What is EF2 kinase in cancer?4 answersEukaryotic elongation factor 2 kinase (eEF2K) plays a crucial role in cancer by regulating protein synthesis, cell survival, and response to DNA damage induced by agents like cisplatin. Studies have shown that eEF2K is overexpressed in various cancers, including breast cancer, where its activity correlates with poor patient outcomes. Inhibiting eEF2K has emerged as a potential therapeutic strategy, with research focusing on developing novel inhibitors to target this kinase in cancer treatment. Various compounds, including pyrano[3,4-b] indole derivatives and coumarin-chalcone core compounds, have shown promising inhibitory effects on eEF2K in cancer cells, highlighting the potential for eEF2K-targeted therapies in cancer treatment.
Is EGFR expressed more in glioblastoma than in gliomas of lower grade?5 answersEGFR expression is notably higher in glioblastoma compared to lower-grade gliomas. Glioblastoma frequently exhibits EGFR alterations, with EGFR amplification being a defining criterion for this aggressive tumor type. Additionally, in recurrent glioblastoma, the EGFR pathway is consistently overexpressed, irrespective of EGFR amplification status, indicating a common genomic endpoint in recurrent disease. Furthermore, the TROY-EGFR complex plays a crucial role in regulating glioblastoma cell invasion, highlighting the significance of EGFR signaling in the aggressive behavior of these tumors. Overall, the data suggest that EGFR is indeed expressed more prominently in glioblastoma compared to lower-grade gliomas, emphasizing its role as a key player in the molecular landscape of this highly malignant brain tumor.
What are conserved amino acide in activation segment of EGFR?4 answersThe conserved amino acids in the activation segment of the Epidermal Growth Factor Receptor (EGFR) include residues such as N771, D770, and R958. These residues play crucial roles in regulating EGFR activity and downstream signaling. Additionally, the activation segment of EGFR contains functionally important residues like N32, D46, K48, and W50, which have been studied for their impact on cellular proliferation. Furthermore, the EGFR-K745_E746insIPVAIK mutation, which is an exon 19 insertion mutation, also contains conserved amino acids that influence sensitivity to EGFR Tyrosine Kinase Inhibitors (TKIs). Understanding the significance of these conserved amino acids in the activation segment of EGFR is crucial for developing targeted therapies and predicting clinical outcomes in EGFR-mutated cancers.
Is there clinical data vailable regarding EGFR alterations in squamous cell non-small cell lung cancer?5 answersEGFR alterations in squamous cell non-small cell lung cancer (NSCLC) have been studied in the available literature. However, the abstracts provided do not specifically mention clinical data regarding EGFR alterations in squamous cell NSCLC. The abstracts primarily focus on EGFR mutations in NSCLC as a whole, including both adenocarcinoma and squamous cell histologies. Therefore, it is unclear if there is specific clinical data available for EGFR alterations in squamous cell NSCLC based on the information provided. Further research or review of additional sources may be necessary to obtain specific clinical data on this topic.
What is the function of EGFR/?5 answersThe epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that plays a fundamental role in tissue development, homeostasis, and tumorigenesis. It is involved in growth, differentiation, maintenance, and repair of various tissues and organs. In addition to its well-known role in regulating epithelial tissue development and homeostasis, EGFR has recently been found to have noncanonical functions in stress-induced trafficking, autophagy, and energy metabolism. Furthermore, EGFR can be transported from the cell surface to the nucleus through endocytosis, where it acts as a transcriptional regulator and is involved in multiple biological functions, including cell proliferation, tumor progression, DNA repair, and resistance to cancer therapies. EGFR is also an important oncogenic drug target and is involved in several cellular functions, including cancer cell growth, survival, proliferation, differentiation, and motility. The transmembrane region of EGFR has an intrinsic propensity to associate in cell membranes, but specific transmembrane dimers do not appear to regulate EGFR function.
What are the mechanisms underlying EGFR-mediated EMT invasion in HNSCC?5 answersEGFR-mediated EMT invasion in HNSCC involves multiple mechanisms. One mechanism is the activation of the MAPK and Akt pathways through EGFR signaling, which promotes cell proliferation and EMT. Another mechanism is the engagement of EGFR in cross talk with TGF-β1/Smad canonical signaling, which further activates EMT. Additionally, EGFR signaling is influenced by cell membrane components such as CD44 and ERM binding protein, as well as MMPs and scaffolding proteins that form links with the cytoskeletal machinery. These components play a role in modulating EGFR signaling and promoting EMT. Overall, the mechanisms underlying EGFR-mediated EMT invasion in HNSCC involve the activation of signaling pathways, cross talk with other signaling pathways, and the involvement of cell membrane components and cytoskeletal machinery.