Lung Cancer and its Relation to Human MolecularGenetic
محل انتشار: کنفرانس بین المللی ژنتیک و ژنومیکس انسانی
سال انتشار: 1400
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 86
نسخه کامل این مقاله ارائه نشده است و در دسترس نمی باشد
- صدور گواهی نمایه سازی
- من نویسنده این مقاله هستم
این مقاله در بخشهای موضوعی زیر دسته بندی شده است:
استخراج به نرم افزارهای پژوهشی:
شناسه ملی سند علمی:
CHGGE01_087
تاریخ نمایه سازی: 22 شهریور 1401
چکیده مقاله:
Genome changes in lung cells cause Lung cancer due to exposure totobacco smoke carcinogens in the workplace. Some studies show that it ishistologically obvious. Lung cancer grows by a lot of specific genetic andmorphological changes in normal lung cells. RAS as a positive signal,oncogene-mediated symptoms, and negative markers, such as tumorsuppressingretinoblastoma (RB) protein mediators, leading to uncontrolledcell growth and proliferation. Other key molecular disorders can besymptoms of cancer, like angiogenesis, tissue injections, apoptosis andaging, and metastases. Gene inactivation through DNA methylation offers anew way to escape the natural mechanisms of cellular control. Humangenome new information, and methods for revealing genetic abnormalitiesand tumor cells, message us pathways of lung cancer cells. This informationcan lead to risk assessment, early diagnosis, prognosis, and treatment oflung cancer. And there are several molecular mechanisms involved in themultistage carcinogenesis through which respiratory epithelial cells becomepreneoplastic and then invasive cancer. In this review, we summarize someof these changes including, genomic alterations such as loss ofheterozygosity and microsatellite alterations, autocrine-paracrine loops,alterations in oncogenes and tumor suppressor genes, and tumorangiogenesis and aberrant promoter methylation and inheritedpredisposition to lung cancer.
کلیدواژه ها:
نویسندگان
Arefe sadat Aghaei
University of Elm o Honar , yazd, Iran