How does EGFR mutations cause cancer?

How does EGFR mutations cause cancer?

EGFR’s job is to help cells grow and divide. In the case of EGFR-positive non small cell lung cancer (NSCLC), a mutation, or damage, in the EGFR gene causes the EGFR protein to remain stuck in the “on” position. This “drives” abnormal cell growth, which is what cancer is.

What happens when EGFR is mutated?

EGFR (epidermal growth factor receptor) is a protein on cells that helps them grow. A mutation in the gene for EGFR can make it grow too much, which can cause cancer.

What are the newest treatments for lung cancer?

Today, the U.S. Food and Drug Administration approved Lumakras (sotorasib) as the first treatment for adult patients with non-small cell lung cancer whose tumors have a specific type of genetic mutation called KRAS G12C and who have received at least one prior systemic therapy.

How are mutations in epidermal growth factor receptor linked to lung cancer?

Abstract. Mutations in epidermal growth factor receptor have been discovered in association with some lung cancers. Lung adenocarcinomas with mutated epidermal growth factor receptor have significant responses to tyrosine kinase inhibitors, although for unselected patients it does not appear to have a survival benefit.

How are EGFR mutations used to treat lung cancer?

Epidermal growth factor receptor mutations in lung cancer The development and clinical application of inhibitors that target the epidermal growth factor receptor (EGFR) provide important insights for new lung cancer therapies, as well as for the broader field of targeted cancer therapies.

How are EGFR mutations related to NSCLC tumours?

EGFR kinase domain mutations hyperactivate the kinase and confer a dependence on the mutated kinase for the survival of the NSCLC tumour cells.

Are there any epidermal growth factor receptor mutations that are targetable?

However, recent studies revealed that these rare genotypes could be targetable if appropriate TKI are selected. For example, G719X (X denotes A, S, C and so on), Del18, E709K, insertions in exon 19 (Ins19), S768I or L861Q showed moderate sensitivities to gefitinib or erlotinb with ORR of 30%-50%.