|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
KRAS mutations and miRNA dysregulation (e.g. miR-21-5p oncomiR) play key roles in Pancreatic Ductal Adenocarcinoma (PDAC), leading to rapid progression of the disease.
|
31523393 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The mutant-type K-ras gene was found in plasma DNA samples of 12 (27%) of 44 patients with pancreatic ductal adenocarcinoma; this finding was related to the tumor stage (P = .05), mainly in the presence of distant metastases (P = .02).
|
10080602 |
1999 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Based on experimental results, we have recently put forward a hypothesis that the coordination of CaM and PI3Kα with K-Ras4B forms a CaM-PI3Kα-K-Ras4B ternary complex, which leads to the formation of pancreatic ductal adenocarcinoma.
|
29300353 |
2018 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Cancer cell-restricted genetic ablation of murine TRAIL-R in autochthonous KRAS-driven models of non-small-cell lung cancer (NSCLC) and pancreatic ductal adenocarcinoma (PDAC) reduces tumor growth, blunts metastasis, and prolongs survival by inhibiting cancer cell-autonomous migration, proliferation, and invasion.
|
25843002 |
2015 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Initiation of pancreatic ductal adenocarcinoma (PDA) is definitively linked to activating mutations in the KRAS oncogene.
|
22975374 |
2012 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The UCA1/KRAS axis promotes human pancreatic ductal adenocarcinoma stem cell properties and tumor growth.
|
30949406 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
KRAS is an attractive pancreatic ductal adenocarcinoma (PDAC) therapeutic target.
|
23288781 |
2013 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
There remains intense interest in tractable approaches to target or silence the KRAS oncoprotein as a rational therapeutic strategy to attack pancreatic ductal adenocarcinoma (PDAC) and other cancers that overexpress it.
|
29321164 |
2018 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In contrast to the peripheral circulation, KRAS mutation- positive CTC thrive in the portal venous blood of patients with pancreatic ductal adenocarcinoma (PDAC).
|
30067440 |
2018 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Despite expression of oncogenic KRAS, premalignant pancreatic intraepithelial neoplasia 1 (PanIN1) lesions rarely become fully malignant pancreatic ductal adenocarcinoma (PDAC).
|
29153842 |
2017 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Oncogenic mutations in KRAS contribute to the development of pancreatic ductal adenocarcinoma, but are not sufficient to initiate carcinogenesis.
|
25623042 |
2015 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Oncogenic KRAS mutation is the signature genetic event in the progression and growth of pancreatic ductal adenocarcinoma (PDAC), an almost universally fatal disease.
|
24388967 |
2014 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
IQ motif containing GTPase-activating protein 1 (IQGAP1) acts as a scaffold for aberrant mitogen-activated protein kinase (MAPK) signaling driven by KRAS mutations in pancreatic ductal adenocarcinoma (PDAC).
|
30540680 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Pancreatic ductal adenocarcinoma (PDAC), like many KRAS-driven tumors, preferentially loses CDKN2A that encodes an endogenous CDK4/6 inhibitor to bypass the RB-mediated cell cycle suppression.
|
30696953 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, preclinical studies have demonstrated that statins exhibit antitumor effects in pancreatic cancer cell lines <i>in vitro</i> and animal models <i>in vivo</i>, in addition to delaying the progression of pancreatic intraepithelial neoplasia to pancreatic ductal adenocarcinoma (PDAC) and inhibiting PDAC formation in conditional K-Ras mutant mice.
|
28454210 |
2017 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
However, in pancreatic ductal adenocarcinoma (PDAC) there are only four abundantly common driver mutations (KRAS, CDKN2A, TP53, and SMAD4), which are not currently actionable.
|
31639254 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
KRAS is one of the most frequently mutated proto-oncogenes in pancreatic ductal adenocarcinoma (PDAC) and aberrantly activated in triple-negative breast cancer (TNBC).
|
30654191 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Oncogenic KRAS mutation plays a key role in pancreatic ductal adenocarcinoma (PDAC) tumorigenesis with nearly 95% of PDAC harboring mutation-activated KRAS, which has been considered an undruggable target.
|
31467540 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the "CKP" mouse pancreatic ductal adenocarcinoma (PDAC) model driven by mutant K-Ras, Ctbp2 haploinsufficiency prolonged survival, abrogated peritoneal metastasis, and caused dramatic downregulation of c-Myc, a known critical dependency for TIC activity and tumor progression in PDAC.
|
31586042 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The KRASG12R mutation displays uneven prevalence among cancers that harbor the highest occurrence of KRAS mutations: it is rare in lung and colorectal cancers (~1%), yet relatively common (~20%) in pancreatic ductal adenocarcinoma (PDAC), suggesting context-specific properties.
|
31649109 |
2020 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In pancreatic ductal adenocarcinoma (PDAC), NF-kB is constitutively activated in most patients and is linked to a mutation in KRAS via IkB kinase complex 1 (IKK1, also known as IKKa).
|
30463064 |
2018 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The highest frequencies of KRAS mutations occur in colorectal carcinoma (CRC) and pancreatic ductal adenocarcinoma (PDAC).
|
31521603 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The high prevalence of KRAS mutations and importance of the RalGEF-Ral pathway downstream of activated K-ras in pancreatic ductal adenocarcinoma (PDAC) emphasize the importance of identifying novel methods by which to therapeutically target these pathways.
|
24222664 |
2014 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Most pancreatic ductal adenocarcinoma (PDAC) develops from pancreatic epithelial cells bearing activating mutant KRAS genes through precancerous lesions, i.e. acinar-to-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN).
|
30705405 |
2019 |
|
Pancreatic Ductal Adenocarcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
KRAS mutation, which occurs in ∼ 95% of pancreatic ductal adenocarcinoma (PDA), has been shown to program tumor metabolism.
|
25497091 |
2014 |