Special Issue "Tobacco-related Cancers"

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A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (20 December 2013)

Special Issue Editor

Guest Editor
Prof. Dr. Gary Stoner

Department of Medicine, Medical College of Wisconsin, 8701 Watertown Plank Road, TBRC Rm C4815 between Watertown Plank Road and Milwaukee, Milwaukee, WI 53226, USA
Website | E-Mail
Interests: lung; oral; esophagus and colon cancer; tobacco-specific nitrosamines; polycyclic aromatic hydrocarbons; DNA adducts; chemoprevention; isothiocyanates; polyphenols; anthocyanins; NSAIDs

Special Issue Information

Dear Colleagues,

Tobacco use is associated with the development of cancers in multiple organ sites in humans. This volume will present the latest information on the epidemiology of tobacco-related cancers, the mechanisms by which tobacco carcinogens and co-carcinogens induce cancer in these organ sites, and strategies for the prevention of tobacco-related cancers. Particular emphasis will be placed on new developments in the epidemiology, carcinogenesis and prevention of tobacco-related cancers in the last 5 – 10 years. Authors are encouraged to submit original manuscripts and review articles on topics of relevance to the role of tobacco in the epidemiology, etiology and prevention of tobacco –related cancers.

Prof. Dr. Gary Stoner
Guest Editor

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 800 CHF (Swiss Francs).

Keywords

  • epidemiology
  • chemical carcinogens
  • tobacco-specific nitrosamines
  • polycyclic hydrocarbons
  • aromatic amines
  • aldehydes
  • co-carcinogens
  • asbestos
  • alcohol
  • viruses
  • chemoprevention
  • isothiocyanates
  • budesonide
  • non-steroidal anti-inflammatory drugs
  • polyphenols
  • other naturally-occurring
  • synthetic agents

Published Papers (5 papers)

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Research

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Open AccessArticle Tobacco Exposure and Complications in Conservative Laryngeal Surgery
Cancers 2014, 6(3), 1727-1735; doi:10.3390/cancers6031727
Received: 18 March 2014 / Revised: 25 July 2014 / Accepted: 11 August 2014 / Published: 19 August 2014
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Abstract
Smoking is an important risk factor in the development of head and neck cancer. However, little is known about its effects on postoperative complications in head and neck cancer surgery. We performed a retrospective analysis on 535 consecutive laryngeal cancer patients submitted to
[...] Read more.
Smoking is an important risk factor in the development of head and neck cancer. However, little is known about its effects on postoperative complications in head and neck cancer surgery. We performed a retrospective analysis on 535 consecutive laryngeal cancer patients submitted to open partial laryngectomy at the Otolaryngology-Head and Neck Surgery Department of Florence University to evaluate a possible correlation between smoking and surgical complications. Patients were grouped in non smokers and smokers and evaluated for airway, swallowing, local and fistula complications by multivariate analysis: 507 (95%) patients were smokers, 69% presented supraglottic, 30% glottic and 1% transglottic cancer. The most common operation was supraglottic horizontal laryngectomy in 58%, followed by supracricoid partial laryngectomy in 27% and frontolateral hemilaryngectomy in 15% of cases. The incidence of overall complications was 30%, airway complications representing the most frequent (14%), followed by swallowing (7%), local (6%) and fistula complications (3%). Smokers developed more local complications (p = 0.05, univariate, p = 0.04, multivariate analysis) and pharyngocutaneous fistula (p = 0.01, univariate, p = 0.03, multivariate analysis). Full article
(This article belongs to the Special Issue Tobacco-related Cancers)
Open AccessArticle The Role of Neutrophil Myeloperoxidase in Models of Lung Tumor Development
Cancers 2014, 6(2), 1111-1127; doi:10.3390/cancers6021111
Received: 4 March 2014 / Revised: 11 April 2014 / Accepted: 6 May 2014 / Published: 9 May 2014
Cited by 16 | PDF Full-text (1057 KB) | HTML Full-text | XML Full-text
Abstract
Chronic inflammation plays a key tumor-promoting role in lung cancer. Our previous studies in mice demonstrated that neutrophils are critical mediators of tumor promotion in methylcholanthrene (MCA)-initiated, butylated hydroxytoluene (BHT)-promoted lung carcinogenesis. In the present study we investigated the role of neutrophil myeloperoxidase
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Chronic inflammation plays a key tumor-promoting role in lung cancer. Our previous studies in mice demonstrated that neutrophils are critical mediators of tumor promotion in methylcholanthrene (MCA)-initiated, butylated hydroxytoluene (BHT)-promoted lung carcinogenesis. In the present study we investigated the role of neutrophil myeloperoxidase (MPO) activity in this inflammation promoted model. Increased levels of MPO protein and activity were present in the lungs of mice administered BHT. Treatment of mice with N-acetyl lysyltyrosylcysteine amide (KYC), a novel tripeptide inhibitor of MPO, during the inflammatory stage reduced tumor burden. In a separate tumor model, KYC treatment of a Lewis Lung Carcinoma (LLC) tumor graft in mice had no effect on tumor growth, however, mice genetically deficient in MPO had significantly reduced LLC tumor growth. Our observations suggest that MPO catalytic activity is critical during the early stages of tumor development. However, during the later stages of tumor progression, MPO expression independent of catalytic activity appears to be required. Our studies advocate for the use of MPO inhibitors in a lung cancer prevention setting. Full article
(This article belongs to the Special Issue Tobacco-related Cancers)

Review

Jump to: Research

Open AccessReview Updates and Controversies in the Rapidly Evolving Field of Lung Cancer Screening, Early Detection, and Chemoprevention
Cancers 2014, 6(2), 1157-1179; doi:10.3390/cancers6021157
Received: 13 February 2014 / Revised: 25 April 2014 / Accepted: 8 May 2014 / Published: 16 May 2014
Cited by 8 | PDF Full-text (654 KB) | HTML Full-text | XML Full-text
Abstract
Lung cancer remains the leading cause of cancer-related death in the United States. Cigarette smoking is a well-recognized risk factor for lung cancer, and a sustained elevation of lung cancer risk persists even after smoking cessation. Despite identifiable risk factors, there has been
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Lung cancer remains the leading cause of cancer-related death in the United States. Cigarette smoking is a well-recognized risk factor for lung cancer, and a sustained elevation of lung cancer risk persists even after smoking cessation. Despite identifiable risk factors, there has been minimal improvement in mortality for patients with lung cancer primarily stemming from diagnosis at a late stage when there are few effective therapeutic options. Early detection of lung cancer and effective screening of high-risk individuals may help improve lung cancer mortality. While low dose computerized tomography (LDCT) screening of high risk smokers has been shown to reduce lung cancer mortality, the high rates of false positives and potential for over-diagnosis have raised questions on how to best implement lung cancer screening. The rapidly evolving field of lung cancer screening and early-detection biomarkers may ultimately improve the ability to diagnose lung cancer in its early stages, identify smokers at highest-risk for this disease, and target chemoprevention strategies. This review aims to provide an overview of the opportunities and challenges related to lung cancer screening, the field of biomarker development for early lung cancer detection, and the future of lung cancer chemoprevention. Full article
(This article belongs to the Special Issue Tobacco-related Cancers)
Open AccessReview Mechanisms of Cancer Induction by Tobacco-Specific NNK and NNN
Cancers 2014, 6(2), 1138-1156; doi:10.3390/cancers6021138
Received: 6 February 2014 / Revised: 13 April 2014 / Accepted: 28 April 2014 / Published: 14 May 2014
Cited by 15 | PDF Full-text (767 KB) | HTML Full-text | XML Full-text
Abstract
Tobacco use is a major public health problem worldwide. Tobacco-related cancers cause millions of deaths annually. Although several tobacco agents play a role in the development of tumors, the potent effects of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) are unique. Metabolically activated NNK and
[...] Read more.
Tobacco use is a major public health problem worldwide. Tobacco-related cancers cause millions of deaths annually. Although several tobacco agents play a role in the development of tumors, the potent effects of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) are unique. Metabolically activated NNK and NNN induce deleterious mutations in oncogenes and tumor suppression genes by forming DNA adducts, which could be considered as tumor initiation. Meanwhile, the binding of NNK and NNN to the nicotinic acetylcholine receptor promotes tumor growth by enhancing and deregulating cell proliferation, survival, migration, and invasion, thereby creating a microenvironment for tumor growth. These two unique aspects of NNK and NNN synergistically induce cancers in tobacco-exposed individuals. This review will discuss various types of tobacco products and tobacco-related cancers, as well as the molecular mechanisms by which nitrosamines, such as NNK and NNN, induce cancer. Full article
(This article belongs to the Special Issue Tobacco-related Cancers)
Open AccessReview Impact of Neuro-Psychological Factors on Smoking-Associated Lung Cancer
Cancers 2014, 6(1), 580-594; doi:10.3390/cancers6010580
Received: 25 December 2013 / Revised: 14 February 2014 / Accepted: 21 February 2014 / Published: 13 March 2014
Cited by 4 | PDF Full-text (441 KB) | HTML Full-text | XML Full-text
Abstract
Smoking has been extensively documented as a risk factor for all histological types of lung cancer and tobacco-specific nitrosamines and polycyclic aromatic hydrocarbons reproducibly cause lung cancer in laboratory rodents. However, the most common lung cancer, non-small cell lung cancer (NSCLC), frequently develops
[...] Read more.
Smoking has been extensively documented as a risk factor for all histological types of lung cancer and tobacco-specific nitrosamines and polycyclic aromatic hydrocarbons reproducibly cause lung cancer in laboratory rodents. However, the most common lung cancer, non-small cell lung cancer (NSCLC), frequently develops in never smokers and is particularly common in women and African Americans, suggesting that factors unrelated to smoking significantly impact this cancer. Recent experimental investigations in vitro and in animal models have shown that chronic psychological stress and the associated hyperactive signaling of stress neurotransmitters via β-adrenergic receptors significantly promote the growth and metastatic potential of NSCLC. These responses were caused by modulation in the expression and sensitization state of nicotinic acetylcholine receptors (nAChRs) that regulate the production of stress neurotransmitters and the inhibitory neurotransmitter γ-aminobutyric acid (GABA). Similar changes in nAChR-mediated neurotransmitter production were identified as the cause of NSCLC stimulation in vitro and in xenograft models by chronic nicotine. Collectively, these data suggest that hyperactivity of the sympathetic branch of the autonomic nervous system caused by chronic psychological stress or chronic exposure to nicotinic agonists in cigarette smoke significantly contribute to the development and progression of NSCLC. A recent clinical study that reported improved survival outcomes with the incidental use of β-blockers among patients with NSCLC supports this interpretation. Full article
(This article belongs to the Special Issue Tobacco-related Cancers)
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