LUNG CARCINOMA
National Institute for Health and Clinical Excellence's
guideline: Referral guidelines for suspected lung cancer -
http://www.prodigy.nhs.uk/ProdigyKnowledge/Guidance/GuidanceView.aspx?GuidanceId=37418
Lung Cancer: a comprehensive overview -
http://en.wikipedia.org/wiki/Lung_cancer
Lung Cancer: a comprehensive overview -
http://www.emedicine.com/med/topic1333.htm
Lung Cancer: a comprehensive overview -
http://www.cancer.gov/cancerinfo/wyntk/lung
CG24 Lung cancer: NICE guideline -
http://www.nice.org.uk/page.aspx?o=cg024niceguideline
CG24 Lung cancer: Full guideline -
http://www.nice.org.uk/page.aspx?o=cg024fullguideline
CG24 Lung cancer: Full guideline, appendices -
http://www.nice.org.uk/page.aspx?o=244782
CG24 Lung cancer: Quick reference guide -
http://www.nice.org.uk/page.aspx?o=cg024quickrefguide
American Society of Clinical Oncology (ASCO) Patient Guide:
Advanced Lung Cancer Treatment -
http://www.plwc.org/plwc/MainConstructor/1,1744,_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 -
http://www.plwc.org/plwc/MainConstructor/1,1744,_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 -
http://www.cancerindex.org/geneweb/X1501.htm#lung
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 -
http://carcin.oxfordjournals.org/cgi/content/full/20/8/1403
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 -
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=99270009&dopt=Abstract
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 -
http://www3.interscience.wiley.com/cgi-bin/fulltext/65501315/HTMLSTART
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 -
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16459173&itool=iconabstr&query_hl=6&itool=pubmed_docsum
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 -
http://cancerres.aacrjournals.org/cgi/content/full/66/4/2116
Screening for lung cancer:
National Cancer Institute (NCI): Lung Cancer Screening -
http://www.cancer.gov/cancertopics/pdq/screening/lung/Patient/page3
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 -
http://www.cancer.gov/newscenter/NLSTQA
National Cancer Institute (NCI): Chest X-Rays Can Detect Early Lung Cancer But
Also Can Produce Many False-Positive Results -
http://www.nih.gov/news/pr/dec2005/nci-20.htm
Statistics:
National Centre for Chronic Disease Prevention
and Health Promotion: Lung Cancer Statistics -
http://www.cdc.gov/lungcancer/statistics/
Measures:
Overview of different investigative
modalities:
Questionnaires:
C-reactive protein:
CT
scan Chest:
Positron Emission Tomography (PET Imaging):
Plain X-Ray Chest:
Chest MRI:
Bone scintigraphy:
Bronchoscopy:
Mediastinoscopy with biopsy:
Percutaneous Transthoracic Needle Aspiration:
Pleural needle biopsy:
Document Author: Dr. Fazal Danish
Document Created: 8th May 2006
Document Edits: