se publicó.
Chronic exposure to carcinogens represents the major risk factor for head and neck squamous cell carcinoma (HNSCC). Beverages derived from broccoli sprout extracts (BSE) that are rich in glucoraphanin and its bioactive metabolite sulforaphane promote detoxication of airborne pollutants in humans. Herein, we investigated the potential chemopreventive activity of sulforaphane using in vitro models of normal and malignant mucosal epithelial cells and an in vivo model of murine oral cancer resulting from the carcinogen 4-nitroquinoline-1-oxide (4NQO). Sulforaphane treatment of Het-1A, a normal mucosal epithelial cell line, and 4 HNSCC cell lines led to dose- and time-dependent induction of NRF2 and the NRF2 target genes NQO1 and GCLC, known mediators of carcinogen detoxication. Sulforaphane also promoted NRF2-independent dephosphorylation/inactivation of pSTAT3, a key oncogenic factor in HNSCC. Compared with vehicle, sulforaphane significantly reduced the incidence and size of 4NQO-induced tongue tumors in mice. A pilot clinical trial in 10 healthy volunteers evaluated the bioavailability and pharmacodynamic activity of three different BSE regimens, based upon urinary sulforaphane metabolites and NQO1 transcripts in buccal scrapings, respectively. Ingestion of sulforaphane-rich BSE demonstrated the greatest, most consistent bioavailability. Mucosal bioactivity, defined as 2-fold or greater upregulation of NQO1 mRNA, was observed in 6 of 9 evaluable participants ingesting glucoraphanin-rich BSE; 3 of 6 ingesting sulforaphane-rich BSE; and 3 of 9 after topical-only exposure to sulforaphane-rich BSE. Together, our findings demonstrate preclinical chemopreventive activity of sulforaphane against carcinogen-induced oral cancer, and support further mechanistic and clinical investigation of sulforaphane as a chemopreventive agent against tobacco-related HNSCC. Cancer Prev Res; 9(7); 547-57. ©2016 AACR.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial.
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