KRAS

(redirected from v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog)

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 ?
On the other hand, using microarray analysis followed by experimental validation, the expression levels of miRNA-143 and V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) were shown to be negatively correlated with each other [37].
Other Ras family members previously implied in NPC-related tumorigenesis are V-Ki-ras2 Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) and Transforming Protein p21 (HRAS) [26].
To demonstrate the application of LDT-COLD-PCR, we selected a 146-bp v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) [2] amplicon, with a [T.sub.m]-decreasing p.G12V mutation, for which a [T.sub.c] of 82.8[degrees]C for 10 s on a finely regulated Cepheid machine demonstrated a 4-5-fold enrichment of mutations over wild-type DNA following PCR (data not shown).
In their proposal, low-grade serous carcinoma develops from serous epithelium that acquires gene mutations for v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) and v-raf murine sarcoma viral oncogene homolog B1 (BRAF).
Summary of Mutations Detected by Multiplex Polymerase Chain Reaction and Sequencing KRas BRaf Patient DNA Protein DNA Protein 1 c.35G>A p.G12D wt wt 4 wt wt c.1799T>A p.V600E 12 c.35G>T p.G12V wt wt 13 c.34G>A p.G12S wt wt c.198A>G p.A66A 14 wt wt c.1799T>A p.V600E 16 wt wt c.1799T>A p.V600E 18 c.35G>A p.G12D wt wt 19 c.38G>A p.G13D wt wt Abbreviations: BRaf, v-raf murine sarcoma viral oncogene homolog B1; KRas, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog;wt, wild type.
[4] Nonstandard abbreviations: ER, estrogen receptor; IHC, immunohistochemistry; ASCO, American Society for Clinical Oncology; CAP, College of American Pathologists; HER2, human epidermal growth factor receptor 2; HR, hazard ratio; FISH, fluorescent in situ hybridization; EGFR, epidermal growth factor receptor; CRC, colorectal cancer; K-RAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; NSCLC, non-small cell lung cancer; TKI, tyrosine kinase inhibitor; FDA, US Food and Drug Administration; ALK, anaplastic lymphoma kinase.
This left 24 distinct mutations, including 16 missense mutations in these genes: CBL, FLT3, IDH2, KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog), NRAS [neuroblastoma RAS viral (v-ras) oncogene homolog], TP53, RUNX1, SRSF2, TET2, KDM6A [lysine (K)-specific demethylase 6A (also known as UTX)], and ZRSR2.
[6] KRAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; EGFR, epidermal growth factor receptor; SPINT1, serine peptidase inhibitor, Kunitz type 1; INTS2, integrator complex subunit 2; MOCS2, molybdenum cofactor synthesis 2; PRP8, pre-mRNA processing factor 8.
In addition to 4 genes that had previously been recognized to be mutated in PC [KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog), TP53 (tumor protein p53), p16/CDKN2A, and SMAD4 (SMAD family member 4)], other gene mutations that were present in the majority of the cancers examined have been identified.
Remarkably, the 3' UTRs of the 3 human RAS genes [HRAS (v-Ha-ras Harvey rat sarcoma viral oncogene homolog), KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog), and NRAS (neuroblastoma RAS viral (v-ras) oncogene homolog)] contained multiple let-7--complementary sites, allowing let-7 to regulate RAS expression.
Moreover, additional genetic characterization for mutations in oncogenes [e.g., KRAS [7] (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog)] or tumor suppressor genes [e.g., TP53 (tumor protein p53)], and fluorescence in situ hybridization-based detection of numerical chromosomal aberrations at the single-cell level may add specificity to current CTC assays.
In contrast, detection oflow-level KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) mutations in metastatic colorectal cancer enhances the prediction of resistance to treatment with an anti-epidermal growth factor receptor monoclonal antibody (7).