12 Facts About KRAS

The oncogene identified was derived from a cellular genome, so KRAS, when found in a cellular genome, is called a proto-oncogene.

In turn, KRAS can bind to proteins of the Guanine Nucleotide Exchange Factor class, which forces the release of bound nucleotide .

Several germline KRAS mutations have been found to be associated with Noonan syndrome and cardio-facio-cutaneous syndrome.

Somatic KRAS mutations are found at high rates in leukemias, colorectal cancer, pancreatic cancer and lung cancer.

Impact of KRAS mutations is heavily dependent on the order of mutations.

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KRAS mutations are more commonly observed in cecal cancers than colorectal cancers located in any other places from ascending colon to rectum.

KRAS mutation is predictive of a very poor response to panitumumab and cetuximab therapy in colorectal cancer.

Emergence of KRAS mutations is a frequent driver of acquired resistance to cetuximab anti-EGFR therapy in colorectal cancers.

In 2012, the FDA cleared QIAGEN's therascreen KRAS test, which is a genetic test designed to detect the presence of seven mutations in the KRAS gene in colorectal cancer cells.

An antisense oligonucleotide targeting KRAS, AZD4785, completed a phase I study but was discontinued from further development because of insufficient knockdown of the target.

Normally amino acid position 12 of the KRAS protein is occupied by glycine but in G12D it is occupied by aspartic acid.

The first clinical trial of a novel gene therapy targeting KRAS G12D is currently recruiting patients and is sponsored by the National Cancer Institute.