The most commonly mutated oncogene in human cancer is rat sarcoma (RAS), with Kirsten rat sarcoma (KRAS) being the most frequently mutated RAS isoform. In the aggregate, KRAS accounts for 85% of RAS mutations in human cancer, and KRAS exists in 35% of lung adenocarcinomas.

The dysregulation of KRAS results in tumor growth and mediates interactions between cancer cells and the tumor microenvironment, thus impacting therapeutic response. KRAS mutations likely occur early in carcinogenesis and facilitate the survival, invasion, and migration of cancer cells. Smoking has been strongly linked to KRAS mutations in lung cancer.

Previously, KRAS was considered “undruggable” due to difficulty with identifying actionable target-inhibitor binding sites. New developments show that targeting the KRAS 12 glycine to cysteine (G12C) mutation, which depends on covalent modification of the cysteine residue, is effective in the treatment of NSCLC.

What is your experience with KRAS-positive lung cancer? In which patients would you consider KRAS inhibitors?

https://pubmed.ncbi.nlm.nih.gov/34089836/

https://pubmed.ncbi.nlm.nih.gov/34151545/

The most commonly mutated oncogene in human cancer is rat sarcoma (RAS), with Kirsten rat sarcoma (KRAS) being the most frequently mutated RAS isoform. In the aggregate, KRAS accounts for 85% of RAS mutations in human cancer, and KRAS exists in 35% of lung adenocarcinomas.

The dysregulation of KRAS results in tumor growth and mediates interactions between cancer cells and the tumor microenvironment, thus impacting therapeutic response. KRAS mutations likely occur early in carcinogenesis and facilitate the survival, invasion, and migration of cancer cells. Smoking has been strongly linked to KRAS mutations in lung cancer.

Previously, KRAS was considered “undruggable” due to difficulty with identifying actionable target-inhibitor binding sites. New developments show that targeting the KRAS 12 glycine to cysteine (G12C) mutation, which depends on covalent modification of the cysteine residue, is effective in the treatment of NSCLC.

What is your experience with KRAS-positive lung cancer? In which patients would you consider KRAS inhibitors?

https://pubmed.ncbi.nlm.nih.gov/34089836/

https://pubmed.ncbi.nlm.nih.gov/34151545/

The most commonly mutated oncogene in human cancer is rat sarcoma (RAS), with Kirsten rat sarcoma (KRAS) being the most frequently mutated RAS isoform. In the aggregate, KRAS accounts for 85% of RAS mutations in human cancer, and KRAS exists in 35% of lung adenocarcinomas.

The dysregulation of KRAS results in tumor growth and mediates interactions between cancer cells and the tumor microenvironment, thus impacting therapeutic response. KRAS mutations likely occur early in carcinogenesis and facilitate the survival, invasion, and migration of cancer cells. Smoking has been strongly linked to KRAS mutations in lung cancer.

Previously, KRAS was considered “undruggable” due to difficulty with identifying actionable target-inhibitor binding sites. New developments show that targeting the KRAS 12 glycine to cysteine (G12C) mutation, which depends on covalent modification of the cysteine residue, is effective in the treatment of NSCLC.

What is your experience with KRAS-positive lung cancer? In which patients would you consider KRAS inhibitors?

https://pubmed.ncbi.nlm.nih.gov/34089836/

https://pubmed.ncbi.nlm.nih.gov/34151545/

The most commonly mutated oncogene in human cancer is rat sarcoma (RAS), with Kirsten rat sarcoma (KRAS) being the most frequently mutated RAS isoform. In the aggregate, KRAS accounts for 85% of RAS mutations in human cancer, and KRAS exists in 35% of lung adenocarcinomas.

The dysregulation of KRAS results in tumor growth and mediates interactions between cancer cells and the tumor microenvironment, thus impacting therapeutic response. KRAS mutations likely occur early in carcinogenesis and facilitate the survival, invasion, and migration of cancer cells. Smoking has been strongly linked to KRAS mutations in lung cancer.

Previously, KRAS was considered “undruggable” due to difficulty with identifying actionable target-inhibitor binding sites. New developments show that targeting the KRAS 12 glycine to cysteine (G12C) mutation, which depends on covalent modification of the cysteine residue, is effective in the treatment of NSCLC.

What is your experience with KRAS-positive lung cancer? In which patients would you consider KRAS inhibitors?

https://pubmed.ncbi.nlm.nih.gov/34089836/

https://pubmed.ncbi.nlm.nih.gov/34151545/

The most commonly mutated oncogene in human cancer is rat sarcoma (RAS), with Kirsten rat sarcoma (KRAS) being the most frequently mutated RAS isoform. In the aggregate, KRAS accounts for 85% of RAS mutations in human cancer, and KRAS exists in 35% of lung adenocarcinomas.

The dysregulation of KRAS results in tumor growth and mediates interactions between cancer cells and the tumor microenvironment, thus impacting therapeutic response. KRAS mutations likely occur early in carcinogenesis and facilitate the survival, invasion, and migration of cancer cells. Smoking has been strongly linked to KRAS mutations in lung cancer.

Previously, KRAS was considered “undruggable” due to difficulty with identifying actionable target-inhibitor binding sites. New developments show that targeting the KRAS 12 glycine to cysteine (G12C) mutation, which depends on covalent modification of the cysteine residue, is effective in the treatment of NSCLC.

What is your experience with KRAS-positive lung cancer? In which patients would you consider KRAS inhibitors?

https://pubmed.ncbi.nlm.nih.gov/34089836/

https://pubmed.ncbi.nlm.nih.gov/34151545/