KRAS

(redirected from KRAS2)

KRAS

A Kirsten ras oncogene homolog from the mammalian ras gene family on chromosome 12p12.1, which encodes a small GTPase in which a single amino acid substitution results in a transforming protein.

Molecular pathology
The KRAS transforming protein has been linked to various malignancies, including lung adenocarcinoma, mucinous adenoma, ductal carcinoma of the pancreas, colorectal carcinoma, acute myelogenous leukaemia, juvenile myelomonocytic leukaemia, gastric cancer, pilocytic astrocytoma, Noonan syndrome type 3, and cardiofaciocutaneous syndrome
References in periodicals archive ?
French, "Low value of detection of KRAS2 mutations in circulating DNA to differentiate chronic pancreatitis to pancreatic cancer [1]," British Journal of Cancer, vol.
Ultrasensitive detection of KRAS2 mutations in bile and serum from patients with biliary tract carcinoma using LigAmp technology.
On the basis of their temporal appearance in this progression model, the molecular abnormalities can be classified as early (KRAS2 mutation, telomere shortening), intermediate (P16/CDKN2A loss), or late (mutations of DPC4/SMAD4, TP53, BRCA2).
KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with PanIN: implications for the human pancreatic cancer cell of origin.
Abe et al., "Sensitive and quantitative detection of KRAS2 gene mutations in pancreatic duct juice differentiates patients with pancreatic cancer from chronic pancreatitis, potential for early detection," Cancer Biology and Therapy, vol.
Subramanian et al., "An oncogenic KRAS2 expression signature identified by cross-species gene-expression analysis," Nature Genetics, vol.
7P5Jand KRAS2 mutations in plasma DNA of healthy subjects and subsequent cancer occurrence: a prospective study.
Similarly, KRAS2 protein with a genetic insertion was shown to play a role in malignant transformation by activating the RAS-activated signaling pathway in acute myeloid leukemia (AML) cells (47).
Detection of mutated KRAS2 sequences as tumor markers in plasma/serum of patients with gastrointestinal cancer.
Hybridization probes (KRAS1 Flu: TAGGCAAGAGTGCCTTGACGA-fluorescein, KRAS2 Red640: LC Red 640-ACAGCTAATTCAGAATCATTTTGTGGACGAATATGATCCA-phosphate) were designed with the LightCycler Probe Design 2.0 software (Roche Diagnostics) and tested for their specificity as described above.
Detection of mutated KRAS2 sequences in plasma from patients with pancreatic carcinoma in comparison with the CA19-9 assay.
These mutations were associated with 12 core signaling pathways.7 Based on the frequency of genetically affected genes in pancreatic cancers, a genetic "topographic map" of the pancreatic cancers can be generated in which the most frequent mutations are represented as 4 "mountains" (high-frequency driver genes) involving KRAS2, CDKN2A/p16, SMAD4/DPC4, and TP53, with numerous "hills" (low-frequency driver genes) involving SMARC4A, CDH1, EPHA3, FBXW7, EGFR, IDH1, and NF1.