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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
High-dose vitamin C impairs tumor growth in Apc/Kras(G12D) mutant mice.
|
26541605 |
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 |
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 |
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 |
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 |
KRAS mutations were detected in 4 (3%) of 117 tumors (3× G12D and 1 G12V mutation).One tumor had a PIK3CA E545K mutation.
|
23158210 |
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 |
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 |
We found that the deletion of Ink4a/Arf in K-Ras(G12D) expressing mice led to high expression of PDGF-D signaling pathway in the tumor and tumor-derived cell line (RInk-1 cells).
|
22806240 |
2013 |
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
KRAS mutations were detected in 4 (3%) of 117 tumors (3× G12D and 1 G12V mutation).One tumor had a PIK3CA E545K mutation.
|
23158210 |
2013 |
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Treatment of Kras(G12D) mice with either of two distinct small molecule Pak inhibitors (PF3758309 and FRAX597) caused tumor regression and loss of Erk and Akt activity.
|
22983922 |
2012 |
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Significant variations in treatment effects were found for tumor response (P = .005) and PFS (P = .046) in patients with G13D-mutant tumors versus all other mutations (including G12V).
|
22734028 |
2012 |
rs121913529
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Because of the potent anti-proliferative effects of KRAS(G12D) in granulosa cells, we sought to determine whether KRAS(G12D) would block precancerous lesion and tumor formation in follicles of the CTNNB1-mutant mice.
|
21860425 |
2012 |