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rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Strength of fascin expression and tumor percentage stained with fascin were scored semi quantitatively. c.34 > C (p.G12R), c.35 g > C (p.G12C), c.34G > A (p.G12S), c.35G > A (p.G12D), c.35G > T (p.G12V), c.35G > C (p.G12A), and c.38G > A (p.G13.D) mutations in K-RAS gene were studied by using RT-PCR.
|
23588415 |
2014 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Notch1 mutations, including exon 34 mutations and recently characterized type 1 and 2 deletions, are detected in 100% of Kras G12D-induced T-ALL tumors.
|
23673656 |
2013 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The tumors that developed differed in their ability to recapitulate normal myogenesis. cdh15:KRAS(G12D) and rag2:KRAS(G12D) fish developed tumors that displayed an inability to complete muscle differentiation as determined by histological appearance and gene expression analyses.
|
23821038 |
2013 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Using genetically engineered mouse models (GEMMs) for human non-small-cell lung cancer (NSCLC), we found that deletion of the essential autophagy gene, Atg7, in KRAS(G12D)-driven NSCLC inhibits tumor growth and converts adenomas and adenocarcinomas to benign oncocytomas characterized by the accumulation of respiration-defective mitochondria.
|
23959381 |
2013 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Treatment of Caggs-Cre/FR-Hras(G12V) mice with TPA alone was sufficient to trigger papilloma development with a shorter latency and an ∼10-fold greater tumor burden than DMBA/TPA-treated WT-controls.
|
24240680 |
2014 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Mutant enriched sequencing of isolated CTCs confirmed that they harbored KRAS G12V mutations, identical to the matched tumors.
|
24586805 |
2014 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The p.G12V mutation was significantly associated with sigmoid tumors (P = 0.021) and negatively associated with left-sided tumors (P = 0.011), with a trend of an association with age ≥70 years (P = 0.062) and rectal tumors (P = 0.063).
|
24675495 |
2014 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
PTEN loss leads to acceleration of Kras(G12D)-driven pancreatic ductal adenocarcinoma (PDAC) in mice and these tumours have high levels of mammalian target of rapamycin (mTOR) signalling.
|
24717934 |
2014 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In combination with p53 silencing, KRAS(G12V) alone was sufficient to fully transform the immortalized HPDECs, and MYC markedly accelerated the development of tumors.
|
24858378 |
2014 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The increased cell survival, invasion, intravasation, and specific molecular regulation observed in KRas G12V tumors is consistent with the higher aggressiveness observed in patients with CRC expressing this oncogene.
|
25359494 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Mutations in primary tumors were identified in three regions; KARS (G13D) and APC (R876*) in P1-2, TP53 (A161S) in P1-3, and KRAS (G12D), PIK3CA (Q546R), and ERBB4 (T272A) in P1-4.
|
25623536 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
We analyzed tumor growth in mice that expressed the oncogenic form of KRAS (KRAS(G12D)) in pancreatic precursor cells, as well as sst2+/- and sst2-/-, and in crossed KRAS(G12D);sst2+/- and KRAS(G12D);sst2-/- mice.
|
25683115 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Orthotopic implantation of PDCs carrying the activated Kras(G12D</span>)-allele and shRNA against p16(Ink4a) or Trp53 resulted in tumor growth, metastasis, and reduced survival of NSG mice.
|
25724428 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The miniature biodegradable implant siG12D-LODER™ was inserted into a tumor and released a siRNA drug against KRAS(G12D) along four months.
|
26009994 |
2015 |
|
rs121913529
|
|
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 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Analysis of a tumor biopsy revealed an activating KRAS mutation (G12D) and the patient was started on first-line treatment with Reolysin in combination with gemcitabine in March 2012.
|
26156229 |
2015 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Visible carcinoma was detected as early as day-15 following oncogenic KRAS(G12V) induction alone, and these tumors proliferate rapidly with a median survival of 28-days accompanied with histological reminiscences to human sarcomatoid SDC variants.
|
26289340 |
2015 |
|
rs121913529
|
|
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 |
|
rs121913529
|
|
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 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The karyotype is highly complex, with a hypotriploid to hypertriploid modal number (3n+/-) (52 to 77 chromosomes); low level of HER2 gene amplification, TP53 deletion, gain of AURKA were identified; K-RAS G12D mutation were maintained from primary tumor to MT-CHC01 cells.
|
26486326 |
2016 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
High-dose vitamin C impairs tumor growth in Apc/Kras(G12D) mutant mice.
|
26541605 |
2015 |
|
rs121913529
|
|
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 |
|
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
SW48 KRAS WT tumors, but neither SW48-KRAS-G13D tumors nor SW48-KRAS-G12V tumors, were sensitive to ixazomib in vivo.
|
26709701 |
2015 |
|
rs121913529
|
|
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 |
|
rs121913529
|
|
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 |