National Institute for Health and Clinical Excellence's guideline: Referral guidelines for suspected lung cancer -

Lung Cancer: a comprehensive overview -

Lung Cancer: a comprehensive overview -

Lung Cancer: a comprehensive overview -

CG24 Lung cancer: NICE guideline -

CG24 Lung cancer: Full guideline -

CG24 Lung cancer: Full guideline, appendices -

CG24 Lung cancer: Quick reference guide -

American Society of Clinical Oncology (ASCO) Patient Guide: Advanced Lung Cancer Treatment -,1744,_12-001129-00_14-00Patient%20Guides-00_17-001029-00_18-0031414-00_19-0031415-00_20-001-00_21-008,00.asp

American Society of Clinical Oncology (ASCO) Patient Guide: Preventing and Treating Nausea and Vomiting Caused by Cancer Treatment -,1744,_12-001129-00_14-00Patient%20Guides-00_17-001029-00_18-008042-00_19-0024556-00_20-001-00_21-008,00.asp

Lung Cancer Genetics:

Cancer Genetics Web: Molecular biology of the lung cancer -

How many tumour suppressor genes are involved in human lung carcinogenesis? To date, only a limited number of tumour suppressor genes have been identified as being inactivated in lung cancer. The p53 and RB genes are frequently inactivated by genetic alterations such as chromosomal deletions and loss-of-function mutations, while the p16 gene is inactivated not only by genetic alterations but also by transcriptional silencing due to hypermethylation. Recently, it was shown that the FHIT gene encompassing the chromosomal fragile site, FRA3B, is also inactivated in a large proportion of lung cancers. Studies on the inherited susceptibility to lung cancer in mice have also indicated the presence of additional tumour suppressor genes for lung cancer -

Is there a genetic basis for lung cancer susceptibility? The major risk factor for lung cancer is exposure to tobacco smoke. Exposure to radon, heavy metals used in smelting, and asbestos also greatly increase risks for lung cancer. However, only about 11% of tobacco smokers ultimately develop lung cancer, suggesting that genetic factors may influence the risk for lung cancer among those who are exposed to carcinogens. Further support for this hypothesis is provided by several epidemiological studies and also from molecular epidemiological studies -


Molecular epidemiology of human cancer risk: gene-environment interactions and p53 mutation spectrum in human lung cancer: The p53 tumour suppressor gene is at the crossroads of a network of cellular pathways including cell cycle checkpoints, DNA repair, chromosomal segregation, and apoptosis. These pathways have evolved to maintain the stability of the genome during cellular stress. The high frequency of p53 mutations in human cancer is a reflection of the importance of p53 involvement in this network of pathways during human carcinogenesis. The focus of this review is on the role of p53 and cancer susceptibility genes in the molecular pathogenesis and epidemiology of human lung cancer -

An update on the role of epidermal growth factor receptor inhibitors in non-small cell lung cancer: Within the past 2 years, epidermal growth factor receptor (EGFR) inhibitors have moved from experimental agents to approved drugs for the management of advanced non-small cell lung cancer (NSCLC). The identification of mutations in the ATP-binding domain of the EGFR that predict for dramatic responses introduces the possibility of truly individualized therapy in a subset of advanced NSCLC patients. The fact that these mutations may be more prevalent in certain patient populations, including patients of Asian ethnicity, female gender, and never-smoker status, raises intriguing questions regarding the pathogenesis of lung cancer. Numerous questions have arisen regarding how to best incorporate EGFR-targeted agents into patient management, as well as the role of the clinical laboratory in these decisions and the design of future trials -

Multiple Oncogenic Changes (K-RASV12, p53 Knockdown, Mutant EGFRs, p16 Bypass, Telomerase) Are Not Sufficient to Confer a Full Malignant Phenotype on Human Bronchial Epithelial Cells: The researchers of this study have evaluated the contribution of three genetic alterations (p53 knockdown, K-RASV12, and mutant EGFR) to lung tumorigenesis using human bronchial epithelial cells (HBEC) immortalized with telomerase and Cdk4-mediated p16 bypass. The study results indicate that (a) the HBEC model system is a powerful new approach to assess the contribution of individual and combinations of genetic alterations to lung cancer pathogenesis; (b) a combination of four genetic alterations, including human telomerase reverse transcriptase over expression, bypass of p16/RB and p53 pathways, and mutant K-RASV12 or mutant EGFR, is still not sufficient for HBECs to completely transform to cancer; and (c) EGFR tyrosine kinase inhibitors inhibit the growth of preneoplastic HBEC cells, suggesting their potential for chemoprevention -

Screening for lung cancer:

National Cancer Institute (NCI): Lung Cancer Screening -


National Cancer Institute (NCI): National Lung Screening Trial - The National Lung Screening Trial (NLST), a cancer screening clinical trial, will compare two ways of detecting lung cancer: spiral computed tomography (CT) and standard chest x-ray -


National Cancer Institute (NCI): Chest X-Rays Can Detect Early Lung Cancer But Also Can Produce Many False-Positive Results -


National Centre for Chronic Disease Prevention and Health Promotion: Lung Cancer Statistics -


Overview of different investigative modalities:


C-reactive protein:

CT scan Chest:

Positron Emission Tomography (PET Imaging):

Plain X-Ray Chest:

Chest MRI:

Bone scintigraphy:


        Bone scan -

       Bone scan: Using nuclear medicine to find bone abnormalities -


Plain X-Ray Bone:


Mediastinoscopy with biopsy:

Percutaneous Transthoracic Needle Aspiration:

Pleural needle biopsy:

Document Provenance and History

Document Author: Dr. Fazal Danish

Document Created: 8th May 2006

Document Edits: