Selected article for: "epidermal EGFR growth factor receptor and growth factor"
Author: Tan, Zhaoli; Gao, Lihua; Wang, Yan; Yin, Huihui; Xi, Yongyi; Wu, Xiaojie; Shao, Yong; Qiu, Weiyi; Du, Peng; Shen, Wenlong; Fu, Ling; Jia, Ru; Zhao, Chuanhua; Zhang, Yun; Zhao, Zhihu; Sun, Zhiwei; Chen, Hongxing; Hu, Xianwen; Xu, Jianming; Wang, Youliang
Title: PRSS contributes to cetuximab resistance in colorectal cancer
  • Document date: 2020_1_1
    • ID: tymoeyoo_1
    Snippet: Colorectal cancer (CRC) is a major contributor to cancer mortality and morbidity in both developed and developing countries (1, 2) and is the world's fourth deadliest cancer (after lung, liver, and stomach cancer), accounting for almost 881,000 deaths in 2018 (3, 4) . Epidermal growth factor receptor (EGFR), a member of the v-erb-b2 erythroblastic leukemia viral oncogene homolog/human epidermal growth factor receptor (ERBB/ HER) family of recepto.....
    Document: Colorectal cancer (CRC) is a major contributor to cancer mortality and morbidity in both developed and developing countries (1, 2) and is the world's fourth deadliest cancer (after lung, liver, and stomach cancer), accounting for almost 881,000 deaths in 2018 (3, 4) . Epidermal growth factor receptor (EGFR), a member of the v-erb-b2 erythroblastic leukemia viral oncogene homolog/human epidermal growth factor receptor (ERBB/ HER) family of receptor tyrosine kinases (RTKs), is one of the most prominent therapeutic targets in metastatic CRC (mCRC). EGFR is commonly overexpressed on the cell membrane in several cancers, including lung, colon, head and neck, and esophageal cancer. Ligand binding causes homo-and heterodimerization between EGFR and other HER family members (ERBB2/HER2, ERBB4/HER4, and kinaseinactive ERBB3/HER3), resulting in downstream activation of the RAS-RAF-mitogen-activated protein kinase kinase (MEK) and phosphatidylinositol 3-kinase (PI3K)-AKT pathways (5) and eventually accelerating cell growth and carcinogenesis. Accordingly, numerous targeted molecules have been developed to either block ligand binding or inhibit EGFR tyrosine kinase activity.

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