ArticleCancer prevention research (Philadelphia, Pa.)2010
Early changes in pulmonary gene expression following tobacco exposure shed light on the role of estrogen metabolism in lung carcinogenesis.
Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Insight into the pulmonary molecular toxicity of heated tobacco products using human bronchial and alveolar mucosa models at air-liquid interface.Scientific reports · 2022Article
- Role of sex hormones in lung cancer.Experimental biology and medicine (Maywood, N.J.) · 2021Review
- A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer.Translational lung cancer research · 2016Review
- Pharmacological Modulation of Lung Carcinogenesis in Smokers: Preclinical and Clinical Evidence.Trends in pharmacological sciences · 2016Review
- Hormone use and risk for lung cancer: a pooled analysis from the International Lung Cancer Consortium (ILCCO).British journal of cancer · 2013Article
- Reproductive and hormonal factors and the risk of lung cancer: the EAGLE study.International journal of cancer · 2013Article
- Invited commentary: the etiology of lung cancer in men compared with women.American journal of epidemiology · 2013Article
- Estrogen and cytochrome P450 1B1 contribute to both early- and late-stage head and neck carcinogenesis.Cancer prevention research (Philadelphia, Pa.) · 2011Article
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Abstract
This perspective on Meireles et al. (beginning on p. 707 in this issue of the journal) discusses the increasing evidence for the role of female steroid hormones in lung cancer development and progression. The novel work of Meireles et al. is the first evidence for the rapid upregulation by tobacco smoke of a key cytochrome P450 gene that can metabolize estrogens such as beta-estradiol to potentially carcinogenic catechol and quinine forms, as well as the first evidence for the colocalization of beta-estradiol and estrogen receptors in murine airway epithelium. Actions of estrogens that contribute to lung carcinogenesis, especially in the presence of tobacco smoke, may involve both reactive intermediates that damage DNA and steroid hormone receptor signaling that promotes growth.
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Registered trials
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