rs121913529, KRAS

N. diseases: 144
Source: ALL
Disease Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE In all components (bilateral serous borderline tumors, low-grade serous carcinoma and mesonephric-like adenocarcinoma), an identical KRAS mutation was detected (NM_004985.4): c.35G>A, p.(G12D) proving a clonal association between the serous and mesonephric-like components and excluding a collision neoplasm. 30575604 2020
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE In all components (bilateral serous borderline tumors, low-grade serous carcinoma and mesonephric-like adenocarcinoma), an identical KRAS mutation was detected (NM_004985.4): c.35G>A, p.(G12D) proving a clonal association between the serous and mesonephric-like components and excluding a collision neoplasm. 30575604 2020
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Furthermore, we observe an in vivo reduction in tumor size of gallbladder xenografts in response to Afatinib is paralleled by a reduction in the amounts of phospho-ERK, in tumors harboring KRAS (G13D) mutation but not in KRAS (G12V) mutation, supporting an essential role of the ErbB pathway. 30304546 2019
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Importantly, FGTI-2734 inhibited the growth of xenografts derived from four patients with pancreatic cancer with mutant KRAS (2 G12D and 2 G12V) tumors. 31227505 2019
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE The results showed that the AZ628 and BP-1-102 combination showed strongly synergistic effects on KRAS(G12D) H838, KRAS(G12S) H292 and KRAS(G12V) H441 cells and significantly enhanced the inhibition of cell proliferation <i>in vitro</i> and tumor growth <i>in vivo</i> by promoting apoptosis compared with one inhibitor alone. 31484165 2019
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Tumors harboring mutant KRAS-G12 V had a significantly higher PD-L1 expression compared to other tumors (p = 0.044), while mutant KRAS-G12D tumors showed an increase in the density of CD66b+ cells (p = 0.001). 29858030 2018
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Next generation sequencing found only the KRAS G12D and RNF43 G659Vfs*41 mutations were retained from the pre-treatment tumor in the treatment-resistant tumor. 30458888 2018
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE In conclusion, whilst oncogenic KRAS mutation might activate Yap in other cell types, we could find no evidence for this in myoblasts because the expression of KRAS G12V expression did not change Yap/Taz activity in myoblasts and there was a limited overlap in gene expression between KRAS G12V and YAP1 S127A-driven tumours. 30353028 2018
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE When the assay was applied to tumor samples with known KRAS or NRAS mutations (G12A, G12D, G12V, and G13D), RAS-mutant and wild-type peptides were successfully detected in 11 of 13 biopsy samples. 29684684 2018
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Three of the four tumors had a BRAF (V600E) driver mutation, an EGFR (del E746-T751/S752V) driver mutation, or driver mutations in both EGFR (E709G) and KRAS (G12V). 29624782 2018
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Importantly, intratumoral injection of the adenoviruses with pro-drug treatment specifically and significantly impeded the growth of xenografted tumors harboring KRAS G12V through a trans-splicing reaction with the target RNA. 28153088 2017
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Co-expression of Kras(G12V) and Braf(D631A) in mouse lung cells markedly enhances tumour initiation, a phenomenon mediated by Craf kinase activity, and effectively accelerates tumour progression when activated in advanced lung adenocarcinomas. 28783725 2017
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Polymerase chain reaction identified a Kirsten rat sarcoma viral oncogene homolog (<i>KRAS</i>) G12V mutation in the tumor. 28932588 2017
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Our results showed that 21 of 34 tumors with high-grade TB had KRAS mutations (P=.001) and KRAS G12D and PIK3CA exon 9 variants were significantly associated with high-grade TB (P=.002 and .006, respectively); furthermore, tumors with KRAS mutations in exons 3 and 4 tended to have lymphovascular tumor emboli and perineural invasion (P=.044 and .049, respectively). 28188750 2017
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Co-administration of BI-2536 and fasudil either in the LSL-KRAS(G12D) mouse model or in a patient tumour explant mouse model of KRAS-mutant lung cancer suppresses tumour growth and significantly prolongs mouse survival, suggesting a strong synergy in vivo and a potential avenue for therapeutic treatment of KRAS-mutant cancers. 27193833 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Since hypoxic microenvironments select for tumor cells with diminished therapeutic response, we investigated whether hypoxia unequally increases resistance to 3-BrPA in wt p53 MelJuso melanoma harbouring (Q61L)-mutant NRAS and wt BRAF, C8161 melanoma with (G12D)-mutant KRAS (G464E)-mutant BRAF, and A549 lung carcinoma with a KRAS (G12S)-mutation. 27863474 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE The K-Ras(V14I) mutation is a mild activating K-Ras protein; thus, we have used this model to study tumour susceptibility in comparison with mice expressing the classical K-Ras(G12V) oncogene. 27174785 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE The percentage of KRAS G12V mutation relative to wild-type sequences in tumor-derived DNA was also determined. 27043547 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE The median progression-free survival (PFS) and overall survival (OS) for patients with tumors harboring G12V/A KRAS mutation was 6.6 and 16.8 compared to 11.6 and 26.3 months for patients with tumors harboring other KRAS mutation type (p < 0.001 and p < 0.001), while the survival of patients harboring other KRAS mutation types was comparable to those with tumors harboring wild-type KRAS gene. 26662311 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Disruption of Acvr1b in LSL-KRAS(G12D);Pdx1-Cre mice accelerated the growth of pancreatic IPMNs compared with LSL-KRAS(G12D);Pdx1-Cre mice, but did not alter growth of pancreatic intraepithelial neoplasias. 26408346 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Consistent with previous findings in vitro, Glut1 transcript and protein expression was up-regulated in the tumors of G22Cre;Apc (flox/flox) ; Kras(G12D) mice. 26361962 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE Coactivation of BRAF(V600E) and KRAS(G12D) markedly reduced lung tumor numbers and overall tumo</span>r burden compared with activation of BRAF(V600E) alone. 26028035 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE In this report, we reveal a previously unidentified tumor cell-autonomous role of KRAS(G12D)-induced CXCR2 signaling in mediating growth of neoplastic PDAC cells. 26771140 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE 44% of the tumors were positive for G12D, 20% for G12V, and 10% for G12C. 27591291 2016
Neoplasms
CUI: C0027651
Disease: Neoplasms
0.100 GeneticVariation BEFREE KRAS mutations were detected in 109 (86.5 %) of the 126 cases; the most common mutation was c.34G > T (p.G12C), which was present in 80 tumors, followed by c.35G > T (p.G12V) in 52 tumors. 26927447 2016