Molecular dignosis of liver cancer
محل انتشار: دومین کنگره بین المللی کنسرژنومیکس
سال انتشار: 1403
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 98
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شناسه ملی سند علمی:
ICGCS02_057
تاریخ نمایه سازی: 17 دی 1403
چکیده مقاله:
Liver is the sixth most common cancer and the third cause of death. Liver carcinoma HCC is the most common primary liver cancer and the fourth leading cause of death. Hepatocellular carcinoma is known to have a high potential to show liver damage through dynamic changes in hepatocytes in homeostasis, and hepatocyte proliferation is responsible for maintaining liver function and mass homeostasis. Hepatocellular carcinoma, primary liver cancer, called hepatoma, is usually One or more round tumors develop in the liver and invade the normal tissue and destroy it. It is called carcinoma, and by multiplying out of control, it causes the beginning of liver cancer, which generally spreads along the bile ducts in the form of finger lines. like they grow and as a result causes changes. In liver cancer, the DNA of liver cells grows. The mutation affects the uncontrolled growth of the cell and eventually turns into a tumor and a mass of cancer cells. The origin of this type of cancer cells are: a) Malignant tumor: liver cells of hepatocellular carcinoma (beginning of primary liver cancer) b) Benign tumor: It originates from the cells of the cholangius bile duct c) Unusual tumors that mainly occur in the liver are: a) Hemangioendothelioma, which is a malignant tumor that originates from the endothelial cells of the liver vessels. b) Hepatoblastoma, which originates in children. c) Angiosarcoma or hemangiosarcoma that grows and originates from the blood vessels of the liver. Genes producing cancer cells are divided into four groups: a) oncogenes b) tumor suppressor genes c) DNA repair genes d) Apoptosis genes The first stage of liver damage is non-alcoholic fatty liver disease (NAFLD), which causes problems with fat breakdown and resulting inflammation, leading to non-alcoholic steatohepatitis (NASH), which leads to liver fibrosis. Increases extracellular matrix accumulation and collagen type III and IV production increases ۱۰-fold during fibrosis. Liver fibrosis leads to activation of HSC۳ hepatic stellate cells, liver dysfunction, accumulation of extracellular matrix proteins. Over time, fibrosis and hepatocellular carcinoma lead to death due to liver failure. Initiation of the damage process by stimulation of fibrogenetic, paracrine, Kupffer cells (with surface markers CD۶۸, CDIIb, F۴/۸۰), endothelial cells, platelets and hepatocytes with proliferation of fibrogenesis and contraction and lack of interaction in matrix metalloproteinase, disruption of gene expression Inhibitors and inflammatory signals, in the expression of inhibitory inflammatory signals causes a stable phenotype in activated HSC. The main role and penetration of cells inside the liver tissue, which regulates the principle of wound tissue, is called chemokine, which is a combination of chemotactic and cytokine, and is the agent of migration and activation of inflammatory cells such as macrophages and non-inflammatory cells. Binding to plasma membrane receptors that perform their actions by binding to G protein-coupled membrane receptors.
کلیدواژه ها:
نویسندگان
Yeganeh Salehi
Naghshejahan University
Amirhossein Asghari
Mazandaran University
Kourosh Khayam Abed
Naghshejahan University