Lung Cancer Causes - Pathogenesis

Lung Cancer Causes - Pathogenesis

Patogenesis lung cancer like cancer of the other, starting early diinduksi agent events of a long period promotion and progress in the process of multi steps. Smoking is started and promote karsinogenesis. The initiation done soon to change the same genetic between smokers and ex-event (z 3P removal of mutated p53), as proven. The smoke thus causing the "effect field" epitel lungs, populations of large cells starting distribution and the increase in the probability transformation. Keep exposure smoke tobacco has been allowed to accumulate mutations extra because of irritating the chronics and promoters in cigarette smoke (amount of nicotine's formalin for example., Is phenol) promotion because. The time delay between smoking and cancer, the early beginning is usually long and requires 20-25 years to the development of cancer. Reduce the risk of cancer after quitting smoking, but cells getting there can flourish. If karsinogen else continue with process.

SCLC and NSCLC were treated different, because it (i) comes from the cells are different, (ii) undergo the process of patogenesis different and (iii) to accumulate genetic mutations are different. SCLC carries frequent mutations in c-KIT, p53 and R.B., while often NSCLC, MYC, Bcl2, mutations EGFR, KRAS, CD44 and p16. This is all well onkogen or gen supresor tumor. See genetics and biology chapter cancer cancer for an explanation of how a mutation like this can cause cancer.

Similar to a lot of cancer other lung cancer begins with the activation onkogen or inaktivasi gen supresor tumor. Karsinogen causing mutation on the gene this causes the development of cancer. Mutation in K-ras proto-onkogen responsible for 10-30% of adenokarsinoma the lungs. About 4% of cancer cell lung non-small involving gene fusion EML4-ALK tyrosine kinase. Change epigenetik - like changes metilasi DNA, modification of histon tails or rules microRNA - it can cause inaktivasi gen supresor tumor. Reseptor to reseptor factor the growth of epidermal (EGFR) regulates proliferation of cells, apoptosis, angiogenesis and invasion of tumor. Mutation and amplifikasi EGFR are common in cell karsinoma lung non-small, and give the basis for treatment with inhibitor EGFR. HER2 / neu is influenced more rare. genes other that is often mutated or amplified are c-MET, NKX2-1, LKB1, PIK3CA, and BRAF. Line cells is not fully understood origin. The mechanism might include activation abnormal stem cells. In stem cells the drains breath proksimal express keratin 5 are more likely to be affected, usually causing karsinoma sel skuamosa the lungs. In the air central, the stem cells involved the club cells and the cells neuroepithelial who expressed protein cell sekretori club. Karsinoma sel small lungs that can be derived from the line cell or cell neuroendokrin and can express CD44. Metastasis of lung cancer requires transition from epitel to cell types mesenchymal. This problem can happen with the path signal activated Akt / GSK3Beta, MEK-ERK, Fas and Par6.