A single change in the KRAS gene causes a normal protein to become a driver of uncontrolled cell growth.
Strongly supported
Multiple high-quality studies back this claim.
Not medical advice. For informational purposes only. Always consult a healthcare professional.
A single change in the KRAS gene causes a normal protein to become a driver of uncontrolled cell growth.
See the technical phrasing
A single point mutation in the KRAS gene is sufficient to transform a normal cellular protein into an oncogenic driver of uncontrolled cell proliferation.
A single change in the KRAS gene causes the KRAS protein to stay permanently switched on, which forces cells to keep dividing nonstop by activating a chain of signals that tell the cell to grow. At the same time, this mutated protein blocks the cell's natural self-destruct system, allowing damaged cells to survive. Without additional damage to other genes that normally stop uncontrolled growth, the cell may stop dividing and enter a resting state, but if those brakes are also broken, the cell becomes cancerous.
What the research says
Supports
2 studies
Study: Abstract CT082: Phase I study of autologous CD8+ and CD4+ transgenic T cells expressing high-affinity KRAS G12V mutation-specific T cell receptors (FH-A11KRASG12V-TCR) in patients with metastatic pancreatic, colorectal and non-small cell lung cancers with KRAS G12V mutations
This study provides evidence supporting the claim.
Contradicts
1 study
Study: Why isn't an oncogenic mutation in KRAS enough to induce and sustain transformation?
This study provides evidence contradicting the claim.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 3 supporting studies