User:CFCF/sandbox/Lung cancer

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This page is about lung carcinomas. For other lung tumors, see Lung tumor.

CFCF/sandbox/Lung cancer
CFCF/sandbox/Lung cancerA chest X-ray showing a tumor in the lung (marked by arrow)
CFCF/sandbox/Lung cancerA chest X-ray showing a tumor in the lung (marked by arrow)
A chest X-ray showing a tumor in the lung (marked by arrow)
Classification and external resources
ICD/CIM-10C33-C34 C33-C34
ICD/CIM-9162 162
DiseasesDB7616
MedlinePlus007194

Lung cancer, also known as carcinoma of the lung or pulmonary carcinoma, is a malignant lung tumor characterized by uncontrolled cell growth in tissues of the lung. If left untreated, this growth can spread beyond the lung by process of metastasis into nearby tissue or other parts of the body. Most cancers that start in the lung, known as primary lung cancers, are carcinomas that derive from epithelial cells. The main primary types are small-cell lung cancer (SCLC), and non-small-cell lung cancer (NSCLC). The most common symptoms are coughing (including coughing up blood), weight loss, shortness of breath, and chest pains.[1]

The vast majority (80–90%) of cases of lung cancer are due to long-term exposure to tobacco smoke.[1][2] About 10–15% of cases occur in nonsmokers.[3] These cases are often caused by a combination of genetic factors[4] and exposure to radon gas,[4] asbestos,[5] or other forms of air pollution,[4] including second-hand smoke.[6][7] Lung cancer may be seen on chest radiographs and computed tomography (CT) scans. The diagnosis is confirmed by biopsy[8] which is usually performed by bronchoscopy or CT-guidance.

Treatment and long-term outcomes depend on the type of cancer, the stage (degree of spread), and the person's overall health, measured by performance status. Common treatments include surgery, chemotherapy, and radiotherapy. NSCLC is sometimes treated with surgery, whereas SCLC usually responds better to chemotherapy and radiotherapy.[9] Overall, 17% of people in the United States diagnosed with lung cancer survive five years after the diagnosis,[10] while outcomes on average are worse in the developing world. Worldwide, lung cancer is the most common cause of cancer-related death in men and women, and was responsible for 1.56 million deaths annually, as of 2012.[11]

Signs and symptoms[edit]

Signs and symptoms which may suggest lung cancer include:[1]

If the cancer grows in the airways, it may obstruct airflow, causing breathing difficulties. The obstruction can lead to accumulation of secretions behind the blockage, and predispose to pneumonia.[1]

Depending on the type of tumor, paraneoplastic phenomena—symptoms not due to the local presence of cancer—may initially attract attention to the disease.[12] In lung cancer, these phenomena may include Lambert–Eaton myasthenic syndrome (muscle weakness due to autoantibodies), hypercalcemia, or syndrome of inappropriate antidiuretic hormone (SIADH, abnormally concentrated urine and dilute blood). Tumors in the top of the lung, known as Pancoast tumors, may invade the local part of the sympathetic nervous system, leading to Horner's syndrome (dropping of the eyelid and a small pupil on that side), as well as damage to the brachial plexus.[1]

Many of the symptoms of lung cancer (poor appetite, weight loss, fever, fatigue) are not specific.[8] In many people, the cancer has already spread beyond the original site by the time they have symptoms and seek medical attention.[13] Symptoms that suggest the presence of metastatic disease include weight loss, bone pain and neurological symptoms (headaches, fainting, convulsions, or limb weakness).[1] Common sites of spread include the brain, bone, adrenal glands, opposite lung, liver, pericardium, and kidneys.[13] About 10% of people with lung cancer do not have symptoms at diagnosis; these cancers are incidentally found on routine chest radiography.[14]

Causes[edit]

Cancer develops following genetic damage to DNA and epigenetic changes. These changes affect the normal functions of the cell, including cell proliferation, programmed cell death (apoptosis) and DNA repair. As more damage accumulates, the risk of cancer increases.[15]

Smoking[edit]

Graph showing how a general increase in sales of tobacco products in the USA in the first four decades of the 20th century (cigarettes per person per year) led to a corresponding rapid increase in the rate of lung cancer during the 1930s, '40s and '50s (lung cancer deaths per 100,000 male population per year)
Cross section of a human lung: The white area in the upper lobe is cancer; the black areas are discoloration due to smoking.
Lung cancer, incidence, mortality and survival, England 1971–2011

Smoking, particularly of cigarettes, is by far the main contributor to lung cancer.[16] Cigarette smoke contains at least 73 known carcinogens,[17] including radioisotopes from the radon decay sequence, nitrosamine, and benzopyrene. Additionally, nicotine appears to depress the immune response to cancerous growths in exposed tissue.[18] Across the developed world, 90% of lung cancer deaths in men during the year 2000 were attributed to smoking (70% for women).[19] Smoking accounts for 80–90% of lung cancer cases.[1]

Passive smoking—the inhalation of smoke from another's smoking—is a cause of lung cancer in nonsmokers. A passive smoker can be defined as someone living or working with a smoker. Studies from the US,[20][21][22] Europe[23] and the UK[24] have consistently shown a significantly increased risk among those exposed to passive smoke.[25] Those who live with someone who smokes have a 20–30% increase in risk while those who work in an environment with second hand smoke have a 16–19% increase in risk.[26] Investigations of sidestream smoke suggest it is more dangerous than direct smoke.[27] Passive smoking causes about 3,400 deaths from lung cancer each year in the USA.[22]

The tar from marijuana smoke contains many of the same carcinogens of that of tobacco smoke.[28]

Radon gas[edit]

Radon is a colorless and odorless gas generated by the breakdown of radioactive radium, which in turn is the decay product of uranium, found in the Earth's crust. The radiation decay products ionize genetic material, causing mutations that sometimes turn cancerous. Radon is the second-most common cause of lung cancer in the USA, after smoking.[22] The risk increases 8–16% for every 100 Bq/m³ increase in the radon concentration.[29] Radon gas levels vary by locality and the composition of the underlying soil and rocks. For example, in areas such as Cornwall in the UK (which has granite as substrata), radon gas is a major problem, and buildings have to be force-ventilated with fans to lower radon gas concentrations. The United States Environmental Protection Agency (EPA) estimates one in 15 homes in the US has radon levels above the recommended guideline of 4 picocuries per liter (pCi/l) (148 Bq/m³).[30]

Asbestos[edit]

Asbestos can cause a variety of lung diseases, including lung cancer. Tobacco smoking and asbestos have a synergistic effect on the formation of lung cancer.[5] Asbestos can also cause cancer of the pleura, called mesothelioma (which is different from lung cancer).[31]

Air pollution[edit]

Outdoor air pollution has a small effect on increasing the risk of lung cancer.[4] Fine particulates (PM2.5) and sulfate aerosols, which may be released in traffic exhaust fumes, are associated with slightly increased risk.[4][32] For nitrogen dioxide, an incremental increase of 10 parts per billion increases the risk of lung cancer by 14%.[33] Outdoor air pollution is estimated to account for 1–2% of lung cancers.[4]

Tentative evidence supports an increased risk of lung cancer from indoor air pollution related to the burning of wood, charcoal, dung or crop residue for cooking and heating.[34] Women who are exposed to indoor coal smoke have about twice the risk and a number of the by-products of burning biomass are known or suspected carcinogens.[35] This risk affects about 2.4 billion people globally,[34] and is believed to account for 1.5% of lung cancer deaths.[35]

Genetics[edit]

It is estimated that 8 to 14% of lung cancer is due to inherited factors.[36] In relatives of people with lung cancer, the risk is increased 2.4 times. This is likely due to a combination of genes.[37] Polymorphisms on chromosomes 5, 6 and 15 are known to affect the risk of lung cancer.[38]

Other causes[edit]

Numerous other substances, occupations, and environmental exposures have been linked to lung cancer. The International Agency for Research on Cancer (IARC) states there is "sufficient evidence" to show the following are carcinogenic in the lungs:[39]

Pathogenesis[edit]

See also: Carcinogenesis

Similar to many other cancers, lung cancer is initiated by activation of oncogenes or inactivation of tumor suppressor genes.[40] Oncogenes are believed to make people more susceptible to cancer. Proto-oncogenes are believed to turn into oncogenes when exposed to particular carcinogens.[41] 70–80% of lung cancers have polyploidy within the tissue.[42]

Mutations in the K-ras proto-oncogene are responsible for 10–30% of lung adenocarcinomas.[43][44] The epidermal growth factor receptor (EGFR) regulates cell proliferation, apoptosis, angiogenesis, and tumor invasion.[43] Mutations and amplification of EGFR are common in non-small-cell lung cancer and provide the basis for treatment with EGFR-inhibitors. Her2/neu is affected less frequently.[43] Chromosomal damage can lead to loss of heterozygosity. This can cause inactivation of tumor suppressor genes. Damage to chromosomes 3p, 5q, 13q, and 17p are particularly common in small-cell lung carcinoma. The p53 tumor suppressor gene, located on chromosome 17p, is affected in 60-75% of cases.[45] Other genes that are often mutated or amplified are c-MET, NKX2-1, LKB1, PIK3CA, and BRAF.[43]

Diagnosis[edit]

CT scan showing a cancerous tumor in the left lung

Performing a chest radiograph is one of the first investigative steps if a person reports symptoms that may suggest lung cancer. This may reveal an obvious mass, widening of the mediastinum (suggestive of spread to lymph nodes there), atelectasis (collapse), consolidation (pneumonia), or pleural effusion.[2] CT imaging is typically used to provide more information about the type and extent of disease. Bronchoscopy or CT-guided biopsy is often used to sample the tumor for histopathology.[14]

Lung cancer often appears as a solitary pulmonary nodule on a chest radiograph. However, the differential diagnosis is wide. Many other diseases can also give this appearance, including tuberculosis, fungal infections, metastatic cancer, or organizing pneumonia. Less common causes of a solitary pulmonary nodule include hamartomas, bronchogenic cysts, adenomas, arteriovenous malformation, pulmonary sequestration, rheumatoid nodules, Wegener's granulomatosis, or lymphoma.[46] Lung cancer can also be an incidental finding, as a solitary pulmonary nodule on a chest radiograph or CT scan done for an unrelated reason.[47] The definitive diagnosis of lung cancer is based on histological examination of the suspicious tissue in the context of the clinical and radiological features.[1]

Classification[edit]

Age-adjusted incidence of lung cancer by histological type[4]
Histological type Incidence per 100,000 per year
All types 66.9
Adenocarcinoma 22.1
Squamous-cell carcinoma 14.4
Small-cell carcinoma 9.8

Lung cancers are classified according to histological type.[8] This classification is important for determining management and predicting outcomes of the disease. Lung cancers are carcinomas—malignancies that arise from epithelial cells. Lung carcinomas are categorized by the size and appearance of the malignant cells seen by a histopathologist under a microscope. For therapeutic purposes, two broad classes are distinguished: non-small cell lung carcinoma and small cell lung carcinoma.[48]

Non-small-cell lung carcinoma[edit]

Micrograph of squamous carcinoma, a type of non-small-cell carcinoma, FNA specimen, Pap stain

The three main subtypes of NSCLC are adenocarcinoma, squamous-cell carcinoma and large-cell carcinoma.[1]

Nearly 40% of lung cancers are adenocarcinoma, which usually originates in peripheral lung tissue.[8] Most cases of adenocarcinoma are associated with smoking; however, among people who have smoked fewer than 100 cigarettes in their lifetimes ("never-smokers"),[1] adenocarcinoma is the most common form of lung cancer.[49] A subtype of adenocarcinoma, the bronchioloalveolar carcinoma, is more common in female never-smokers, and may have a better long term survival.[50]

Squamous-cell carcinoma accounts for about 30% of lung cancers. They typically occur close to large airways. A hollow cavity and associated cell death are commonly found at the center of the tumor.[8] About 9% of lung cancers are large-cell carcinoma. These are so named because the cancer cells are large, with excess cytoplasm, large nuclei and conspicuous nucleoli.[8]

Small-cell lung carcinoma[edit]

Small-cell lung carcinoma (microscopic view of a core needle biopsy)

In small-cell lung carcinoma (SCLC), the cells contain dense neurosecretory granules (vesicles containing neuroendocrine hormones), which give this tumor an endocrine/paraneoplastic syndrome association.[51] Most cases arise in the larger airways (primary and secondary bronchi).[14] These cancers grow quickly and spread early in the course of the disease. Sixty to seventy percent have metastatic disease at presentation. This type of lung cancer is strongly associated with smoking.[1]

Others[edit]

Four main histological subtypes are recognized, although some cancers may contain a combination of different subtypes.[48] Rare subtypes include glandular tumors, carcinoid tumors, and undifferentiated carcinomas.[1]

Metastasis[edit]

Typical immunostaining in lung cancer[1]
Histological type Immunostain
Squamous-cell carcinoma CK5/6 positive
CK7 negative
Adenocarcinoma CK7 positive
TTF-1 positive
Large-cell carcinoma TTF-1 negative
Small-cell carcinoma TTF-1 positive
CD56 positive
Chromogranin positive
Synaptophysin positive

The lung is a common place for the spread of tumors from other parts of the body. Secondary cancers are classified by the site of origin; e.g., breast cancer that has spread to the lung is called metastatic breast cancer. Metastases often have a characteristic round appearance on chest radiograph.[52]

Primary lung cancers themselves most commonly metastasize to the brain, bones, liver, and adrenal glands.[8] Immunostaining of a biopsy is often helpful to determine the original source.[53]

Staging[edit]

See also: Lung cancer staging

Lung cancer staging is an assessment of the degree of spread of the cancer from its original source. It is one of the factors affecting the prognosis and potential treatment of lung cancer.[1]

The initial evaluation of non-small-cell lung cancer (NSCLC) staging uses the TNM classification. This is based on the size of the primary tumor, lymph node involvement, and distant metastasis. After this, using the TNM descriptors, a group is assigned, ranging from occult cancer, through stages 0, IA (one-A), IB, IIA, IIB, IIIA, IIIB and IV (four). This stage group assists with the choice of treatment and estimation of prognosis.[54] Small-cell lung carcinoma (SCLC) has traditionally been classified as 'limited stage' (confined to one half of the chest and within the scope of a single tolerable radiotherapy field) or 'extensive stage' (more widespread disease).[1] However, the TNM classification and grouping are useful in estimating prognosis.[54]

For both NSCLC and SCLC, the two general types of staging evaluations are clinical staging and surgical staging. Clinical staging is performed prior to definitive surgery. It is based on the results of imaging studies (such as CT scans and PET scans) and biopsy results. Surgical staging is evaluated either during or after the operation, and is based on the combined results of surgical and clinical findings, including surgical sampling of thoracic lymph nodes.[8]

Prevention[edit]

See also: Smoking ban

Prevention is the most cost-effective means of decreasing lung cancer development. While in most countries industrial and domestic carcinogens have been identified and banned, tobacco smoking is still widespread. Eliminating tobacco smoking is a primary goal in the prevention of lung cancer, and smoking cessation is an important preventive tool in this process.[55]

Policy interventions to decrease passive smoking in public areas such as restaurants and workplaces have become more common in many Western countries.[56] Bhutan has had a complete smoking ban since 2005[57] while India introduced a ban on smoking in public in October 2008.[58] The World Health Organization has called for governments to institute a total ban on tobacco advertising to prevent young people from taking up smoking. They assess that such bans have reduced tobacco consumption by 16% where instituted.[59]

The long-term use of supplemental vitamin A,[60][61] vitamin C,[60] vitamin D[62] or vitamin E[60] does not reduce the risk of lung cancer. Some studies suggest that people who eat diets with a higher proportion of vegetables and fruit tend to have a lower risk,[22][63] but this may be due to confounding—with the lower risk actually due to the association of a high fruit/vegetables diet with less smoking. More rigorous studies have not demonstrated a clear association between diet and lung cancer risk.[63]

Screening[edit]

Main article: Lung cancer screening

Screening refers to the use of medical tests to detect disease in asymptomatic people. Possible screening tests for lung cancer include sputum cytology, chest radiograph (CXR), and computed tomography (CT). Screening programs using CXR or cytology have not demonstrated benefit.[64] Screening those at high risk (i.e. age 55 to 79 who have smoked more than 30 pack years or those who have had previous lung cancer) annually with low-dose CT scans may reduce the chance of death from lung cancer by an absolute amount of 0.3% (relative amount of 20%).[65][66] There is, however, a high rate of falsely positive scans which may result in unneeded invasive procedures as well as substantial financial cost.[67] For each true positive scan there are more than 19 false positives.[68] Radiation exposure is another potential harm from screening.[69]

Management[edit]

Main article: Treatment of lung cancer

Treatment for lung cancer depends on the cancer's specific cell type, how far it has spread, and the person's performance status. Common treatments include palliative care,[70] surgery, chemotherapy, and radiation therapy.[1] Targeted therapy of lung cancer is growing in importance for advanced lung cancer.

Surgery[edit]

Main article: Lung cancer surgery
Pneumonectomy specimen containing a squamous-cell carcinoma, seen as a white area near the bronchi

If investigations confirm NSCLC, the stage is assessed to determine whether the disease is localized and amenable to surgery or if it has spread to the point where it cannot be cured surgically. CT scan and positron emission tomography are used for this determination.[1] If mediastinal lymph node involvement is suspected, mediastinoscopy may be used to sample the nodes and assist staging.[71] Blood tests and pulmonary function testing are used to assess whether a person is well enough for surgery.[14] If pulmonary function tests reveal poor respiratory reserve, surgery may not be a possibility.[1]

In most cases of early-stage NSCLC, removal of a lobe of lung (lobectomy) is the surgical treatment of choice. In people who are unfit for a full lobectomy, a smaller sublobar excision (wedge resection) may be performed. However, wedge resection has a higher risk of recurrence than lobectomy.[72] Radioactive iodine brachytherapy at the margins of wedge excision may reduce the risk of recurrence.[73] Rarely, removal of a whole lung (pneumonectomy) is performed.[72] Video-assisted thoracoscopic surgery (VATS) and VATS lobectomy use a minimally invasive approach to lung cancer surgery.[74] VATS lobectomy is equally effective compared to conventional open lobectomy, with less postoperative illness.[75]

In SCLC, chemotherapy and/or radiotherapy is typically used.[76] However the role of surgery in SCLC is being reconsidered. Surgery might improve outcomes when added to chemotherapy and radiation in early stage SCLC.[77]

Radiotherapy[edit]

Radiotherapy is often given together with chemotherapy, and may be used with curative intent in people with NSCLC who are not eligible for surgery. This form of high-intensity radiotherapy is called radical radiotherapy.[78] A refinement of this technique is continuous hyperfractionated accelerated radiotherapy (CHART), in which a high dose of radiotherapy is given in a short time period.[79] Postoperative thoracic radiotherapy generally should not be used after curative intent surgery for NSCLC.[80] Some people with mediastinal N2 lymph node involvement might benefit from post-operative radiotherapy.[81]

For potentially curable SCLC cases, chest radiotherapy is often recommended in addition to chemotherapy.[8]

If cancer growth blocks a short section of bronchus, brachytherapy (localized radiotherapy) may be given directly inside the airway to open the passage.[82] Compared to external beam radiotherapy, brachytherapy allows a reduction in treatment time and reduced radiation exposure to healthcare staff.[83]

Prophylactic cranial irradiation (PCI) is a type of radiotherapy to the brain, used to reduce the risk of metastasis. PCI is most useful in SCLC. In limited-stage disease, PCI increases three-year survival from 15% to 20%; in extensive disease, one-year survival increases from 13% to 27%.[84]

Recent improvements in targeting and imaging have led to the development of stereotactic radiation in the treatment of early-stage lung cancer. In this form of radiotherapy, high doses are delivered in a small number of sessions using stereotactic targeting techniques. Its use is primarily in patients who are not surgical candidates due to medical comorbidities.[85]

For both NSCLC and SCLC patients, smaller doses of radiation to the chest may be used for symptom control (palliative radiotherapy).[86]

Chemotherapy[edit]

The chemotherapy regimen depends on the tumor type.[8] Small-cell lung carcinoma (SCLC), even relatively early stage disease, is treated primarily with chemotherapy and radiation.[87] In SCLC, cisplatin and etoposide are most commonly used.[88] Combinations with carboplatin, gemcitabine, paclitaxel, vinorelbine, topotecan, and irinotecan are also used.[89][90] In advanced non-small cell lung carcinoma (NSCLC), chemotherapy improves survival and is used as first-line treatment, provided the person is well enough for the treatment.[91] Typically, two drugs are used, of which one is often platinum-based (either cisplatin or carboplatin). Other commonly used drugs are gemcitabine, paclitaxel, docetaxel,[92][93] pemetrexed,[94] etoposide or vinorelbine.[93]

Adjuvant chemotherapy refers to the use of chemotherapy after apparently curative surgery to improve the outcome. In NSCLC, samples are taken of nearby lymph nodes during surgery to assist staging. If stage II or III disease is confirmed, adjuvant chemotherapy improves survival by 5% at five years.[95][96] The combination of vinorelbine and cisplatin is more effective than older regimens.[96] Adjuvant chemotherapy for people with stage IB cancer is controversial, as clinical trials have not clearly demonstrated a survival benefit.[97][98] Trials of preoperative chemotherapy (neoadjuvant chemotherapy) in resectable NSCLC have been inconclusive.[99]

Chemotherapy may be combined with palliative care in the treatment of the NSCLC. In advanced cases, appropriate chemotherapy improves average survival over supportive care alone, as well as improving quality of life.[100] With adequate physical fitness maintaining chemotherapy during lung cancer palliation offers 1.5 to 3 months of prolongation of survival, symptomatic relief, and an improvement in quality of life, with better results seen with modern agents.[101][102] The NSCLC Meta-Analyses Collaborative Group recommends if the recipient wants and can tolerate treatment, then chemotherapy should be considered in advanced NSCLC.[91][103]

Palliative care[edit]

Palliative care when added to usual cancer care benefits people even when they are still receiving chemotherapy.[104] These approaches allow additional discussion of treatment options and provide opportunities to arrive at well-considered decisions.[105][106] Palliative care may avoid unhelpful but expensive care at the end of life.[106] For individuals who have more advanced disease, hospice care may also be appropriate.[14]

Prognosis[edit]

Main articles: Lung cancer staging and Manchester score
Outcomes in lung cancer according to clinical stage[54]
Clinical stage Five-year survival (%)
Non-small cell lung carcinoma Small cell lung carcinoma
IA 50 38
IB 47 21
IIA 36 38
IIB 26 18
IIIA 19 13
IIIB 7 9
IV 2 1

Of all people with lung cancer in the US, 16.8% survive for five years after diagnosis.[107] Outcomes are generally worse in the developing world.[108] Stage is often advanced at the time of diagnosis. At presentation, 30–40% of cases of NSCLC are stage IV, and 60% of SCLC are stage IV.[8]

Prognostic factors in NSCLC include presence or absence of pulmonary symptoms, tumor size, cell type (histology), degree of spread (stage) and metastases to multiple lymph nodes, and vascular invasion. For people with inoperable disease, outcomes are worse in those with poor performance status and weight loss of more than 10%.[109] Prognostic factors in small cell lung cancer include performance status, gender, stage of disease, and involvement of the central nervous system or liver at the time of diagnosis.[110]

For NSCLC, the best prognosis is achieved with complete surgical resection of stage IA disease, with up to 70% five-year survival.[111] For SCLC, the overall five-year survival is about 5%.[1] People with extensive-stage SCLC have an average five-year survival rate of less than 1%. The average survival time for limited-stage disease is 20 months, with a five-year survival rate of 20%.[2]

According to data provided by the National Cancer Institute, the median age at diagnosis of lung cancer in the United States is 70 years,[112] and the median age at death is 72 years.[113] In the US, people with medical insurance are more likely to have a better outcome.[114]

Epidemiology[edit]

Age-standardized death from tracheal, bronchial, and lung cancers per 100,000 inhabitants in 2004[115]
Lung cancer distribution in the United States

Worldwide, lung cancer is the most common cancer in terms of both incidence and mortality. In 2012, there were 1.82 million new cases, and 1.56 million deaths due to lung cancer.[11] The highest rates are in Europe and North America.[116] The population segment most likely to develop lung cancer is people aged over 50 who have a history of smoking. In contrast to the mortality rate in men, which began declining more than 20 years ago, women's lung cancer mortality rates have been rising over the last decades, and are just recently beginning to stabilize.[117] In the USA, the lifetime risk of developing lung cancer is 8% in men and 6% in women.[1]

For every 3–4 million cigarettes smoked, one lung cancer death occurs.[1][118] The influence of "Big Tobacco" plays a significant role in the smoking culture.[119] Young nonsmokers who see tobacco advertisements are more likely to take up smoking.[120] The role of passive smoking is increasingly being recognized as a risk factor for lung cancer,[25] leading to policy interventions to decrease undesired exposure of nonsmokers to others' tobacco smoke.[121] Emissions from automobiles, factories, and power plants also pose potential risks.[4]

Eastern Europe has the highest lung cancer mortality among men, while northern Europe and the US have the highest mortality among women. In the United States, black men and women have a higher incidence.[122] Lung cancer rates are currently lower in developing countries.[123] With increased smoking in developing countries, the rates are expected to increase in the next few years, notably in China[124] and India.[125]

From the 1960s, the rates of lung adenocarcinoma started to rise relative to other types of lung cancer. This is partly due to the introduction of filter cigarettes. The use of filters removes larger particles from tobacco smoke, thus reducing deposition in larger airways. However, the smoker has to inhale more deeply to receive the same amount of nicotine, increasing particle deposition in small airways where adenocarcinoma tends to arise.[126] The incidence of lung adenocarcinoma continues to rise.[127]

History[edit]

Lung cancer was uncommon before the advent of cigarette smoking; it was not even recognized as a distinct disease until 1761.[128] Different aspects of lung cancer were described further in 1810.[129] Malignant lung tumors made up only 1% of all cancers seen at autopsy in 1878, but had risen to 10–15% by the early 1900s.[130] Case reports in the medical literature numbered only 374 worldwide in 1912,[131] but a review of autopsies showed the incidence of lung cancer had increased from 0.3% in 1852 to 5.66% in 1952.[132] In Germany in 1929, physician Fritz Lickint recognized the link between smoking and lung cancer,[130] which led to an aggressive antismoking campaign.[133] The British Doctors Study, published in the 1950s, was the first solid epidemiological evidence of the link between lung cancer and smoking.[134] As a result, in 1964 the Surgeon General of the United States recommended smokers should stop smoking.[135]

The connection with radon gas was first recognized among miners in the Ore Mountains near Schneeberg, Saxony. Silver has been mined there since 1470, and these mines are rich in uranium, with its accompanying radium and radon gas.[136] Miners developed a disproportionate amount of lung disease, eventually recognized as lung cancer in the 1870s.[137] Despite this discovery, mining continued into the 1950s, due to the USSR's demand for uranium.[136] Radon was confirmed as a cause of lung cancer in the 1960s.[138]

The first successful pneumonectomy for lung cancer was performed in 1933.[139] Palliative radiotherapy has been used since the 1940s.[140] Radical radiotherapy, initially used in the 1950s, was an attempt to use larger radiation doses in patients with relatively early-stage lung cancer, but who were otherwise unfit for surgery.[141] In 1997, continuous hyperfractionated accelerated radiotherapy was seen as an improvement over conventional radical radiotherapy.[142] With small-cell lung carcinoma, initial attempts in the 1960s at surgical resection[143] and radical radiotherapy[144] were unsuccessful. In the 1970s, successful chemotherapy regimens were developed.[145]

References[edit]

  1. ^ a b c d e f g h i j k l m n o p q r s t u Horn, L; Pao W; Johnson DH (2012). "Chapter 89". In Longo, DL; Kasper, DL; Jameson, JL; Fauci, AS; Hauser, SL; Loscalzo, J (eds.). Harrison's Principles of Internal Medicine (18th ed.). McGraw-Hill. ISBN 978-0-07-174889-6.
  2. ^ a b c "Lung Carcinoma: Tumors of the Lungs". Merck Manual Professional Edition, Online edition. Retrieved 15 August 2007.
  3. ^ Thun, Michael J.; Hannan, Lindsay M.; Adams-Campbell, Lucile L.; Boffetta, Paolo; Buring, Julie E.; Feskanich, Diane; Flanders, W. Dana; Jee, Sun Ha; Katanoda, Kota; Kolonel, Laurence N.; Lee, I-Min; Marugame, Tomomi; Palmer, Julie R.; Riboli, Elio; Sobue, Tomotaka; Avila-Tang, Erika; Wilkens, Lynne R.; Samet, Jon M. (September 2008). "Lung cancer occurrence in never-smokers: an analysis of 13 cohorts and 22 cancer registry studies". PLOS Medicine. 5 (9): e185. doi:10.1371/journal.pmed.0050185. PMC 2531137. PMID 18788891.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  4. ^ a b c d e f g h Alberg AJ, Samet JM (2010). "Chapter 46". Murray & Nadel's Textbook of Respiratory Medicine (5th ed.). Saunders Elsevier. ISBN 978-1-4160-4710-0.
  5. ^ a b O'Reilly, KM; Mclaughlin AM; Beckett WS; Sime PJ (March 2007). "Asbestos-related lung disease". American Family Physician. 75 (5): 683–688. PMID 17375514.
  6. ^ Carmona, RH (27 June 2006). "The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General". U.S. Department of Health and Human Services. Secondhand smoke exposure causes disease and premature death in children and adults who do not smoke. Retrieved 2014-06-16
  7. ^ "Tobacco Smoke and Involuntary Smoking" (PDF). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. 83. WHO International Agency for Research on Cancer. 2002. There is sufficient evidence that involuntary smoking (exposure to secondhand or 'environmental' tobacco smoke) causes lung cancer in humans. ... Involuntary smoking (exposure to secondhand or 'environmental' tobacco smoke) is carcinogenic to humans (Group 1).
  8. ^ a b c d e f g h i j k Lu, C (2010). "78: Cancer of the Lung". Holland-Frei Cancer Medicine (8th ed.). People's Medical Publishing House. ISBN 978-1-60795-014-1. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  9. ^ Chapman, S; Robinson G; Stradling J; West S (2009). "Chapter 31". Oxford Handbook of Respiratory Medicine (2nd ed.). Oxford University Press. ISBN 978-0-19-954516-2.
  10. ^ "http://seer.cancer.gov/statfacts/html/lungb.html". National Cancer Institute. Retrieved 18 June 2014. {{cite web}}: External link in |title= (help)
  11. ^ a b World Cancer Report 2014. World Health Organization. 2014. pp. Chapter 1.1. ISBN 978-9283204299.
  12. ^ Honnorat, J; Antoine JC (May 2007). "Paraneoplastic neurological syndromes". Orphanet Journal of Rare Diseases. 2 (1). BioMed Central: 22. doi:10.1186/1750-1172-2-22. PMC 1868710. PMID 17480225.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  13. ^ a b Greene, Frederick L. (2002). AJCC cancer staging manual. Berlin: Springer-Verlag. ISBN 0-387-95271-3.
  14. ^ a b c d e Collins, LG; Haines C; Perkel R; Enck RE (January 2007). "Lung cancer: diagnosis and management". American Family Physician. 75 (1). American Academy of Family Physicians: 56–63. PMID 17225705.
  15. ^ Brown, KM (2010). "Chapter 8". Holland-Frei Cancer Medicine (8th ed.). People's Medical Publishing House USA. ISBN 978-1-60795-014-1. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  16. ^ Biesalski, H. K.; De Mesquita, B. B.; Chesson, A.; Chytil, F.; Grimble, R.; Hermus, R. J.; Kohrle, J.; Lotan, R.; Norpoth, K.; Pastorino, U.; Thurnham, D. (1998). "European Consensus Statement on Lung Cancer: risk factors and prevention. Lung Cancer Panel". CA Cancer J Clin. 48 (3). Smoking is the major risk factor, accounting for about 90% of lung cancer incidence.: 167–176, discussion 164–166. doi:10.3322/canjclin.48.3.167. PMID 9594919.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: location (link)
  17. ^ Hecht, SS (2012). "Lung carcinogenesis by tobacco smoke". International Journal of Cancer. 131 (12): 2724–2732. doi:10.1002/ijc.27816. PMC 3479369. PMID 22945513.
  18. ^ Sopori, M (May 2002). "Effects of cigarette smoke on the immune system". Nature Reviews Immunology. 2 (5): 372–7. doi:10.1038/nri803. PMID 12033743.
  19. ^ Peto, R (2006). Mortality from smoking in developed countries 1950–2000: Indirect estimates from National Vital Statistics. Oxford University Press. ISBN 0-19-262535-7. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  20. ^ California Environmental Protection Agency (1997). "Health effects of exposure to environmental tobacco smoke. California Environmental Protection Agency". Tobacco Control. 6 (4): 346–353. doi:10.1136/tc.6.4.346. PMC 1759599. PMID 9583639.
  21. ^ Centers for Disease Control and Prevention (CDC) (December 2001). "State-specific prevalence of current cigarette smoking among adults, and policies and attitudes about secondhand smoke—United States, 2000". Morbidity and Mortality Weekly Report. 50 (49). Atlanta, Georgia: CDC: 1101–1106. PMID 11794619.
  22. ^ a b c d Alberg, AJ; Samet JM (September 2007). "Epidemiology of lung cancer". Chest. 132 (S3). American College of Chest Physicians: 29S–55S. doi:10.1378/chest.07-1347. PMID 17873159.
  23. ^ Jaakkola, MS; Jaakkola JJ (August 2006). "Impact of smoke-free workplace legislation on exposures and health: possibilities for prevention". European Respiratory Journal. 28 (2): 397–408. doi:10.1183/09031936.06.00001306. PMID 16880370.
  24. ^ Parkin, DM (December 2011). "Tobacco—attributable cancer burden in the UK in 2010". British Journal of Cancer. 105 (Suppl. 2): S6–S13. doi:10.1038/bjc.2011.475. PMC 3252064. PMID 22158323.
  25. ^ a b Taylor, R; Najafi F; Dobson A (October 2007). "Meta-analysis of studies of passive smoking and lung cancer: effects of study type and continent". International Journal of Epidemiology. 36 (5): 1048–1059. doi:10.1093/ije/dym158. PMID 17690135.
  26. ^ "Frequently asked questions about second hand smoke". World Health Organization. Retrieved 25 July 2012.
  27. ^ Schick, S; Glantz S (December 2005). "Philip Morris toxicological experiments with fresh sidestream smoke: more toxic than mainstream smoke". Tobacco Control. 14 (6): 396–404. doi:10.1136/tc.2005.011288. PMC 1748121. PMID 16319363.
  28. ^ Tomar, Rajpal C.; Beaumont and Hsieh (August 2009). "Evidence on the carcinogenicity of marijuana smoke" (PDF). Reproductive and Cancer Hazard Assessment Branch Office of Environmental Health Hazard Assessment, California Environmental Protection Agency. Retrieved 23 June 2012.
  29. ^ Schmid K, Kuwert T, Drexler H (March 2010). "Radon in Indoor Spaces: An Underestimated Risk Factor for Lung Cancer in Environmental Medicine". Dtsch Arztebl Int. 107 (11): 181–6. doi:10.3238/arztebl.2010.0181. PMC 2853156. PMID 20386676.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  30. ^ EPA (October 2006). "Radiation information: radon". EPA. Retrieved 11 August 2007.
  31. ^ Davies, RJO; Lee YCG (2010). "18.19.3". Oxford Textbook Medicine (5th ed.). OUP Oxford. ISBN 978-0-19-920485-4.
  32. ^ Chen, H; Goldberg MS; Villeneuve PJ (October–December 2008). "A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases". Reviews on Environmental Health. 23 (4): 243–297. doi:10.1515/reveh.2008.23.4.243. PMID 19235364.
  33. ^ Clapp, RW; Jacobs MM; Loechler EL (January–March 2008). "Environmental and Occupational Causes of Cancer New Evidence, 2005–2007". Reviews on Environmental Health. 23 (1): 1–37. doi:10.1515/REVEH.2008.23.1.1. PMC 2791455. PMID 18557596.
  34. ^ a b Lim, WY; Seow, A (January 2012). "Biomass fuels and lung cancer". Respirology (Carlton, Vic.). 17 (1): 20–31. doi:10.1111/j.1440-1843.2011.02088.x. PMID 22008241.
  35. ^ a b Sood, A (December 2012). "Indoor fuel exposure and the lung in both developing and developed countries: an update". Clinics in Chest Medicine. 33 (4): 649–65. doi:10.1016/j.ccm.2012.08.003. PMC 3500516. PMID 23153607.
  36. ^ Dudley, Joel (2013). Exploring Personal Genomics. Oxford University Press. p. 25. ISBN 978-0-19-964448-3.
  37. ^ Kern JA, McLennan G (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. p. 1802. ISBN 978-0-07-145739-2.
  38. ^ Larsen, JE; Minna D (December 2011). "Molecular biology of lung cancer: clinical implications". Clinics in Chest Medicine. 32 (4): 703–740. doi:10.1016/j.ccm.2011.08.003. PMC 3367865. PMID 22054881.
  39. ^ Cogliano, V. J.; Baan, R.; Straif, K.; Grosse, Y.; Lauby-Secretan, B.; El Ghissassi, F.; Bouvard, V.; Benbrahim-Tallaa, L.; Guha, N.; Freeman, C.; Galichet, L.; Wild, C. P. (21 December 2011). "Preventable exposures associated with human cancers" (PDF). Journal of the National Cancer Institute. 103 (24): 1827–39. doi:10.1093/jnci/djr483. PMC 3243677. PMID 22158127.
  40. ^ Fong, KM; Sekido Y; Gazdar AF; Minna JD (October 2003). "Lung cancer • 9: Molecular biology of lung cancer: clinical implications". Thorax. 58 (10). BMJ Publishing Group Ltd.: 892–900. doi:10.1136/thorax.58.10.892. PMC 1746489. PMID 14514947.
  41. ^ Salgia, R; Skarin AT (March 1998). "Molecular abnormalities in lung cancer". Journal of Clinical Oncology. 16 (3): 1207–1217. doi:10.1200/JCO.1998.16.3.1207. PMID 9508209.
  42. ^ Masuda, A; Takahashi T (October 2002). "Chromosome instability in human lung cancers: possible underlying mechanisms and potential consequences in the pathogenesis". Oncogene. 21 (45): 6884–6897. doi:10.1038/sj.onc.1205566. PMID 12362271.
  43. ^ a b c d Herbst, RS; Heymach JV; Lippman SM (September 2008). "Lung cancer". New England Journal of Medicine. 359 (13): 1367–1380. doi:10.1056/NEJMra0802714. PMID 18815398.
  44. ^ Aviel-Ronen, S; Blackhall FH; Shepherd FA; Tsao MS (July 2006). "K-ras mutations in non-small-cell lung carcinoma: a review". Clinical Lung Cancer. 8 (1). Cancer Information Group: 30–38. doi:10.3816/CLC.2006.n.030. PMID 16870043.
  45. ^ Devereux, TR; Taylor JA; Barrett JC (March 1996). "Molecular mechanisms of lung cancer. Interaction of environmental and genetic factors". Chest. 109 (Suppl 3). American College of Chest Physicians: 14S–19S. doi:10.1378/chest.109.3_Supplement.14S. PMID 8598134.
  46. ^ Miller, WT (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. p. 486. ISBN 978-0-07-145739-2.
  47. ^ Kaiser, LR (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. pp. 1815–1816. ISBN 978-0-07-145739-2.
  48. ^ a b Maitra, A; Kumar V (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 528–529. ISBN 978-1-4160-2973-1.
  49. ^ Subramanian, J; Govindan R (February 2007). "Lung cancer in never smokers: a review". Journal of Clinical Oncology. 25 (5). American Society of Clinical Oncology: 561–570. doi:10.1200/JCO.2006.06.8015. PMID 17290066.
  50. ^ Raz, DJ; He B; Rosell R; Jablons DM (March 2006). "Bronchioloalveolar carcinoma: a review". Clinical Lung Cancer. 7 (5): 313–322. doi:10.3816/CLC.2006.n.012. PMID 16640802.
  51. ^ Rosti, G.; Bevilacqua, G.; Bidoli, P.; Portalone, L.; Santo, A.; Genestreti, G. (March 2006). "Small cell lung cancer". Annals of Oncology. 17 (Suppl. 2): 5–10. doi:10.1093/annonc/mdj910. PMID 16608983.
  52. ^ Seo, Joon Beom; Im, Jung-Gi; Goo, Jin Mo; Chung, Myung Jin; Kim, Mi-Young (1 March 2001). "Atypical pulmonary metastases: spectrum of radiologic findings". Radiographics. 21 (2): 403–417. doi:10.1148/radiographics.21.2.g01mr17403. PMID 11259704.
  53. ^ Tan D, Zander DS (2008). "Immunohistochemistry for Assessment of Pulmonary and Pleural Neoplasms: A Review and Update". Int J Clin Exp Pathol. 1 (1): 19–31. PMC 2480532. PMID 18784820.
  54. ^ a b c Rami-Porta, R; Crowley JJ; Goldstraw P (February 2009). "The revised TNM staging system for lung cancer" (PDF). Annals of Thoracic and Cardiovascular Surgery. 15 (1): 4–9. PMID 19262443.
  55. ^ Goodman, GE (November 2002). "Lung cancer. 1: prevention of lung cancer". Thorax. 57 (11): 994–999. doi:10.1136/thorax.57.11.994. PMC 1746232. PMID 12403886.
  56. ^ McNabola, A; Gill LW (February 2009). "The control of environmental tobacco smoke: a policy review". International Journal of Environmental Research and Public Health. 6 (2): 741–758. doi:10.3390/ijerph6020741. PMC 2672352. PMID 19440413.
  57. ^ Pandey, G (February 2005). "Bhutan's smokers face public ban". BBC. Retrieved 7 September 2007.
  58. ^ Pandey, G (2 October 2008). "Indian ban on smoking in public". BBC. Retrieved 25 April 2012.
  59. ^ "UN health agency calls for total ban on tobacco advertising to protect young" (Press release). United Nations News service. 30 May 2008.
  60. ^ a b c Fabricius, P; Lange P (July–September 2003). "Diet and lung cancer". Monaldi Archives for Chest Disease. 59 (3): 207–211. PMID 15065316.
  61. ^ Fritz, Heidi; Kennedy, Deborah; Fergusson, Dean; Fernandes, Rochelle; Doucette, Steve; Cooley, Kieran; Seely, Andrew; Sagar, Stephen; Wong, Raimond; Seely, Dugald (2011). "Vitamin A and Retinoid Derivatives for Lung Cancer: A Systematic Review and Meta Analysis". PLOS ONE. 6 (6): e21107. doi:10.1371/journal.pone.0021107. PMC 3124481. PMID 21738614.{{cite journal}}: CS1 maint: date and year (link)
  62. ^ Herr, Christian; Greulich, Timm; Koczulla, Rembert A.; Meyer, Silke; Zakharkina, Tetyana; Branscheidt, Meret; Eschmann, Rebecca; Bals, Robert (March 2011). "The role of vitamin D in pulmonary disease: COPD, asthma, infection, and cancer". Respiratory Research. 12 (1): 31. doi:10.1186/1465-9921-12-31. PMC 3071319. PMID 21418564.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  63. ^ a b Key, TJ (January 2011). "Fruit and vegetables and cancer risk". British Journal of Cancer. 104 (1): 6–11. doi:10.1038/sj.bjc.6606032. PMC 3039795. PMID 21119663.
  64. ^ Manser, Renée; Irving, Louis B.; Stone, Christine; Byrnes, Graham; Abramson, Michael J.; Campbell, Donald (2004). Manser, Renée (ed.). "Screening for lung cancer". Cochrane Database of Systematic Reviews (1): CD001991. doi:10.1002/14651858.CD001991.pub2. PMID 14973979.{{cite journal}}: CS1 maint: date and year (link)
  65. ^ Jaklitsch, Michael T.; Jacobson, Francine L.; Austin, John H.M.; Field, John K.; Jett, James R.; Keshavjee, Shaf; MacMahon, Heber; Mulshine, James L.; Munden, Reginald F.; Salgia, Ravi; Strauss, Gary M.; Swanson, Scott J.; Travis, William D.; Sugarbaker, David J. (July 2012). "The American Association for Thoracic Surgery guidelines for lung cancer screening using low-dose computed tomography scans for lung cancer survivors and other high-risk groups". Journal of Thoracic and Cardiovascular Surgery. 144 (1): 33–38. doi:10.1016/j.jtcvs.2012.05.060. PMID 22710039.
  66. ^ Bach, P. B.; Mirkin, J. N.; Oliver, T. K.; Azzoli, C. G.; Berry, D. A.; Brawley, O. W.; Byers, T.; Colditz, G. A.; Gould, M. K.; Jett, J. R.; Sabichi, A. L.; Smith-Bindman, R.; Wood, D. E.; Qaseem, A.; Detterbeck, F. C. (June 2012). "Benefits and harms of CT screening for lung cancer: a systematic review". JAMA: The Journal of the American Medical Association. 307 (22): 2418–2429. doi:10.1001/jama.2012.5521. PMC 3709596. PMID 22610500.
  67. ^ Boiselle, PM (20 March 2013). "Computed tomography screening for lung cancer". JAMA: The Journal of the American Medical Association. 309 (11): 1163–70. doi:10.1001/jama.2012.216988. PMID 23512063.
  68. ^ Bach PB, Mirkin JN, Oliver TK; et al. (June 2012). "Benefits and harms of CT screening for lung cancer: a systematic review". JAMA. 307 (22): 2418–29. doi:10.1001/jama.2012.5521. PMC 3709596. PMID 22610500. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  69. ^ Aberle, Denise R.; Abtin, Fereidoun; Brown, Kathleen (10 March 2013). "Computed tomography screening for lung cancer: has it finally arrived? Implications of the national lung screening trial". Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology. 31 (8): 1002–8. doi:10.1200/JCO.2012.43.3110. PMC 3589698. PMID 23401434.
  70. ^ Ferrell, B; Koczywas M; Grannis F; Harrington A (April 2011). "Palliative care in lung cancer". Surgical Clinics of North America. 91 (2): 403–417. doi:10.1016/j.suc.2010.12.003. PMC 3655433. PMID 21419260.
  71. ^ Kaiser LR (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. pp. 1853–1854. ISBN 978-0-07-145739-2.
  72. ^ a b Kaiser LR (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. pp. 1855–1856. ISBN 978-0-07-145739-2.
  73. ^ Odell, DD; Kent MS; Fernando HC (Spring 2010). "Sublobar resection with brachytherapy mesh for stage I non-small cell lung cancer". Seminars in Thoracic and Cardiovascular Surgery. 22 (1): 32–37. doi:10.1053/j.semtcvs.2010.04.003. PMID 20813314.
  74. ^ Alam, N; Flores RM (July–September 2007). "Video-assisted thoracic surgery (VATS) lobectomy: the evidence base". Journal of the Society of Laparoendoscopic Surgeons. 11 (3): 368–374. PMC 3015831. PMID 17931521.
  75. ^ Rueth, NM; Andrade RS (June 2010). "Is VATS lobectomy better: perioperatively, biologically and oncologically?". Annals of Thoracic Surgery. 89 (6): S2107–S2111. doi:10.1016/j.athoracsur.2010.03.020. PMID 20493991.
  76. ^ Simon GR, Turrisi A (September 2007). "Management of small cell lung cancer: ACCP evidence-based clinical practice guidelines (2nd edition)". Chest. 132 (3 Suppl): 324S–339S. doi:10.1378/chest.07-1385. PMID 17873178.
  77. ^ Goldstein, SD; Yang SC (October 2011). "Role of surgery in small cell lung cancer". Surgical Oncology Clinics of North America. 20 (4): 769–777. doi:10.1016/j.soc.2011.08.001. PMID 21986271.
  78. ^ Arriagada, R; Goldstraw P; Le Chevalier T (2002). Oxford Textbook of Oncology (2nd ed.). Oxford University Press. p. 2094. ISBN 0-19-262926-3.
  79. ^ Hatton, MQ; Martin JE (June 2010). "Continuous hyperfractionated accelerated radiotherapy (CHART) and non-conventionally fractionated radiotherapy in the treatment of non-small cell lung cancer: a review and consideration of future directions". Clinical Oncology (Royal College of Radiologists). 22 (5): 356–364. doi:10.1016/j.clon.2010.03.010. PMID 20399629.
  80. ^ PORT Meta-analysis Trialists Group (2005). Rydzewska, Larysa (ed.). "Postoperative radiotherapy for non-small cell lung cancer". Cochrane Database of Systematic Reviews (2): CD002142. doi:10.1002/14651858.CD002142.pub2. PMID 15846628.
  81. ^ Le Péchoux, C (2011). "Role of postoperative radiotherapy in resected non-small cell lung cancer: a reassessment based on new data". Oncologist. 16 (5): 672–681. doi:10.1634/theoncologist.2010-0150. PMC 3228187. PMID 21378080.
  82. ^ Cardona Zorrilla, Andrés Felipe; Reveiz, Ludovic; Ospina, Edgar Guillermo; Yepes, Andrés; Yepes, A. (April 2008). Reveiz, Ludovic (ed.). "Palliative endobronchial brachytherapy for non-small cell lung cancer". Cochrane Database of Systematic Reviews (2): CD004284. doi:10.1002/14651858.CD004284.pub2. PMID 18425900.
  83. ^ Ikushima, H (February 2010). "Radiation therapy: state of the art and the future". Journal of Medical Investigation. 57 (1–2): 1–11. doi:10.2152/jmi.57.1. PMID 20299738.
  84. ^ Paumier, A; Cuenca X; Le Péchoux C (June 2011). "Prophylactic cranial irradiation in lung cancer". Cancer Treatment Reviews. 37 (4): 261–265. doi:10.1016/j.ctrv.2010.08.009. PMID 20934256.
  85. ^ Girard, N; Mornex F (October 2011). "Stereotactic radiotherapy for non-small cell lung cancer: From concept to clinical reality. 2011 update". Cancer Radiothérapie. 15 (6–7): 522–526. doi:10.1016/j.canrad.2011.07.241. PMID 21889901.
  86. ^ Fairchild, Alysa; Harris, Kristin; Barnes, Elizabeth; Wong, Rebecca; Lutz, Stephen; Bezjak, Andrea; Cheung, Patrick; Chow, Edward (August 2008). "Palliative thoracic radiotherapy for lung cancer: a systematic review". Journal of Clinical Oncology. 26 (24): 4001–4011. doi:10.1200/JCO.2007.15.3312. PMID 18711191.
  87. ^ Hann CL, Rudin CM (30 November 2008). "Management of small-cell lung cancer: incremental changes but hope for the future". Oncology (Williston Park). 22 (13): 1486–92. PMC 4124612. PMID 19133604.
  88. ^ Murray, N; Turrisi AT (March 2006). "A review of first-line treatment for small-cell lung cancer". Journal of Thoracic Oncology. 1 (3): 270–278. doi:10.1016/s1556-0864(15)31579-3. PMID 17409868.
  89. ^ Azim, HA; Ganti AK (March 2007). "Treatment options for relapsed small-cell lung cancer". Anticancer Drugs. 18 (3): 255–261. doi:10.1097/CAD.0b013e328011a547. PMID 17264756.
  90. ^ MacCallum, C; Gillenwater HH (July 2006). "Second-line treatment of small-cell lung cancer". Current Oncology Reports. 8 (4): 258–264. doi:10.1007/s11912-006-0030-8. PMID 17254525.
  91. ^ a b NSCLC Meta-Analyses Collaborative Group (October 2008). "Chemotherapy in Addition to Supportive Care Improves Survival in Advanced Non–Small-Cell Lung Cancer: A Systematic Review and Meta-Analysis of Individual Patient Data From 16 Randomized Controlled Trials". J. Clin. Oncol. 26 (28): 4617–25. doi:10.1200/JCO.2008.17.7162. PMC 2653127. PMID 18678835.
  92. ^ Mehra R, Treat J (2008). Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. p. 1876. ISBN 978-0-07-145739-2.
  93. ^ a b Clegg, A.; Scott, D. A.; Hewitson, P.; Sidhu, M.; Waugh, N. (January 2002). "Clinical and cost effectiveness of paclitaxel, docetaxel, gemcitabine, and vinorelbine in non-small cell lung cancer: a systematic review". Thorax. 57 (1). BMJ Publishing Group: 20–28. doi:10.1136/thorax.57.1.20. PMC 1746188. PMID 11809985.
  94. ^ Fuld AD, Dragnev KH, Rigas JR (June 2010). "Pemetrexed in advanced non-small-cell lung cancer". Expert Opin Pharmacother. 11 (8): 1387–402. doi:10.1517/14656566.2010.482560. PMID 20446853.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  95. ^ Carbone, DP; Felip E (September 2011). "Adjuvant therapy in non-small cell lung cancer: future treatment prospects and paradigms". Clinical Lung Cancer. 12 (5): 261–271. doi:10.1016/j.cllc.2011.06.002. PMID 21831720.
  96. ^ a b Le Chevalier, T (October 2010). "Adjuvant chemotherapy for resectable non-small-cell lung cancer: where is it going?". Annals of Oncology. 21 (Suppl. 7): vii196–198. doi:10.1093/annonc/mdq376. PMID 20943614.
  97. ^ Horn, L; Sandler AB; Putnam JB Jr; Johnson DH (May 2007). "The rationale for adjuvant chemotherapy in stage I non-small cell lung cancer". Journal of Thoracic Oncology. 2 (5): 377–383. doi:10.1097/01.JTO.0000268669.64625.bb. PMID 17473651.
  98. ^ Wakelee, HA; Schiller JH; Gandara DR (July 2006). "Current status of adjuvant chemotherapy for stage IB non-small-cell lung cancer: implications for the New Intergroup Trial". Clinical Lung Cancer. 8 (1). Cancer Information Group: 18–21. doi:10.3816/CLC.2006.n.028. PMID 16870041.
  99. ^ BMJ (December 2005). Clinical evidence concise : the international resource of the best available evidence for effective health care. London: BMJ Publishing Group. pp. 486–488. ISBN 1-905545-00-2. ISSN 1475-9225.
  100. ^ Souquet PJ, Chauvin F, Boissel JP, Bernard JP (April 1995). "Meta-analysis of randomised trials of systemic chemotherapy versus supportive treatment in non-resectable non-small cell lung cancer". Lung Cancer. 12 (Suppl 1): S147–54. doi:10.1016/0169-5002(95)00430-9. PMID 7551923.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  101. ^ Sörenson S, Glimelius B, Nygren P (2001). "A systematic overview of chemotherapy effects in non-small cell lung cancer". Acta Oncologica. 40 (2–3): 327–39. doi:10.1080/02841860151116402. PMID 11441939.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  102. ^ Clegg A, Scott DA, Sidhu M, Hewitson P, Waugh N (2001). "A rapid and systematic review of the clinical effectiveness and cost-effectiveness of paclitaxel, docetaxel, gemcitabine and vinorelbine in non-small-cell lung cancer". Health Technology Assessment. 5 (32): 1–195. doi:10.3310/hta5320. PMID 12065068.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  103. ^ Non-Small Cell Lung Cancer Collaborative Group (2010). Burdett, Sarah (ed.). "Chemotherapy and supportive care versus supportive care alone for advanced non-small cell lung cancer". Cochrane Database of Systematic Reviews (5). CD007309 (2nd rev.). doi:10.1002/14651858.CD007309.pub2. PMID 20464750.
  104. ^ Parikh, Ravi B.; Kirch, Rebecca A.; Smith, Thomas J.; Temel, Jennifer S. (12 December 2013). "Early specialty palliative care--translating data in oncology into practice". The New England Journal of Medicine. 369 (24): 2347–51. doi:10.1056/nejmsb1305469. PMC 3991113. PMID 24328469.
  105. ^ Kelley AS, Meier DE (August 2010). "Palliative care—a shifting paradigm". New England Journal of Medicine. 363 (8): 781–2. doi:10.1056/NEJMe1004139. PMID 20818881.
  106. ^ a b Prince-Paul M (April 2009). "When hospice is the best option: an opportunity to redefine goals". Oncology (Williston Park, N.Y.). 23 (4 Suppl Nurse Ed): 13–7. PMID 19856592.
  107. ^ Ridge, CA; McEarlean AM; Ginsberg MS (June 2013). "Epidemiology of lung cancer". Seminars in Interventional Radiology. 30 (2): 93–98. doi:10.1055/s-0033-1342949. PMC 3709917. PMID 24436524.
  108. ^ Majumder, edited by Sadhan (2009). Stem cells and cancer (Online-Ausg. ed.). New York: Springer. p. 193. ISBN 978-0-387-89611-3. {{cite book}}: |first= has generic name (help)
  109. ^ "Non-Small Cell Lung Cancer Treatment". PDQ for Health Professionals. National Cancer Institute. Retrieved 22 November 2008.
  110. ^ "Small Cell Lung Cancer Treatment". PDQ for Health Professionals. National Cancer Institute. 2012. Retrieved 16 May 2012.
  111. ^ Spiro, SG (2010). "18.19.1". Oxford Textbook Medicine (5th ed.). OUP Oxford. ISBN 978-0-19-920485-4.
  112. ^ SEER data (SEER.cancer.gov) Median Age of Cancer Patients at Diagnosis 2002–2003
  113. ^ SEER data (SEER.cancer.gov) Median Age of Cancer Patients at Death 2002–2006
  114. ^ Slatore, CG; Au DH; Gould MK (November 2010). "An official American Thoracic Society systematic review: insurance status and disparities in lung cancer practices and outcomes". American Journal of Respiratory and Critical Care Medicine. 182 (9): 1195–1205. doi:10.1164/rccm.2009-038ST. PMID 21041563.
  115. ^ "WHO Disease and injury country estimates". World Health Organization. 2009. Retrieved 11 November 2009.
  116. ^ Ferlay, Jacques; Shin, Hai-Rim; Bray, Freddie; Forman, David; Mathers, Colin; Parkin, Donald Maxwell (December 2010). "Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008". International Journal of Cancer. 127 (12): 2893–2917. doi:10.1002/ijc.25516. PMID 21351269.
  117. ^ Jemal A, Tiwari RC, Murray T; et al. (2004). "Cancer statistics, 2004". CA: A Cancer Journal for Clinicians. 54 (1): 8–29. doi:10.3322/canjclin.54.1.8. PMID 14974761. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  118. ^ Proctor, RN (March 2012). "The history of the discovery of the cigarette-lung cancer link: evidentiary traditions, corporate denial, global toll". Tobacco Control. 21 (2): 87–91. doi:10.1136/tobaccocontrol-2011-050338. PMID 22345227.
  119. ^ Lum, KL; Polansky JR; Jackler RK; Glantz SA (October 2008). "Signed, sealed and delivered: "big tobacco" in Hollywood, 1927–1951". Tobacco Control. 17 (5): 313–323. doi:10.1136/tc.2008.025445. PMC 2602591. PMID 18818225.
  120. ^ Lovato, C; Watts A; Stead LF (October 2011). "Impact of tobacco advertising and promotion on increasing adolescent smoking behaviours". Cochrane Database of Systematic Reviews. 2011 (10): CD003439. doi:10.1002/14651858.CD003439.pub2. PMC 7173757. PMID 21975739.
  121. ^ Kemp, FB (July–September 2009). "Smoke free policies in Europe. An overview". Pneumologia. 58 (3): 155–158. PMID 19817310.
  122. ^ National Cancer Institute; SEER stat fact sheets: Lung and Bronchus. Surveillance Epidemiology and End Results. 2010 [1]
  123. ^ "Gender in lung cancer and smoking research" (PDF). World Health Organization. 2004. Retrieved 26 May 2007.
  124. ^ Zhang, J; Ou JX; Bai CX (November 2011). "Tobacco smoking in China: prevalence, disease burden, challenges and future strategies". Respirology. 16 (8): 1165–1172. doi:10.1111/j.1440-1843.2011.02062.x. PMID 21910781.
  125. ^ Behera, D; Balamugesh T (2004). "Lung cancer in India" (PDF). Indian Journal of Chest Diseases and Allied Sciences. 46 (4): 269–281. PMID 15515828.
  126. ^ Charloux, A.; Quoix, E.; Wolkove, N.; Small, D.; Pauli, G.; Kreisman, H. (February 1997). "The increasing incidence of lung adenocarcinoma: reality or artefact? A review of the epidemiology of lung adenocarcinoma". International Journal of Epidemiology. 26 (1): 14–23. doi:10.1093/ije/26.1.14. PMID 9126499.
  127. ^ Kadara, H; Kabbout M; Wistuba II (January 2012). "Pulmonary adenocarcinoma: a renewed entity in 2011". Respirology. 17 (1): 50–65. doi:10.1111/j.1440-1843.2011.02095.x. PMC 3911779. PMID 22040022.
  128. ^ Morgagni, Giovanni Battista (1761). De sedibus et causis morborum per anatomen indagatis. OL 24830495M.
  129. ^ Bayle, Gaspard-Laurent (1810). Recherches sur la phthisie pulmonaire (in French). Paris. OL 15355651W.
  130. ^ a b Witschi, H (November 2001). "A short history of lung cancer". Toxicological Sciences. 64 (1): 4–6. doi:10.1093/toxsci/64.1.4. PMID 11606795.
  131. ^ Adler, I (1912). Primary Malignant Growths of the Lungs and Bronchi. New York: Longmans, Green, and Company. OCLC 14783544. OL 24396062M., cited in Spiro SG, Silvestri GA (2005). "One hundred years of lung cancer". American Journal of Respiratory and Critical Care Medicine. 172 (5): 523–529. doi:10.1164/rccm.200504-531OE. PMID 15961694.
  132. ^ Grannis, FW. "History of cigarette smoking and lung cancer". smokinglungs.com. Archived from the original on 18 July 2007. Retrieved 6 August 2007.
  133. ^ Proctor, R (2000). The Nazi War on Cancer. Princeton University Press. pp. 173–246. ISBN 0-691-00196-0.
  134. ^ Doll, R; Hill AB (November 1956). "Lung Cancer and Other Causes of Death in Relation to Smoking". British Medical Journal. 2 (5001): 1071–1081. doi:10.1136/bmj.2.5001.1071. PMC 2035864. PMID 13364389.
  135. ^ US Department of Health Education and Welfare (1964). "Smoking and health: report of the advisory committee to the Surgeon General of the Public Health Service" (PDF). Washington, DC: US Government Printing Office.
  136. ^ a b Greaves, M (2000). Cancer: the Evolutionary Legacy. Oxford University Press. pp. 196–197. ISBN 0-19-262835-6.
  137. ^ Greenberg, M; Selikoff IJ (February 1993). "Lung cancer in the Schneeberg mines: a reappraisal of the data reported by Harting and Hesse in 1879". Annals of Occupational Hygiene. 37 (1): 5–14. doi:10.1093/annhyg/37.1.5. PMID 8460878.
  138. ^ Samet, JM (April 2011). "Radiation and cancer risk: a continuing challenge for epidemiologists". Environmental Health. 10 (Suppl. 1): S4. doi:10.1186/1476-069X-10-S1-S4. PMC 3073196. PMID 21489214.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  139. ^ Horn, L; Johnson DH (July 2008). "Evarts A. Graham and the first pneumonectomy for lung cancer". Journal of Clinical Oncology. 26 (19): 3268–3275. doi:10.1200/JCO.2008.16.8260. PMID 18591561.
  140. ^ Edwards, AT (1946). "Carcinoma of the Bronchus". Thorax. 1 (1): 1–25. doi:10.1136/thx.1.1.1. PMC 1018207. PMID 20986395.
  141. ^ Kabela, M (1956). "Erfahrungen mit der radikalen Röntgenbestrahlung des Bronchienkrebses" [Experience with radical irradiation of bronchial cancer]. Ceskoslovenská Onkológia (in German). 3 (2): 109–115. PMID 13383622.
  142. ^ Saunders, Michele; Dische, Stanley; Barrett, Ann; Harvey, Angela; Gibson, Della; Parmar, Mahesh (July 1997). "Continuous hyperfractionated accelerated radiotherapy (CHART) versus conventional radiotherapy in non-small-cell lung cancer: a randomised multicentre trial". Lancet. 350 (9072). Elsevier: 161–165. doi:10.1016/S0140-6736(97)06305-8. PMID 9250182.
  143. ^ Lennox, S.C.; Flavell, Geoffrey; Pollock, D.J.; Thompson, Vernonc.; Wilkins, J.L. (November 1968). "Results of resection for oat-cell carcinoma of the lung". Lancet. 2 (7575). Elsevier: 925–927. doi:10.1016/S0140-6736(68)91163-X. PMID 4176258.
  144. ^ Miller, AB; Fox W; Tall R (September 1969). "Five-year follow-up of the Medical Research Council comparative trial of surgery and radiotherapy for the primary treatment of small-celled or oat-celled carcinoma of the bronchus". Lancet. 2 (7619). Elsevier: 501–505. doi:10.1016/S0140-6736(69)90212-8. PMID 4184834.
  145. ^ Cohen, M. H.; Creaven, P. J.; Fossieck Jr, B. E.; Broder, L. E.; Selawry, O. S.; Johnston, A. V.; Williams, C. L.; Minna, J. D. (1977). "Intensive chemotherapy of small cell bronchogenic carcinoma". Cancer Treatment Reports. 61 (3): 349–354. PMID 194691.{{cite journal}}: CS1 maint: date and year (link)

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