Browse protocols, FAQs, guidelines, and technical articles tagged “KRAS”, newest first. For research use only.
Non-small cell lung cancer exhibits substantial histological and molecular heterogeneity. Alterations involving EGFR, ALK, ROS1, KRAS, BRAF, RET, MET, HER2, and other oncogenic drivers can continuously activate tumor-cell proliferation and survival signaling and generate molecular subtypes with ...
RAS mutations drive many tumors, including pancreatic cancer, colorectal cancer, and lung cancer. However, RAS was long considered difficult to drug because of its shallow structural pockets and tight GTP binding. The emergence of RAS(ON) inhibitors, molecular glues, and PROTACs has shifted RAS ...
In the field of cancer research, the KRAS gene has always occupied an important and unique position. For many years, due to its complex structure and functional characteristics, KRAS has been regarded as an "undruggable" target.
KRAS (Kirsten Rat Sarcoma Viral Oncogene Homolog) is a key member of the RAS family. Mutations in KRAS are among the most common oncogenic drivers in several malignancies, including non-small cell lung cancer (NSCLC), pancreatic cancer, and colorectal cancer. It is estimated that KRAS mutations ...
The KRAS G12C mutation is one of the common driver mutations in malignant tumors such as colorectal cancer (CRC) and non-small cell lung cancer (NSCLC). Recently approved KRAS G12C inhibitors like Adagrasib (MRTX849) and Sotorasib have provided unprecedented therapeutic options for patients.
In recent years, protein tyrosine phosphatase SHP2 has become a highly regarded research target in the field of oncology in mediating the RAS-driven MAPK signaling pathway. Its treatment methods are not limited to single drug use, but also can work together with KRAS inhibitors, showing good ...
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