Patent ductus arteriosus
|
0.200 |
Biomarker
|
disease |
BEFREE |
Here we show that deletion of the ataxia-telangiectasia group D-complementing (<i>Atdc</i>) gene, whose human homolog is up-regulated in the majority of pancreatic adenocarcinoma, completely prevents PDA development in the context of oncogenic KRAS.
|
31048544 |
2019 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
CEACAM6 over-expression is universally a poor prognostic marker in KRAS mutant and wild type PDA.
|
31797958 |
2019 |
Patent ductus arteriosus
|
0.200 |
Biomarker
|
disease |
BEFREE |
These findings demonstrate that TBK1 is central to an Axl-driven epithelial-mesenchymal transition in KRAS-mutant PDA and suggest that interruption of the Axl-TBK1 signaling cascade above or below KRAS has potential therapeutic efficacy in this recalcitrant disease.
|
30938713 |
2019 |
Patent ductus arteriosus
|
0.200 |
Biomarker
|
disease |
BEFREE |
KRAS is the driving oncogene in PDA and many of the metabolic changes are downstream of its activation.
|
29702208 |
2018 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Pancreatic ductal adenocarcinoma (PDA) is characterized by epithelial mutations in KRAS and prominent tumor-associated inflammation, including macrophage infiltration.
|
29756386 |
2018 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Although KRAS mutations are one of the major driver mutations in PDA, KRAS mutation alone is not sufficient to induce invasive pancreatic cancer in mice model.
|
29670173 |
2018 |
Patent ductus arteriosus
|
0.200 |
AlteredExpression
|
disease |
BEFREE |
We performed <i>KRAS</i> mutation analysis by direct sequencing and found that tumours with <i>KRAS</i> mutations have a significantly higher mean <i>KRAS</i> signal per cell from PDA samples compared with tumours with wild-type <i>KRAS.
|
29695486 |
2018 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Mutations in KRAS, the major PDA oncogene, were only detected in 10/34 (29%) blood samples, compared to 20/23 (87%) tumor tissue biopsies.
|
29137355 |
2017 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
However, in PDA mouse models, expression of oncogenic mutant KRAS during development gives rise to tumors only after a prolonged latency or following induction of pancreatitis.
|
25593307 |
2015 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Oncogenic BRAF mutations are mutually exclusive with KRAS and define sensitivity to vemurafenib in PDA models.
|
25855536 |
2015 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
KRAS mutation, which occurs in ∼ 95% of pancreatic ductal adenocarcinoma (PDA), has been shown to program tumor metabolism.
|
25497091 |
2014 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Mutations in the KRAS oncogene are dominant features in pancreatic ductal adenocarcinoma (PDA).
|
23918833 |
2013 |
Patent ductus arteriosus
|
0.200 |
AlteredExpression
|
disease |
BEFREE |
PDA is addicted to the activity of the mutated KRAS oncogene which is considered so far an undruggable therapeutic target.
|
24297898 |
2013 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
KRAS mutation is a hallmark of pancreatic ductal adenocarcinoma (PDA) but remains an intractable pharmacologic target.
|
22628411 |
2012 |
Patent ductus arteriosus
|
0.200 |
GeneticVariation
|
disease |
BEFREE |
Initiation of pancreatic ductal adenocarcinoma (PDA) is definitively linked to activating mutations in the KRAS oncogene.
|
22975374 |
2012 |
Patent ductus arteriosus
|
0.200 |
Biomarker
|
disease |
BEFREE |
OCs and coffee may have independent roles in the aetiopathogenesis of PDA through modulation of KRAS activation, acquisition or persistence, plausibly through non-genotoxic or epigenetic mechanisms.
|
19797353 |
2009 |
Patent ductus arteriosus
|
0.200 |
Biomarker
|
disease |
HPO |
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|
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