Cancer is an umbrella term covering more than types of different diseases. These diseases are usually described as an uncontrolled growth and spread of abnormal cells in the body. Broadly cancer can be divided into two categories — carcinomas cancers that originate in epithelial cells and sarcomas cancer that originates in connective tissue.
NSCLC is further divided histologically into three main disease subtypes of: Whilst in certain countries, adenocarcinoma is now the most common disease subtype seen, in other countries, whilst the relative frequency of adenocarcinoma is rising, squamous cell carcinoma still predominates.
Clinics and Pathology Etiology The smoking of tobacco is the primary cause of lung cancer and patterns of occurrence are largely determined by historical exposure.
In general, the contribution of genetic or other environmental factors to lung cancer risk is thought to be small but some may synergise with smoking.
Such additional environmental factors include exposure to radon gas an indoor environmental pollutantworkplace exposures to inorganic fibres asbestos or toxic chemical entities, air pollution and ionising radiation.
As for many cancers, poor diet appears to be associated with increased disease risk.
Epidemiology Smoking increases the risk of all histological subtypes but is most strongly associated with squamous cell and small cell disease. Adenocarcinoma is more common in women than in men and more common in non-smokers with disease than smokers.
The number of cases attributable to tobacco smoking varies between countries and regions depending on the historical levels of smoking for those regions. The observation that perhaps only of every 10 smokers develops clinical lung cancer during their lifetime has been used as an argument to suggest that some level of genetic predisposition modifies disease risk.
Whilst this argument is perhaps not compelling, it is not unreasonable and indeed a small number of genetic polymorphisms have been associated with modest increases in lung cancer risk.
As lung cancer is usually caused by a chronic exposure of the bronchial epithelium to multiple procarcinogenic and carcinogenic agents, it is not surprising that many of these polymorphisms lie in genes associated with the activation cytochrome Ps or deactivation Glutathione S-transferases of such entities or the repair of subsequently induced damage TP In general, epidemiological analysis has not suggested the existence of highly-penetrant, strongly-predisposing lung cancer associated genetic variants.
Clinics In the early stages of disease, lung cancer tends to be asymptomatic. The potential benefits and costs of CT screening for the detection of early, asymptomatic lung cancer are currently being evaluated in large randomised trials in several countries.
Pathology Tumours are classified primarily on their cytological appearance. The relative frequency of subtypes varies in different regions and the figures cited therefore represent broad approximations. Small cell tumours metastasise very early in the course of the disease but are relatively responsive to chemotherapeutic drugs: Lung cancers are generally heterogeneous, consisting frequently of cells of different histological subtypes.
Pathological classifications therefore emphasise the major cell type present in the tissue analysed and may note significant minor components. When components are roughly equal, designations such as adenosquamous carcinoma may be used.
This common intra-tumour heterogeneity has led to the suggestion that lung carcinomas arise from a multipotent stem cell-like or stem cell component of the bronchial epithelium.
Whilst microarray analyses have shown that gene expression can be used effectively to subdivide disease into existing or novel subtypes, it has also highlighted the similarity that lies between these subtypes at the level of gene expression. Such observations are consistent with a common stem cell progenitor.
This is therefore to some extent a default classification, made when other specific histology has been excluded. They mostly arise centrally in a large bronchus and are highly invasive and highly metastatic.
Treatment Before the appropriate treatment can be defined a careful staging of the disease must be made. SCLC is very seldom surgically resectable, usually widespread at presentation and is generally both more chemosensitive and radiosensitive. Stage I-II are usually resected adjuvant chemotherapy can be discussed with the patient and locally advanced stages III are treated by combined modality treatments neoadjuvant chemotherapy, resection if stage IIIA or radiotherapy.
If overt distant metastases are detected, therapy is palliative and chemotherapy has been shown to improve median survival and quality of life.
If the tumour is confined to one hemithorax limited diseasea combined modality therapy chemo- and radiotherapy is indicated: New therapies based on an improved understanding of the molecular basis of the disease are currently in use or are under development.
For example, Gefitinib, a tyrosine kinase inhibitor, is one such example that has been launched on the market in different countries for patients with relapsed or refractory NSCLC after chemotherapy.
Further drugs with other defined molecular targets are anticipated. Prognosis Once a diagnosis of lung cancer has been made biopsy, cytology the disease is staged I - IV according to established international criteria.
This is a combined grading incorporating tumour size and location Tlymph node involvement N and presence of distant metastasis M. Loss of chromosome 3 sequence appears to occur frequently at the very earliest stages of neoplastic transformation, when epithelial cells may show no evidence of morphological alteration.
Note The loss of p53 function, generally through mutation of the coding sequence is seen in the majority of lung carcinomas. Microarray analyses have shown that many other genes show dramatic differences in expression between lung tumours and normal lung tissue. These differences may be driven by tumour gene amplification, deletion, control region mutation or chromosomal translocation all apparently relatively rare in primary disease or perhaps more commonly, may be associated with changes in various types of epigenetic modification of the DNA sequence.
The differential expressions may be disease-related in the sense that they are induced directly by DNA damage events in the tumour cell, or they may be only indirectly linked to the disease, in the sense that they are typical of the gene expression patterns of progenitor cells and atypical for the majority of normally differentiated lung cells.Fluorescence Digital Image Gallery Human Lung Carcinoma Cells (A Line) The A cell line was originally cultivated in by D.
J. Giard, along with several collaborators, from the human lung carcinoma of a year-old Caucasian male. Lung cancer is a leading cause of cancer-related deaths worldwide. Lung cancer risk factors, including smoking and exposure to environmental carcinogens, have been linked to chronic inflammation.
An integral feature of inflammation is the activation, expansion and infiltration of diverse immune cell. Carcinoma is a type of cancer that develops from epithelial cells. Specifically, a carcinoma is a cancer that begins in a tissue that lines the inner or outer surfaces of the body, and that arises from cells originating in the endodermal, mesodermal  or ectodermal germ layer during embryogenesis.
14 Frederick, BA, Helfrich, BA, Coldren, CD et al. Epithelial to mesenchymal transition predicts gefitinib resistance in cell lines of head and neck squamous cell carcinoma and non-small cell lung carcinoma.
of Paclitaxel(Taxol) resistance in lung cancer cells, iv) Analyzing the response of lung cancer cells to Smoothened Inhibitors and v) Determining the effects of Transforming Growth Factor Beta-1(TGF-1) induced Epithelial to Mesenchymal Transition(EMT) in lung cancer cells.
Introduction. Lung cancer kills more than , individuals in the United States annually. Reduction of lung cancer–related mortality may be achieved by identification and treatment of higher risk individuals with effective cancer-preventive agents.