International Conference on Frontiers in Lung Cancer November 16-17, 2020 Brisbane, Australia

Only a fraction of cigarette smokers develops lung cancer, suggesting that people differ in their susceptibility to this disease. We investigated whether differences in DNA Repair Capacity (DRC) for repairing tobacco carcinogen-induced DNA damage are associated with differential susceptibility to lung cancer.

Small cell lung cancer (SCLC) makes up less than 20% of lung cancers and is typically caused by tobacco smoking. It often starts in the bronchi, then quickly grows and spreads to other parts of the body, including the lymph nodes.

Non-small cell lung cancer (NSCLC) makes up about 85% of diagnosed lung cancers. These includes all kinds of epithelial lung cancer excluding the small cell lung carcinoma types and are generally more insensitive to chemotherapy.

 Risk factors increase an individual’s chance of developing cancer. Risk factors for lung cancer includ

Tobacco smoking

Contact with radon,

asbestos or other cancer-causing agents

Personal history of smoking related cancer

Family history of lung cancer

Lung cancer symptoms may include chronic cough, breathing changes, chest ache, wheezing, hoarse voice, tiredness, weight loss, headache and even bone pain. In certain chronic lung diseases, people with lung cancer don't have symptoms until the cancer is advanced.

 Lung disease ranges from bronchitis and pneumonia to pulmonary hypertension. Lung function tests and X-rays are used to diagnosis the problem. Many symptoms can be eased with proper treatment. If not treated they may directly or indirectly lead to lung cancer.

Alpha-1 antitrypsin lack (Alpha1-antitrypsin insufficiency, A1AD, or AATD) is a hereditary issue that causes faulty creation of alpha-1 antitrypsin (A1AT), prompting diminished A1AT movement in the blood and lungs, and affidavit of intemperate irregular A1AT protein in liver cells leading to lung illness and liver infection. Influenced people frequently develop emphysema, which is a lung infection caused by damage to alveoli. Alpha-1 antitrypsin deficiency (A1AD or AATD) is a genetic disorder that may result in lung disease or liver disease. Onset of lung problems is typically between 20 and 50 years old. This may result in shortness of breath, wheezing, or an increased risk of lung infections.

Genetic mutations that are known to play critical roles in the development and progression of NSCLC include:

•  Epidermal growth factor receptor (EGFR) – the EGFR gene is responsible for a protein that helps a cell respond to its environment and can trigger cell growth, division, and survival.
•  KRAS – the KRAS gene is involved in regulating cell division.
•  Anaplastic lymphoma kinase (ALK) – the ALK gene provides instructions for a protein that plays an important role in cell growth, division, and maturation.
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ARDS, or acute respiratory distress syndrome, is a lung condition that leads to low oxygen levels in the blood. ARDS can be life threatening because organs, such as the kidneys and brain, need oxygen-rich blood to work properly. Most people who develop ARDS are in the hospital for other serious health problems. Rarely, people who aren't hospitalized have health problems that lead to ARDS, such as severe pneumonia. Causes of ARDS includes infections, injuries, or other conditions that cause the lung's tiny blood vessels to leak more fluid than normal into the lungs' air sacs. This prevents the lungs from filling with air and moving enough oxygen into the bloodstream.

 The implementation of molecular biomarkers in routine practice continues to be challenging. First, physicians must know which biomarkers should be analyzed in routine practice and be aware that additional markers may soon become standard. In this context, regularly updated guidelines can support physicians in their decisions. Nevertheless, clinical implementation of molecular biomarkers may differ among regions based on prevalence of the biomarker, availability of test methods, and access to corresponding treatments.