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The Relative Odds for Adeno and Squamous Cell Carcinoma In Women Across Different Categories of Lung FunctionThe cells contain odds ratio (OR) and the 95% confidence intervals
Source publication
Reduced forced expiratory volume in one second (FEV1) has been linked to non small cell lung cancer (NSCLC). However, it is unclear whether all or only certain histological subtypes of NSCLC are associated with reduced FEV1. Moreover, there is little information on whether gender modifies this relationship. Using a large tissue registry, we sought...
Context in source publication
Context 1
... patients had slightly lower FEV 1 , FVC and arterial oxygen tension (P a O 2 ) than did female patients (Table 1). Table 2 summarizes the unadjusted and adjusted odds ratios (controlling for covariates which included age, BMI and cigarette smoking) for adenocarcinoma and squa- mous cell carcinoma in women across quartiles of FEV 1 . ...
Citations
... The percentage predicted FEV 1 has been classically related to the disease severity. The lower the FEV 1 , the poorer the overall survival [8,9,10] but also the higher the risk for cardiovascular events [11,12] and for lung malignancy development [13,14,15]. Similarly, spirometric parameters, namely FEV 1 , forced vital capacity (FVC) and FEV 1 /FVC ratio are important population-level predictors (but not necessarily accurate) of poor COPD outcome. ...
Introduction:
In 2011, the GOLD recommendations for the treatment of Chronic Obstructive Pulmonary Disease (COPD) introduced new clinical elements to classify the severity of the disease and to guide pharmacological choice. For the first time in the GOLD documents, treatment decision was no longer guided only by pulmonary function, but by a more complex combination of pulmonary function and clinical aspects. The recent versions of the GOLD recommendations introduce new aspects for the clinicians and pose new question for the management of the disease. In addition, inflammatory biomarkers and blood eosinophil levels, have been considered to guide treatment selection.
Area covered:
The evolution of disease management proposed by the GOLD document opens several areas of debate. A series of roundtable discussions among respiratory physicians took place in Italy to address key clinical questions. Particularly, the role of lung function and the use of biomarkers, the adherence to international guidelines and the possibility to personalize the pharmacological approach in COPD patients have been discussed, summarized and analyzed.
Expert opinion:
The authors believe that the development of a precision medicine approach tailoring the specific treatment for each patient is the goal of COPD management and may be achieved by considering the phenotypic classification of COPD patients.
... Prostaglandin E2 release, then activated the EP2 and EP4 prostanoid receptor signaling, which induces cell proliferation, survival, and angiogenesis (Malhotra, 2006). Chemical evaluation of betel quid with tobacco (BQT) at the pH of oral cavity (7.4) and stomachic (2.1) found that the first treatment did not rise NNN levels, but at stomach pH the amount of this compound significantly increased (Luch, 2005). ...
Cancer is the second cause of death worldwide. According to the WHO, 14 million new cancers and 8.2 million of cancer-related deaths occurred in 2012, and it is expected that the number of new cases will rise by about 70% over the next 20 years. Lung cancer alone was responsible for approximately 1,590,000 deaths in 2012, being the leading cause of cancer death worldwide. Overall, it is estimated that exposure to tobacco accounts for about 21% of cancer mortality worldwide. A stron causative relationship between tobacco consumption and several types of cancers have been established, including oral, oropharyngeal, digestive and bladder, among others, but the most relevant association occurs between lung cancer and smoking. Regarding lung cancer, the principal carcinogens in cigarette smoke are the tobacco specific nitrosamines and polycylic aromatic hydrocarbons, which alter the smoker's DNA, causing mutations that stimulate cancer development. Carcinogenesis begins years before symptoms or clinical diagnosis, when a malignant cell losses its protective cell-cycle control mechanisms and begins uncontrolled replication. The clinical presentation and the different diagnostic methods varies depending on the distinctive histological type of lung cancer. In this chapter we will review the epidemiology of the most frequent tobacco-related cancers, some clinical aspects, and how carcinogens from tobacco lead to the development of cancer.
... Both in N. rustica tobacco varieties and N. tabacum green leaves have important levels of NNK and NNN, but green tobacco have near an order of magnitude less amount of these substances than sun-dried tobacco (Dipple, 1984). In gastric cancer, NNK promotes the activity of Cyclooxygenase 2 with a subsequent increase of Prostaglandin E2 release, then activated the EP2 and EP4 prostanoid receptor signaling, which induces cell proliferation, survival, and angiogenesis (Malhotra, 2006). Chemical evaluation of betel quid with tobacco (BQT) at the pH of oral cavity (7.4) and stomachic (2.1) found that the first treatment did not rise NNN levels, but at stomach pH the amount of this compound significantly increased (Luch, 2005). ...
Cigarette smoke exposure is strongly related to premature mortality and morbidity worldwide, being a risk factor of numerous pathologies. In fact, smoking is widely recognized as one of the most relevant risk factors of several inflammatory conditions and non-communicable diseases, including different lung cancers and other malignant pathologies, as well as coronary heart disease, stroke, and chronic obstructive pulmonary disease. Cigarette smoke consists in a complex matrix of thousands of different chemical compounds and substances, which by different mechanisms generate damage in biochemical * Camilo Sotomayor, Ignacio Cortés, Matías Libuy et al. 2 pathways and biological molecules both directly and indirectly. Most of these substances have carcinogenic, oxidative and pro-inflammatory effects as well as a combination of them. Specifically, reactive oxygen species (ROS) and reactive nitrogen species (RNS), reactive carbonyl compounds, and other molecules may generate oxidative injury in almost all kinds of biomolecules, compromising their function and/or structure. As a result, cigarette smoking generates oxidative stress, chronic inflammation and structural and functional alterations of the cell, leading to unspecific cell damage such as malignant cell proliferation, apoptosis and angiogenesis. These mechanisms, among others, are the cellular basis of all smoking related diseases.
... Smokers with COPD have a higher risk of developing a specific histological subtype of non-small-cell lung cancer, squamous cell carcinoma. [25][26][27][28] Consistently, subjects with squamous cell carcinoma in this study had larger quantity of smoking exposure and more severe COPD than those with adenocarcinoma (Table 3). ...
Background and objective:
Chronic obstructive pulmonary disease (COPD) is a risk factor and important coexisting disease for lung cancer; however, the current status of management of COPD in lung cancer patients is not fully described. This study addressed this issue in a general teaching hospital in China.
Methods:
Medical records of hospitalized lung cancer patients in Zhongshan Hospital, Fudan University, between January 2006 and December 2010 were reviewed. The definition of COPD was according to the spirometric criteria of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) document. The diagnostic rate (COPD recorded as a discharge diagnosis/spirometry-defined percentage) and conformity to GOLD treatment guidelines were investigated. The factors influencing diagnosis were analysed.
Results:
During the study period, the prevalence of spirometry-defined COPD in hospitalized lung cancer patients was 21.6% (705/3263). The overall diagnostic rate of COPD was 7.1%, and the treatment conformity for stable and acute exacerbation of COPD was 27.1% and 46.8%, respectively. Respiratory physicians had a higher diagnostic rate than non-respiratory doctors (34.8% vs 2.9%, P < 0.001) and a better treatment conformity for acute exacerbation of COPD (63.6% vs 37.5%, P = 0.048). Patients with COPD as a discharge diagnosis had more chance to receive guideline-consistent treatment. The diagnostic rate of COPD was higher among patients with a history of smoking, respiratory diseases or symptoms.
Conclusions:
COPD is substantially underdiagnosed and undertreated in a hospitalized lung cancer population. History of smoking, respiratory diseases and symptoms promotes diagnosis. Education of COPD knowledge among patients and doctors is urgently required in this special population.
... Anywhere, here the difficulty is finding reliable biomarkers to detect the real process and not false starts; sensitivity and specificity are two essential features and the key to both is finding better biomarkers (genes, proteins and cellular metabolites) that can be measured and associated with the development of cancer. Phosphatidylinositol-3kinase (PI3K) signalling pathway might be used for chemoprevention and early trials have shown that the administration of a drug that decreases PI3K activity causes regression of abnormal lesions in the airways of high-risk smokers [116]. Other proposals include alteration in gene expression, levels of death-associated-protein kinase or DAR kinase (enzyme implicated in apoptosis), antibodies to mutant p53 (as signal of damage of cell tumour suppressor system), changes in cancer-related genes or markers of inflammation [115]. ...
Inflammatory bowel disease (IBD) is a chronic inflammatory disorder caused by deregulated immune responses in a genetically predisposed individual. This is a complex process mediated by cytokines, chemokines, adhesion molecules, cytoplasm nuclear receptors, among others. Recent data support a participation of the endoplasmic reticulum (ER) stress and mitochondrial dysfunctions in IBD. Moreover, now it is evident that chronic degenerative pathologies, including IBD, share comparable disease mechanisms at the cellular level with alteration of the autophagy mechanisms. Mounting evidence suggests that the risk of developing colorectal cancer (CRC) is dramatically increased in patients with chronic inflammatory disease. Chronic inflammation in IBD exposes these patients to a number of signals known to have tumorigenic effects including nuclear factor kappa B (NF-κB) activation, proinflammatory cytokines and prostaglandins release and reactive oxygen species (ROS) production. Chemoprevention consists in the use of drugs, vitamins, or nutritional supplements to reduce the risk of developing, or having a recurrence of cancer. Numerous in vitro and animal studies have established the potential colon cancer chemopreventive properties of phytochemicals derived from both plants (curcumin, resveratrol, epigallocatechin gallate, quercetin or genistein) and substances from marine environment, including microalgae species and their products. This review summarizes the mechanisms by which these naturally occurring compounds may mediate chemopreventive effects on cancer. These actions include induction of cell cycle arrest and apoptosis, inhibition of cell proliferation, stimulation of antimetastatic and antiangiogenic responses and increased antioxidant and anti-inflammatory activity.
... Among lifetime non-smokers, lung cancer is much more common in women than in men worldwide (Siegfried, 2001) and odds ratios for different histological types of lung cancer are consistently higher for women than for men with equivalent tobacco exposures (Zang and Wynder, 1996). In addition, adenocarcinoma of the lung is more common in women than in men regardless of smoking status (Ben-Zaken Cohen et al., 2007;Malhotra et al., 2006;Patel, 2005;Patel et al., 2004;Siegfried, 2001). Furthermore, DNA repair capacity has been shown to be 10%-15% lower in female lung cancer patients than in their male counterparts (Wei et al., 2000) and a previous study found a higher frequency of a specific mutation (i.e. ...
... In a study on patients undergoing lung resection for non-small cell lung cancer (NSCLC), impaired FEV1% was associated with significant increase in risk for SCC subtype [17]. In another study, Malhotra et al. also reported that impaired FEV1 was associated with greater chance of SCC [30]. We observed that ILF was associated with a 3 to 7 fold increased risk of identifying SM and SD, precursors of SCC. ...
Background: Chronic obstructive pulmonary disease (COPD) and the presence of endobronchial premalignant lesions (EPL) are individual risk factors for lung cancer (LC). However, effect of impaired lung function (ILF) on the natural history of EPL has not been explored. Patients and Methods: This study included 217 high-risk participants from a hospital-based LC surveillance cohort who underwent pulmonary function testing followed by bronchoscopy with en-dobronchial biopsies. Baseline histopathology diagnoses included 91 cases (41.9%) with squamous metaplasia (SM), 25 (11.5%) with squamous dysplasia (SD), 1 (0.5%) with in-situ carcinoma and 5 (2.3%) with invasive LC. Follow-up biopsies were obtained for 69 patients, and 16 (23.2%) patients demonstrated progression to a higher grade lesion. Re-gression models were used to evaluate the relationship between ILF and EPL. All the models were adjusted for age, gender and tobacco smoking. Results: Patients with FEV 1 % of <50% had 4.5 times greater risk of being diagnosed with an EPL [95% confidence interval: 1.93 -10.80] and 8-fold greater risk of SD, compared to patients with FEV1% ≥ 80. COPD was associated with 2.7 and 4.8 times greater risk of SM and SD, respectively. The mean time to progression to a higher-grade lesion was shorter in COPD patients compared to patients without COPD (27 versus 50 months, p = 0.02). Conclusion: Our results indicate that ILF may be a predictor of prevalence and progression of EPLs among pa-tients at high risk of LC. Therefore, spirometry can be a complementary pre-screening tool for identifying patients with EPL who need more intense LC surveillance.
... Among lifetime nonsmokers, worldwide, lung cancer is much more common in women than in men (2), and odds ratios for different histological types of lung cancer are consistently higher for women than for men with equivalent tobacco exposure (3). In addition, adenocarcinoma of the lung is more common in women than in men regardless of smoking status (2,(4)(5)(6)(7). Interestingly, DNA repair capacity has been shown to be 10-15% lower in female lung cancer patients than in their male counterparts (8), and a previous study has found a higher frequency of a specific mutation (G to T transversion) in the p53 gene in lung tumours of women, than in those of men (9). ...
Accumulating evidence suggests that gender affects the incidence and severity of several pulmonary diseases. Previous studies on mice have shown gender differences in susceptibility to naphthalene-induced lung injury, where Clara cell damage was found to occur earlier and to be more extensive in females than in males. However, very little is known about whether there are any gender differences in subsequent lung repair responses. The aim of this study was to investigate whether gender plays an important role in pulmonary regenerative response to naphthalene-induced Clara cell ablation.
Adult male and female mice were injected with a low, medium, or high dose of naphthalene, and lung tissue regeneration was examined by immunohistochemical staining for cell proliferation marker (Ki-67) and mitosis marker (phosphohistone-3).
Histopathological analysis showed that naphthalene-induced Clara cell necrosis was more prominent in the lungs of female mice as compared to male mice. Cell proliferation and mitosis in both the distal bronchiolar airway epithelium and peribronchiolar interstitium of female mice was significantly greater than that of male mice after treatment with the low and medium doses. However, after treatment with high dose of naphthalene, lung regeneration was delayed in female mice, while male mice mounted a timely regenerative response.
These findings show that there are clear gender differences in naphthalene-induced lung injury and repair.
... 8 -10 In addition, there is some evidence that this association is weaker in women compared with men. 11,12 A recent review by Ben Zaken-Cohen et al. 13 in explored gender-related differences in the development of COPD and lung cancer and in the metabolism of tobacco smoke constituents. They showed that certain cytochrome P450 enzymes, CYP1A1, CYP1A2, and CYP3A4 have increased expression in women and suggest that these differences may lead to gender-related differences in susceptibility to tobacco smoke (and presumably other smoke) toxins. ...
