Lung Cancer
Publisher:Wiley-Blackwell | Pages:480 | 2008-02-15 | ISBN: 1405151129 | PDF | 3.45 MB
Lung cancer is a major cause of cancer-related deaths in men and women. However, since the first edition of Lung Cancer was published 14 years ago, rapid progress in the biology, prevention, diagnosis, and treatment of the disease has been made.
This outstanding team from the M.D. Anderson Cancer Center takes an evidence-based approach to lung cancer management and explains these advances in depth. Comprehensive treatment guidelines are provided, the third edition of Lung Cancer explores vital issues such as:
- Lung cancer susceptibility and risk assessment
- The pathology and pathogenesis of peripheral lung adenocarcinoma including bronchioloalveolar carcinoma
- Screening for early detection
- Advances in molecular and genetic markers
- The detection and treatment of pre-neoplastic lesions and screening for lung cancer
- Novel therapies such as angiogenesis and multi-tyrosine kinase inhibitors
Lung Cancer is a concise summary of advances in lung cancer clinical research and treatment for the clinician and is an invaluable reference for respiratory physicians, medical oncologists, clinical and surgical oncologists.
Lung Cancer
Read This E book
Lung Cancer Susceptibility Genes
Joan E. Bailey-Wilson
Introduction
After heart disease, cancer is the most common cause of death and lung cancer is the most common cause of cancer death in the United States [1]. From 1950 to 1988, lung cancer experienced the largest increase in mortality rate of all the cancers and lung cancer caused an estimated 146,000 deaths in the United States in 1992 [2]. Lung cancer became the
leading cause of cancer death in men in the early 1950s and in women in 1987. Cancer of the lung has frequently been cited as an example of a malignancy that is solely determined by the environment [3,4] and the risks associated with cigarette smoking [3–7] and certain occupations, such as mining [8], asbestos exposure, shipbuilding, and petroleum refining [9–14], are well
established. Most lung cancers are attributable to cigarette smoking (e.g. [15]). Dietary studies have found reduction in risk associated with high compared to low consumption of carotene-containing fruits and vegetables (for reviews see [16–19]). Atleast one recent, very large meta-analysis [20] has found significant protective effects of increased levels of dietary β-cryptoxanthin although recent trials of beta-carotene and vitamin A supplements have not shown any significant reduction in lung cancer risk; instead they showed an increased risk of lung cancer death in the treated group [21–24]. Environmental tobacco smoke (ETS, passive smoking) has also been shown to be associated with increased risk
of lung cancer (for review see [3,4,25–27]) with a recent prospective European study estimating that between 16 and 24%of lung cancers in nonsmokers and long-term ex-smokers were attributable to ETS [28]. A recent meta-analysis of 22 studies showed that exposure to workplace ETS increased risk of lung cancer in workers by 24% and that this risk was highly correlated with duration of exposure [29]. These environmental risk factors cannot be reviewed in detail here. There is little doubt that the majority of lung cancer cases are attributable to
(i.e., would not occur in the absence of) cigarette smoking and other behavioral and environmental risk factors [2,7,25,30]. However, some investigators have long hypothesized that individuals differ in their susceptibility to these environmental insults (e.g. [31–34]). It is well known that mutations and loss of heterozygosity at genetic loci such as oncogenes and tumor suppressor genes are involved in lung carcinogenesis (see [35,36] for reviews) but most of these changes are thought to be accumulated at the somatic cell level. However, evidence has been mounting that certain allelic variants at some genetic loci may affect susceptibility to lung cancer, although these effects may be small. Furthermore, mounting epidemiologic evidence has suggested lung cancer may show familial aggregation after adjusting for cigarette smoking and other risk factors, and that differential susceptibility to lung cancer may be inherited in a Mendelian fashion. There is evidence that both lung
cancer and smoking-associated cancer in general have an inherited genetic component, but the existence of such a genetic component has not been definitely proven. This chapter will detail the evidence Lung Cancer, 3rd edition. Edited by Jack A. Roth, James D. Cox, and Waun Ki Hong.
leading cause of cancer death in men in the early 1950s and in women in 1987. Cancer of the lung has frequently been cited as an example of a malignancy that is solely determined by the environment [3,4] and the risks associated with cigarette smoking [3–7] and certain occupations, such as mining [8], asbestos exposure, shipbuilding, and petroleum refining [9–14], are well
established. Most lung cancers are attributable to cigarette smoking (e.g. [15]). Dietary studies have found reduction in risk associated with high compared to low consumption of carotene-containing fruits and vegetables (for reviews see [16–19]). Atleast one recent, very large meta-analysis [20] has found significant protective effects of increased levels of dietary β-cryptoxanthin although recent trials of beta-carotene and vitamin A supplements have not shown any significant reduction in lung cancer risk; instead they showed an increased risk of lung cancer death in the treated group [21–24]. Environmental tobacco smoke (ETS, passive smoking) has also been shown to be associated with increased risk
of lung cancer (for review see [3,4,25–27]) with a recent prospective European study estimating that between 16 and 24%of lung cancers in nonsmokers and long-term ex-smokers were attributable to ETS [28]. A recent meta-analysis of 22 studies showed that exposure to workplace ETS increased risk of lung cancer in workers by 24% and that this risk was highly correlated with duration of exposure [29]. These environmental risk factors cannot be reviewed in detail here. There is little doubt that the majority of lung cancer cases are attributable to
(i.e., would not occur in the absence of) cigarette smoking and other behavioral and environmental risk factors [2,7,25,30]. However, some investigators have long hypothesized that individuals differ in their susceptibility to these environmental insults (e.g. [31–34]). It is well known that mutations and loss of heterozygosity at genetic loci such as oncogenes and tumor suppressor genes are involved in lung carcinogenesis (see [35,36] for reviews) but most of these changes are thought to be accumulated at the somatic cell level. However, evidence has been mounting that certain allelic variants at some genetic loci may affect susceptibility to lung cancer, although these effects may be small. Furthermore, mounting epidemiologic evidence has suggested lung cancer may show familial aggregation after adjusting for cigarette smoking and other risk factors, and that differential susceptibility to lung cancer may be inherited in a Mendelian fashion. There is evidence that both lung
cancer and smoking-associated cancer in general have an inherited genetic component, but the existence of such a genetic component has not been definitely proven. This chapter will detail the evidence Lung Cancer, 3rd edition. Edited by Jack A. Roth, James D. Cox, and Waun Ki Hong.
0 comments:
Post a Comment