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Frequency of Mortality Related to Lung Cancer - Research Paper Example

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From the paper "Frequency of Mortality Related to Lung Cancer", lung cancer is one of the most devastating pulmonary diseases and is considered a leading cause of death from neoplastic conditions. In many countries, lung cancer is one of the highest deaths causing disease such as in the USA…
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Frequency of Mortality Related to Lung Cancer
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Lung cancer Lung cancer is one of the most devastating pulmonary diseases and is considered as a leading cause of death from neoplastic conditions. In many countries lung cancer is one of the highest deaths causing disease such as in United States. Lung cancer is marked as the most commonly occurring cancer and the major and leading cause of death due to cancers in both the genders. Not only in United States, lung cancer is the cause of cancer-related death world-wide killing and estimated amount of 1.5 million people every year (Keshamouni et al 2009). In UK lung cancer accounts for 33,400 deaths per year from the 39,000 cases diagnosed. Those who survive have only a five-year survival rate of only 8-11% (Leary 2012). The current figures reflect the severity and grave nature of lung cancer. The incidence of lung cancer is high and the related death is also increasing. Lung cancer is divided into further various types depending on the pathological and histological criteria. The diagnosis of lung cancer can be made through proper evaluation of significant clinical manifestations, past history of patient and analysis of the risk factors and etiological factors. The causes of lung cancer are described by different scholars in terms of both genetic causes and non-genetic causes. The proceeding study includes the epidemiology, pathology, classification, causes, clinical manifestations and diagnostic and therapeutic strategies for lung cancer. The common age at which the lung cancer presents is usually during the elder years of life. In United States 70 is considered as the median age for lung cancer. The advancing age of the patients acts as a hindrance to the anti-cancer therapies as they are usually suffering from various co-morbidities and have a difficulty coping with the treatment (Keshamouni et al 2009). The incidence of lung cancer is more in males as compared to the females, however, the sex gap is not large and with the passage of time if it is not controlled it might be eliminated. Lung cancer was evident in males earlier because of the late introduction of tobacco smoking in the females however, since the last decade the incidence has increased in both males and females. During geographical variations, male incidence rates are 60-fold and female incidence rates are 30-fold (Spiro et al 2009). In United States a clear racial difference is seen when it comes to epidemiological data relevant to lung cancer. Lung cancer is more common in black men as compared to white men however, no difference in incidence rates is observed in the white women and black women (Keshamouni et al 2009). According to the United Kingdom epidemiological data collected in 2009 it was observed that the rate of lung cancer was higher in an all white ethnic group as compared to non-white ethnic groups. In white ethnic group the rate was 61.1-62.6 per 100,000 while the rates was found to be 22.4-48.6 per 100,000 in the Chinese group, 23.1-37.2 per 100,000 in an Asian group and 21.9-43.1 per 100,000 in a mixed ethnic group (Leary 2012). The geographical variation of lung cancer shows predominance in developed countries especially in North America and Europe. It is less prevalent in developing countries such as South America and Africa (Spiro et al 2009). The incidence of lung cancer and the frequency of mortality related to lung cancer have been increased from the first half of the twentieth century, as established through the epidemiological studies. In 1930s first it was noticed that lung cancer is becoming a leading cause of mortality at an alarmingly increasing frequency. Various case-control studies conducted in the 1950s established a strong link between the occurrence of lung cancer and smoking cigarettes. Although tobacco had been used for smoking purposes for hundreds of years, it was proved through epidemiological data that the occurrence of cancer of the lung has enhanced due to smoking because of the introduction of cigarettes with different properties. Cigarettes were produced at a massive rate, had a cheaper price and were easily available to the general population. It had lesser smoke yet increased addictive properties and thus, a persistent exposure of the cigarettes to the lungs occurred due to daily usage and easy availability (Keshamouni et al 2009). The incidence of smoking in the American men reached its peak during the 1980s and in women lung cancer became increasingly prevalent during the World War II when tobacco smoking was progressively more pursued. During the years 2000 to 2004 the epidemiological data in US depicted a mortality rate due to lung cancer of 73.4/100,000 in men and 41.4/100,000 in women. The lung cancer occurrence was estimated 81.2/100,000 in men and 52.3/100,000 in women (Keshamouni et al 2009). Passive smoking was also established as an important cause of lung cancer (Spiro et al 2009). Passive smoking is described as the involuntary inhalation of the smoke by the nonsmokers who are in close vicinity of the smokers. They inhale a complex form of smoke which is termed as second-hand smoke. Epidemiological data showed that non-smoker spouses married to smokers had a chance of 30% to develop lung cancer. One-quarter of the cases of lung cancer diagnosed had no history of smoking, however were passive smokers. It has been estimated that every year passive smoking is the cause of 3000 deaths due to lung cancer (Spiro et al 2009). Although passive smoking is a weaker agent as compared to active smoking, yet it is a potential risk factor for lung cancer as the passive smokers are persistently exposed to the carcinogenic effects of the tobacco. Although the major reason for the occurrence of cancer of the lung is tobacco smoking, other predominant were also highlighted. Many indoor and outdoor respiratory materials are labeled as potential risk factors for lung cancer. Radon is identified as the first occupational carcinogen in the early 20th century that led to the development of lung cancer in the underground miners. Radon is also now considered as the major cause of lung cancer in the indoor environments. Other occupational carcinogens that can lead to lung cancer include asbestos, arsenic, chromates, nickel, polycyclic aromatic hydrocarbons and chloromethyl ethers. Outdoor air pollutants like combustion gases and other combustion generated products are considered as carcinogenic and potential risk factors for lung cancer. Indoor environments contain smoking particles, radon, and asbestos and in some countries sustained exposure to fumes and fires from cooking stoves are also causes of lung cancer (Spiro et al 2009). Lung cancer is also associated with those areas which have higher economic and social deprivation. Incidence of lung cancer in men living in economically deprived areas was found to be 2.5 times higher and in women 3 times higher as compared to those who lived in social and economically established areas. Data from the 2008 studies carried in UK established that the incidence rates remained the same for lung cancer in the deprived areas of the country (Leary 2012). A poor socioeconomic status is linked with several other factors that determine the occurrence of lung cancer. Diet, tobacco smoking, poor workplace and home environments are associated with the poor socioeconomic status that leads to lung cancer. Furthermore, the diagnosis of lung cancer is also made usually at an advanced stage of the disease which makes it difficult to manage the cancer (Keshamouni et al 2009). Dietary factors are also considered as risk factors for lung cancer. Foods rich in vegetables and fruits are linked with a reduced occurrence of lung cancer. B-carotene in blood levels is associated with 30-80% lower risk for lung cancer. However, some studies showed that smokers with increased levels of B-carotene have increased chances of developing lung cancer because of the oxidative effects of the carotene owing to the fact that lungs of the smokers have an oxygen environment of high tension (Keshamouni et al 2009). Fruits and vegetables have high anti-oxidative properties which give them protective properties against lung cancer. Phytochemicals such as flavinoids and isothiocyanates have been found important in relation to lung cancer. These are found in many plants and help in reducing the risk for lung cancer. Alcohol drinking in association with smoking has been considered as a potential cause of risk for the occurrence of lung cancer (Spiro et al 2009). Despite of the fact that smoking is marked to be the major reason for cancer of the lung, only 10-15% of the smokers develop lung cancer. This points towards other factors that are associated with lung cancer. Individual susceptibility caused by genetic variations is described as the possible explanation in such cases. Genetic susceptibility causes carcinogen activation in particular individuals as compared to those who are not genetically susceptible. Studies regarding this aspect have showed that familial aggregation is an important cause of lung cancer is smokers. Any particular lung cancer gene has not been specified however certain genes that cause the genetic variation include CYP1A1 gene polymorphisms, deficiency of GSTM1 and inherited variability in the DNA repair capabilities of the body (Keshamouni et al 2009). The epigenetic changes that lead to lung cancer are now better understood due to the analysis through more advanced tools. Methylation of the DNA component cytosine which leads to the process of hypermethylation in the promoter regions is considered as an important and most frequent type of alteration in lung cancer (Spiro et al 2009). Hence, host factors such as genetic susceptibility plays an important role along with tobacco smoking and other environmental factors in the development of lung cancer. Radiation is also a potential risk factor for lung cancer. Epidemiological studies of individuals who have been exposed to high doses of radiation proved that radiation is an important etiological factor for lung cancer. Low linear energy transfer that includes X-rays and gamma rays and high linear energy transfer (LET) that includes radon and neutrons are associated with lung cancer. High LET is associated with increased risk for lung cancer. Low LET risks associated to lung cancer are difficult to characterize however, the survivors of the Japanese atomic bomb helped in understanding the effects of low LET (Spiro et al 2009). Lung cancer is classified on the basis of histological variation- Adenocarcinoma, squamous cell carcinoma, small cell carcinoma and large cell carcinoma. Adenocarcinoma and small cell carcinoma are predominant in females constituting 47% and 18% while in males the ratio is 37% 14% respectively. The other two carcinomas are more common in males as compared to females. For diagnostic and therapeutic purposes, lung cancers are broadly classified as small cell lung carcinomas and non-small cell lung carcinomas (NSCLCs). Small cell lung carcinoma (SCLC) usually metastasizes till the time of diagnosis and surgical interventions are impossible hence are best treated with chemotherapy and radiotherapy (Porth 2011). According to this classification the NSCLCs include Adenocarcinoma, squamous cell carcinomas and large cell carcinoma. This classification is primarily based on prognosis and therapeutic techniques (Keshamouni et al 2009). Carcinoma of lung is caused by a progressive of various sequential events. Various genetic accumulate which ultimately result in the alteration of the bronchial epithelium and transform it into benign bronchial epithelium. The earliest event is the inactivation of the tumor suppressor genes which are located on the 3p chromosome. The later genetic events involve p53 mutation and activation of the KRAS genes. An important aspect is the”field effect”. It has been observed that smokers who have not developed lung cancer also have certain mutations in their respiratory epithelium such as loss of chromosome 3p material. Hence, this field effect is described as the mutagenzied large areas of the respiratory epithelium after exposure to the carcinogens which serves as a fertile soil for the further carcinogenic events to occur, ultimately ending in lung cancer (Kumar et al 2007). Some molecular changes are stopped or reversed after the cessation of smoking however, certain are irreversible and cannot be changed (Keshamouni et al 2009). The histological morphology for the lung cancers differ for each variant. SCLC are characterized by small or oval cells and grow in cluster patterns. Neurose-secretory granules are found in these cells which make them capable of secreting polypeptide hormones resulting in the presence of certain neuroendocrine markers in SCLCs such as neuron-specific enolase and parathormone-like markers. SCLC is strongly associated to a history of smoking as compared to the other variants. SCLC is highly invasive ad malignant and 70% of the carcinomas show metastasis at the time of diagnosis. The NSCLCs include squamous carcinoma, large cell carcinoma and Adenocarcinoma. Squamous cell carcinoma is also associated strongly with smoking and it has a tendency to affect the bronchi and the hilar lymph nodes. It moves into the other parts of the thorax later as compared to other carcinomas. Squamous cell carcinomas are strongly associated with the development of paraneoplastic syndromes causing hypercalemia. Squamous cell carcinomas are preceded by years of squamous dysplasia and metaplasia occurring in the respiratory epithelium which later transforms into carcinoma in situ. Eventually the carcinoma reaches a symptomatic stage (Porth 2011; Kumar et al 2007). The adenocarcinoma is weakly associated with smoking and is mostly common in women and non-smokers. It originates from the alveolar tissues or the bronchial tissues of the lung. The location of adenocarcinoma is comparatively more in the peripheral regions of the lung as compared to the squamous carcinoma. They are also originated in areas of scarring caused by foreign bodies, old infarcts, granulomatous infections and wounds. The precursor of adenocarcinoma is described as atypical adenomatous hyperplasia which is characterized by cuboidal and low-columnar cells presenting with cellular atypia. The large cell carcinomas constitute of large polygonal cells and are highly anaplastic with difficult characterization. They have a poor prognosis (Porth 2011; Kumar et al 2007). All lung cancers are locally invasive and arise from the epithelium of majorly the bronchus. Beginning as small lesions they form intraluminal masses and then invade the bronchial mucosa and entering into the adjacent lung tissue. Some tumors form central necrotic areas with hemorrhagic transformation while others invade the intrathoracic structures, pleural cavity and the chest wall. Specifically small cell carcinomas produce bioactive products that produce paraneoplastic syndrome, however, other tumors also have the capability to do so. The clinical presentation of the lung cancer is characterized by three underlying mechanisms. Manifestation of the lung tissue involvement, effects of metastasis and local spread and the non-metastatic paraneoplastic syndrome that presents as endocrine, neurological and connective tissue disorders (Porth 2011). Carcinomas of lung are usually silent and progressive and produce symptoms during the later stages. Chronic cough and hemoptysis are important presenting features. Other earliest symptoms produced due to local irritation are shortness of breath, wheezing and dull intermittent chest pain. Symptoms occurring due to local spread present as hoarseness due to laryngeal nerve invasion, chest pain, dyspnea and atelactasis due to pleural effusion or pneumonitis and disrupted blood supply to head, chest and neck due to superior vena caval syndrome. When the later symptoms appear, the cancer is usually at later and advancing stages. Metastatic spread to brain presents as neurological changes, liver as hepatomegaly and bones as bone pain (Porth 2011; Kumar et al 2007). The diagnostic strategies involve majorly the radiological investigations and tissue confirmation tests for lung cancer. Chest radiography, computed tomography, ultrasonography and magnetic resonance imaging are some recommended investigations. Sputum cytology is a non-invasive method which helps in indentifying the exfoliated malignant cells. Bronchosocpy has a sensitivity of 80% and is performed as an outpatient procedure. Trans-thoracic needle aspiration is considered as the treatment of choice for the peripheral lung cancers (Leary 2012). Treatment methods include surgery chemotherapy and radiation therapy. Lobectomy, penumonectomy or segmental resection of the lesion is recommended in small NSCLCs. Radiation can be used alone or along with the other procedures or for palliation of the symptoms. Chemotherapy and radiotherapy are the treatment of choice for SCLCs. Prophylactic cranial radiotherapy is recommended to prevent brain metastasis in SCLCs (Porth 2011). Better therapeutic strategies are under process to improve the prognosis of the lung cancer patients. Lung cancer is one of the commonest causes of cancer related deaths and the frequency of its incidence is growing with progressing time. Epidemiological data and carious clinical studies reflect the geographical pattern, gender variations, median age and associations with race and ethnicity. Furthermore, the risk factors and etiological factors of lung cancer have been described through various researches and epidemiological data. Smoking has been described as the major risk factor. On the basis of its histological types, lung cancers have different therapeutic interventions and present different prognostic picture. However, with modern technologies, early diagnosis and improved scientific research the prognosis and treatment options for lung cancer can be improved. Works Cited Keshamouni, Venkateshwar, Douglas Arenberg, and Gregory Kalemkerian. Lung Cancer Metastasis: Novel Biological Mechanisms and Impact on Clinical Practice. New York: Springer, 2009. Print. Kumar, Vinay, and Stanley L. Robbins. Robbins Basic Pathology. Philadelphia, PA: Saunders/Elsevier, 2007. Print. Leary, A. Lung Cancer: A Multidisciplinary Approach. Chichester, West Sussex, UK: Wiley-Blackwell, 2012. Print. Porth, Carol. Essentials of Pathophysiology: Concepts of Altered Health States. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2011. Print. Spiro, Stephen G, R M. Huber, and Samuel M. A. Janes.Thoracic Malignancies. Sheffield: European Respiratory Society, 2009. Print. Read More
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