What type of gene is KRAS?
Table of Contents
What type of gene is KRAS?
The KRAS gene belongs to a class of genes known as oncogenes. When mutated, oncogenes have the potential to cause normal cells to become cancerous. The KRAS gene is in the Ras family of oncogenes, which also includes two other genes: HRAS and NRAS.
Where is KRAS gene located?
KRAS
| Gene location (Human) | ||
|---|---|---|
| Chr. | Chromosome 12 (human) | |
| Band | 12p12.1 | 25,205,246 bp |
| 25,250,936 bp |
What is KRAS mutation in lung cancer?
Lung cancer, the most common cancer type with the highest mortality, can largely be categorized by the genetic mutations that cause it. KRAS is a type of mutation in a group of genes that help regulate cell growth and division.
What does KRAS gene stand for?
KRAS is a short name for the gene Kirsten rat sarcoma viral oncogene homolog. It is one of a group of genes involved in a pathway called the epidermal growth factor receptor (EGFR) pathway.
What type of protein is KRAS?
1. Introduction. GTPase KRas (KRAS) is a signal transducer protein, which plays an important role in various cellular signalling events such as in regulation of cell proliferation.
Is KRAS an oncogene or tumor suppressor?
The KRAS gene (Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) is an oncogene that encodes a small GTPase transductor protein called KRAS. KRAS is involved in the regulation of cell division as a result of its ability to relay external signals to the cell nucleus.
What does a mutation in KRAS result in?
Mutated (changed) forms of the KRAS gene have been found in some types of cancer, including non-small cell lung cancer, colorectal cancer, and pancreatic cancer. These changes may cause cancer cells to grow and spread in the body.
How common is KRAS mutation in lung cancer?
KRAS mutations occur in 20–40% of lung adenocarcinomas, a prevalence that is higher in Western vs Asian populations (26% vs. 11%) and smokers vs non-smokers (30% vs. 10%) [11]. The most frequent mutations occur in codons 12 and 13, with the most common subtypes including G12C, G12 V, and G12D (Fig.
How many types of KRAS mutations are there?
KRAS mutation occurs mainly in codon 12, 13 or 61. Most common types of KRAS mutation are G12C, G12V, and G12D (8,9). In addition, in vitro data reported by Garassino et al suggested that NSCLC cell lines harboring a G12C, G12V or G12D KRAS mutation had differential sensitivity to chemotherapeutic agents (15).
Why is KRAS Undruggable?
For more than 30 years after its discovery, KRAS was considered undruggable target due to the intrinsic characteristics of KRAS proteins. The KRAS is small and has a considerably smooth and shallow surface, resulting in difficulty of small molecule binding to the KRAS.
Is KRAS a membrane protein?
KRAS is a small GTPase and the central switch in the MAPK signaling pathway. In cells, most signals are relayed and processed by proteins attached to or embedded in the membrane; KRAS signaling is no exception.
What is BRAF KRAS mutation?
BRAF and KRAS are two key oncogenes in the RAS/RAF/MEK/MAP-kinase signaling pathway. While previously considered mutually exclusive, concomitant mutations in both KRAS and BRAF genes have been identified in colorectal cancer (CRC). The clinical outcome of these patients remains undetermined.
How does KRAS mutation occur?
KRAS mutations are found in both current and former smokers and are rare in never-smokers. In the majority of cases, these are missense mutations that introduce an amino acid substitution at position 12, 13, or 61. The result of these mutations is constitutive activation of KRAS signaling pathways.
What is KRAS and BRAF?
What is KRAS G12C?
KRAS G12C is an oncogenic driver mutation in multiple cancer types. KRAS mutations play a role in some of the most common and deadly carcinomas, including lung, colorectal, and pancreatic cancers. One single type of KRAS mutation — called KRAS G12C — accounts for about 44% of all KRAS mutations.
What is the difference between KRAS and BRAF?
For one, BRAF mutations disallow the critical feedback from ERK to RAF to occur, while KRAS mutations leave this feedback intact [114]. As a consequence, higher levels of MEK inhibitor are required in KRAS mutated CRC cells as compared to BRAF mutated cells to suppress MEK/ERK activation.
