European Journal of Clinical Oncology

The Study of Lung Cancer

Jennie Jones^{* *}Correspondence: Jennie Jones, Editorial office, Clinical Oncology, Belgium, Email:

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Introduction

Small Cell Lung Carcinoma (SCLC) and Non-Small Cell Lung Carcinoma (NSCLC) kinds of squamous cell carcinoma, adenocarcinoma (including the noninvasive variety of bronchioloalveolar carcinoma), and large cell carcinoma are all histological types of lung cancer. Lung malignancies can develop in the major bronchi (central tumours) or the minor bronchi, bronchioles, or alveoli (peripheral tumours) of the lung's distant airway. Adenocarcinomas and large cell carcinomas normally start in the periphery, whereas squamous cell carcinomas and SCLCs start in the center. The particular respiratory epithelial cell type from which each lung cancer type arises, however, has yet to be determined. Researchers believe lung tumours develop following a series of gradual pathological alterations known as preneoplastic or premalignant lesions, similar to other epithelial malignancies. Although the sequence of preneoplastic alterations in centrally originating squamous carcinomas of the lung has been identified, the other major types of lung malignancies have been poorly described. Although several molecular abnormalities have been identified in clinically apparent lung malignancies, little is understood about the molecular events that precede lung carcinoma development and the underlying genetic foundation of lung carcinogenesis. Several research published in the previous decade have shed light on the molecular characterization of preneoplastic alterations involved in the aetiology of lung cancer, particularly squamous cell carcinoma and adenocarcinoma. Many of these molecular alterations have been found in smokers' normally histologically normal respiratory mucosa. Heavy smokers and individuals who have survived an upper aerodigestive tract cancer are among the high-risk groups targeted for early detection efforts. Traditional morphologic approaches for identifying premalignant cell populations in the pulmonary airways, on the other hand, have significant limitations.

This has led to research into the biological features of the respiratory epithelium and its related preneoplastic cells and lesions, including molecular and genetic modifications. More research in this area could lead to novel approaches for predicting the risk of invasive lung cancer in smokers, as well as early detection and monitoring of their response to chemopreventive treatments.

Lung cancer is the most prevalent main cancer cause of death and incidence worldwide. Lung cancer is expected to account for more than 169,500 new cases and more than 157,400 cancer deaths in the United States in 2001. Although the incidence of lung cancer in men began to fall in the early 1980s in the United States,124 it continues to rise in women. Histology or cytology can be used to provide a pathologic diagnosis of lung cancer. The histology of lung cancer is the topic of this review. Bronchoscopic or needle biopsies, as well as surgical biopsy procedures such as thoracoscopy, excisional wedge biopsy, lobectomy, or pneumonectomy, may be used for histologic examination for lung cancer diagnosis. In almost all cases, light microscopy is sufficient for lung cancer diagnosis, with only a few histologic types requiring histochemical stains or immunohistochemistry. The World Health Organization (WHO) and the International Association for the Study of Lung Cancer have recommended an international standard for histologic classification of lung tumours. Squamous cell carcinoma, adenocarcinoma, small cell carcinoma (SCLC), and large cell carcinoma are the four major histologic forms of lung cancer. These basic forms can be further divided into subcategories, such as the bronchioloalveolar carcinoma (BAC) adenocarcinoma variation. More comprehensive reviews of lung cancer pathology, cytology, and molecular biology can be found elsewhere. Although lung cancer has several subtypes, the differentiation between SCLC and non–small cell lung carcinoma is the most crucial (NSCLC). This is due to the significant clinical disparities in presentation, metastatic dissemination, and therapeutic response. Histologic heterogeneity, which is a variety of histologic types that represents a manifestation of lung cancer's derivation from a pluripotent stem cell, is another key hallmark of lung cancer pathology. For these reasons, when the histologic subtype of a tiny tissue samples cannot be determined, it is permissible to use the term NSCLC [1-3]. The foundation for primary and secondary illness prevention is epidemiologic evidence. To track the prevalence of disease, assess natural history, and find disease drivers, epidemiologic approaches are applied. Epidemiologic methodologies are also used to analyse the benefits of intervention programmes, whether they are based on risk factor interventions or screening. Routine mortality statistics for lung cancer have validated the clinical sense that the disease became more common in the first half of the twentieth century. In research published from the 1950s to the present, case-control and cohort studies, the epidemiologic study designs used to investigate exposure-disease correlations, causally linked smoking to lung cancer. As we've tracked lung cancer incidence and mortality rates, it's become clear that they're on the rise. The conclusion that smoking causes lung cancer is unassailably supported by epidemiologic evidence and a complementary scientific understanding of respiratory carcinogenesis. Patient care is also influenced by epidemiologic studies; as trained doctors weigh alternate diagnoses based on the risk factor profiles of their patients [4]. Several historic breakthroughs have occurred over the century, but none has been more significant than Sir Richard Doll and Austin Hill's groundbreaking study, published in the British Medical Journal in 1950, which proved suspicions that cigarette smoking was linked to lung cancer. The significance of this piece cannot be overstated, as smoking rates were at an all-time high in the United States and Europe following WWII, physicians were shown endorsing smoking in cigarette commercials, and the tobacco industry's claims that smoking was safe went uncontested. The second seminal document was the 1964 report by the United States Surgeon General, which said that smoking was damaging to one's health and that efforts should be made to avoid or quit the habit. Since that publication, smoking rates have decreased, with a proportional fall in lung cancer rates lagging 20 years behind. While lung cancer rates in the United States were less than 5 per 100,000 at the turn of the century, by 1998, the age-adjusted mortality rate per 100,000 populations for men had risen to 77.2 in Belgium and 75.5 in Scotland, with the ten countries with the highest rates all being in Europe.

The ten countries with the lowest male mortality rates were mostly in South America and Asia. The most alarming trend is the rapidly spreading epidemic in emerging countries. In 1985, it was estimated that 921,000 people died from lung cancer over the world, up 17 percent from 1980. Lung cancer rates in Africa in 1994 were equivalent to those in the United States in the 1930s, according to the International Agency for Research on Cancer in France. By 1999, the rate of lung cancer in men in poor nations was 14.1 per 100,000 and increasing, compared to 71.4 per 100,000 and decreasing in rich countries. In underdeveloped countries, the lung cancer rate for women is 5.1 per 100,000, compared to 21.2 per 100,000 in developed ones. The true prevalence of lung cancer in underdeveloped countries will be underestimated since many cases go undetected or unreported in areas where health care is scarce. In the United States, squamous cell carcinoma accounts for roughly 20% of all lung malignancies. In the past, two-thirds of squamous cell carcinomas manifested as central lung tumours, whereas the remaining third presented as peripheral lung tumours. Recent findings, however, show that a growing number of squamous cell carcinomas are discovered in the periphery, with some studies reporting as high as 50%. Intercellular bridging, squamous pearl formation, and individual cell keratinization are morphologic traits that show squamous differentiation. These characteristics are easily visible in well-differentiated tumours, whereas they are difficult to spot in poorly differentiated tumours. Squamous cell carcinoma most commonly develops in segmental bronchi, but it can also affect the lobar and mainstem bronchi. Papillary, clear cell, small cell, and basaloid subtypes of squamous cell carcinoma exist. This subtyping, however, requires revision because it does not adequately address the morphologic spectrum of lung squamous cell carcinoma appearances and does not allow for meaningful linkages with clinical, prognostic, or molecular aspects. The small cell variant, for example, should definitely be dropped because most of these instances are basaloid variants, and the phrase small cell causes confusion with actual small cell carcinoma. Exophytic endobronchial development is common in papillary squamous cell carcinomas [5]. Epidemiologic research on lung cancer has increased in frequency in the four decades after the 1964 Surgeon General's report. While cigarette smoking has long been a key issue, additional reasons have been investigated, and much research has been focused on environmental and genetic factors that may influence smoking risk. In 1981 the first large epidemiologic research on passive smoking and lung cancer were published, and since then, more than 50 papers have been published on the subject.

Researchers have been studying genetic factors of lung cancer risk for several decades, and much of the current epidemiologic research is based on a hybrid methodology called molecular epidemiology, which combines laboratory and population research approaches. Because of the still tragically high case fatality rate of patients with lung cancer, trends in population prevalence of cigarette smoking substantially predict lung cancer incidence and mortality rates, which closely follow incidence. From the publishing of the 1964 Surgeon General's report until around 1990, when the frequency of cigarette smoking in males levelled off at around 25%, the prevalence of cigarette smoking in males dropped steadily in the United States. Female smoking prevalence in the United States levelled out around the same time and at the same level as male smoking prevalence. The historical trends in smoking prevalence in the United States thus explain past changes in lung cancer rates as well as current rates, while also serving as a good predictor of future occurrence. According to current smoking prevalence patterns, lung cancer mortality rates will continue to decline until around 2020, assuming a 30-year lag between population smoking patterns and subsequent lung cancer incidence, and then stabilise, reflecting the current, relative stability of smoking prevalence. By 2030, lung cancer cases will no longer be dominated by men, but will comprise an equal number of men and women, reflecting the current smoking pattern. This prognosis is a compelling reason to keep up the fight against cigarette use [6].

References

1. Wistuba, Ignacio I., and Adi F. Gazdar. "Lung cancer preneoplasia." Annu Rev Pathol Mech Dis 1 (2006): 331-348.

   [Google Scholar]     [Cross Ref]

2. Alberg, Anthony J., and Jonathan M. Samet. "Epidemiology of lung cancer." Chest 123.1 (2003): 21S-49S.

   [Google Scholar]     [Cross Ref]

3. Spiro, Stephen G., and Gerard A. Silvestri. "One hundred years of lung cancer." Am J Respir Crit Care Med 172.5 (2005): 523-529.

   [Google Scholar]     [Cross Ref]

4. Travis, William D. "Pathology of lung cancer." Clin Chest Med 32.4 (2011): 669-692.

   [Google Scholar]   [Cross Ref]

5. Travis, William D. "Pathology of lung cancer." Clin Chest Med 23.1 (2002): 65-81.

   [Google Scholar]  [Cross Ref]

6. Alberg, Anthony J., Malcolm V. Brock, and Jonathan M. Samet. "Epidemiology of lung cancer: looking to the future." J Clin Oncol 23.14 (2005): 3175-3185.

   [Google Scholar]     [Cross Ref]