A Review on Anaplastic Lymphoma Kinase (ALK) Rearrangements and Mutations: Implications for Gastric Carcinogenesis and Target Therapy.
Felipe Pantoja MesquitaLuina Benevides LimaEmerson Lucena da SilvaPedro Filho Noronha SouzaMaria Elisabete Amaral de MoraesRommel Mario Rodrigues BurbanoRaquel Carvalho MontenegroPublished in: Current protein & peptide science (2024)
Gastric adenocarcinoma is a complex disease with diverse genetic modifications, including Anaplastic Lymphoma Kinase (ALK) gene changes. The ALK gene is located on chromosome 2p23 and encodes a receptor tyrosine kinase that plays a crucial role in embryonic development and cellular differentiation. ALK alterations can result from gene fusion, mutation, amplification, or overexpression in gastric adenocarcinoma. Fusion occurs when the ALK gene fuses with another gene, resulting in a chimeric protein with constitutive kinase activity and promoting oncogenesis. ALK mutations are less common but can also result in the activation of ALK signaling pathways. Targeted therapies for ALK variations in gastric adenocarcinoma have been developed, including ALK inhibitors that have shown promising results in pre-clinical studies. Future studies are needed to elucidate the ALK role in gastric cancer and to identify predictive biomarkers to improve patient selection for targeted therapy. Overall, ALK alterations are a relevant biomarker for gastric adenocarcinoma treatment and targeted therapies for ALK may improve patients' overall survival.
Keyphrases
- radiation therapy
- advanced non small cell lung cancer
- tyrosine kinase
- copy number
- epidermal growth factor receptor
- genome wide
- squamous cell carcinoma
- genome wide identification
- cell proliferation
- stem cells
- diffuse large b cell lymphoma
- oxidative stress
- case report
- ejection fraction
- mesenchymal stem cells
- endoplasmic reticulum stress
- binding protein
- amino acid
- patient reported outcomes