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There are many different subclasses of lung cancer if meticulously observed under the light microscope, but only the SCLC (small cell lung cancer) and the non-SCLC are the most distinguishable. Based upon the histological behavior, the SCLC, a neuroendocrine (receives neural input and releases molecular messages (hormones) on the bloodstream) lesion, is almost completely a different tissue or cell than that of the non-SCLC. Highly aggressive and metastatic even in early stages, chemotherapy and radiotherapy can only achieve short term positive response. Even surgical resections as a means of intervention are rare due to its highly metastatic nature.
SCLC is usually located at the central bronchus or in a large bronchus with branching lesions. The tumor grows aggressively and invades surrounding structures and tissues. It obstructs the airway and can asphyxiate the patient in severe cases.
SCLC origin is strongly associated with smoking cigarettes and there is substantial evidence regarding molecular mutations in the formation of SCLC. Neuroendocrines are major components of these SCLC and supposedly auto regulates the growth factors of the cell. In SCLC, the auto regulations of hormone release have been compromised and never cease sending growth hormonal signals. With the understanding of genetics and small cell lung cancer treatment, patients will then have a fighting chance for survival.
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Genes Linked with SCLC
The TSG (tumor necrosis factor-inducible gene or TNF-stimulated gene) p53 which is responsible for tumor suppression have been mutated and inactivated in more than 90% of SCLC cases. Again, with the inactivation of the TSG p53 tumor suppressing gene, the uncontrolled cell growth becomes prevalent and eventually leads to SCLC.
Thru the use of gene specific probes, the regions encoding MYCL, MYCN, and MYC genes are amplified in SCLC patients. This suggests a regulatory failure of the MYC family gene functions and relates to the pathogenesis of SCLC. MYC genes controls cell proliferation by encoding transcription factors and that influences the growth-promoting gene’s activity.
RB1 is another gene most likely involved with the proliferation of SCLC. There two negative progression gene regulators in the sequence towards the G1 phase of the cell cycle - RB1 and CDKN2A. The CDKN2A byproduct (cyclin dependent kinase inhibitor p16) is retained in SCLC, but RB1’s byproduct (the retinoblastoma protein, pRB) is not. So, with the missing pRB protein in SCLC, tumor cells are not inactivated during mutations.
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Medical Interventions for SCLC
Treatment of choice for SCLC is chemotherapy where there is a response rate of about 50-90% depending on patient’s tolerance to chemotherapy and stage of the disease. On severe cases, platinum containing combination therapy is administered up to six cycles. In case of relapse, chemotherapy is given again, but with less success rate. Examples of these OTC (over the counter) drugs for chemotherapy include; Topotecan, Cisplatin, Platinol-AQ , Blastolem , Tecnoplatin, and Hycamtin . If caught in the early stages, a combination of chemotherapy and prophylactic cranial irradiation therapy are utilized for management of the disease. Surgical resection may be used on rare cases, but usually advisable only in the early stages of the disease where tumor cells are still localized. With better understanding of genetics and small cell lung cancer treatment, the patient’s condition can be improved.