KRAS

(redirected from Kirsten Rat Sarcoma)
AcronymDefinition
KRASKirsten Rat Sarcoma
KRASKnowledge Representation for Autonomous Systems
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A, In this tumor, a Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation is detected (c.37G>T, p.Gly13Cys), at an allele fraction of 15%.
[3] Human genes: IDH1, isocitrate dehydrogenase 1; IDH2, isocitrate dehydrogenase 2; MET, MET proto-oncogene, receptor tyrosine kinase; ERBB2, erb-b2 receptor tyrosine kinase 2; EGFR, epidermal growth factor receptor; TP53, tumor protein p53; PIK3CA, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; KRAS, Kirsten rat sarcoma viral oncogene homolog; ALK, anaplastic lymphoma receptor tyrosine kinase; BRAF, b-raf proto-oncogene, serine/threonine kinase.
[2] Human genes: KRAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; TP53, tumor protein p53.
[3] Human genes: KRAS, Kirsten rat sarcoma viral oncogene homolog; ERBB2, v-erb-b2 avian erythroblastic leukemia viral oncogene homolog 2 (also known as HER2).
[6] Human genes: KRAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; HER2, human epidermal growth factor receptor 2; current symbol and name: ERBB2, v-erb-b2 erythroblastic leukemia viral oncogene homolog 2, neuro/ glioblastoma derived oncogene homolog (avian); BRAF, v-raf murine sarcoma viral oncogene homolog B1; BCR, breakpoint cluster region; ABL, c-abl oncogene 1, non-receptor tyrosine kinase; ALK, anaplastic lymphoma receptor tyrosine kinase.
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] Genes: let-7; HRAS, v-Ha-ras Harvey rat sarcoma viral oncogene homolog; KRAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; NRAS, neuroblastoma RAS viral (v-ras) oncogene homolog; CCND2, cyclin D2; CDK6, cyclin-dependent kinase 6; CDC25, cell division cycle 25 homolog C (S.
[3] Human genes: HRAS, v-Ha-ras Harvey rat sarcoma viral oncogene homolog; CDKN2C, cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4); NRAS, neuroblastoma RAS viral (v-ras) oncogene homolog; CDK8, cyclin-dependent kinase 8; KRAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; BRAF, v-raf murine sarcoma viral oncogene homolog B1.
In particular, mutations were infrequent among common, broadly mutated oncogenes, such as PIK3CA (phosphoinositide-3-kinase, catalytic, alpha polypeptide), KRAS (v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog), and BRAF (v-raf murine sarcoma viral oncogene homolog B1).
(3) Human genes: ERBB2, v-erb-b2 erythroblastic leukemia viral oncogene homolog 2, neuro/glioblastoma derived oncogene homolog (avian); KRAS, v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; BRAF, v-raf murine sarcoma viral oncogene homolog B1.
Several studies have shown that mutations that cause constitutive activation of the KRAS [3] oncogene (v-Kiras2 Kirsten rat sarcoma viral oncogene homolog) predict resistance to anti-EGFR therapy (1-3), whereas activating mutations in EGFR predict response to therapy and favorable clinical outcome (4, 5).