The latest research on the two most common cancer-causing mutations found a new treatment strategy for the "king of cancer"

Pancreatic cancer is one of the cancer types with the highest mortality rate among all solid tumors.

An important feature of pancreatic cancer is the accumulation of two oncogene mutations that are most common in all cancer types.

KRAS and p53 proteins are two "notorious" "non-drugable" targets.

In this study, the scientists designed a mouse model that simultaneously expresses the oncogenic KRAS mutant and p53 mutant in pancreatic cancer tumor cells without changing the microenvironment surrounding the tumor.

Further research found that the KRAS mutant can activate a transcription factor called CREB1, and it can directly interact with the mutant p53, resulting in abnormal expression of hundreds of genes.

After discovering that CREB1 is a key factor in the interaction between KRAS and p53 mutants, the researchers inhibited its activity with small-molecule drugs targeting CREB1.

Reference materials:

[1] Mutant KRAS and p53 cooperate to drive pancreatic cancer metastasis.

[3] Kim et al.

Note: This article aims to introduce the progress of medical and health research, not to recommend treatment options.