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.

The Use of Biomarkers in Early Diagnostics of Pancreatic Cancer

Ultrasensitive detection of KRAS2 mutations in bile and serum from patients with biliary tract carcinoma using LigAmp technology.

Evaluation of Intraductal Ultrasonography, Endoscopic Brush Cytology and K-ras, P53 Gene Mutation in the Early Diagnosis of Malignant Bile Duct Stricture

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).

Pancreatic carcinoma: review of literature

KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with PanIN: implications for the human pancreatic cancer cell of origin.

Differentiation of Pancreatic Ductal Adenocarcinoma From Chronic Pancreatitis by PAM4 Immunohistochemistry

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.

K-ras mutational status in cytohistological tissue as a molecular marker for the diagnosis of pancreatic cancer: a systematic review and meta-analysis

Subramanian et al., "An oncogenic KRAS2 expression signature identified by cross-species gene-expression analysis," Nature Genetics, vol.

Downregulation of type II diabetes mellitus and maturity onset diabetes of young pathways in human pancreatic islets from hyperglycemic donors

7P5Jand KRAS2 mutations in plasma DNA of healthy subjects and subsequent cancer occurrence: a prospective study.

Seasonal variation in TP53 R249S-mutated serum DNA with aflatoxin exposure and hepatitis B virus infection

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).

The importance of protein profiling in the diagnosis and treatment of hematologic malignancies / Hematolojik malignitelerin tani ve tedavisinde protein profillemenin onemi

Detection of mutated KRAS2 sequences as tumor markers in plasma/serum of patients with gastrointestinal cancer.

Clinical implementation of KRAS testing in metastatic colorectal carcinoma: the pathologist's perspective

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.

High-resolution melting analysis as a sensitive prescreening diagnostic tool to detect KRAS, BRAF, PIK3CA, and AKT1 mutations in formalin-fixed, paraffin-embedded tissues

Detection of mutated KRAS2 sequences in plasma from patients with pancreatic carcinoma in comparison with the CA19-9 assay.

Circulating cell-free DNA in plasma/serum of lung cancer patients as a potential screening and prognostic tool

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.