INT60060

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Context Info
Confidence 0.67
First Reported 1993
Last Reported 2010
Negated 1
Speculated 2
Reported most in Body
Documents 17
Total Number 20
Disease Relevance 11.68
Pain Relevance 1.21

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

signal transduction (KRAS) mitochondrion (KRAS) plasma membrane (KRAS)
GTPase activity (KRAS)
Anatomy Link Frequency
arm 2
SVR 2
mucous cell 2
colon 1
reproductive tract 1
KRAS (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 6 97.44 Very High Very High Very High
endometriosis 7 97.32 Very High Very High Very High
pain pelvic 1 97.00 Very High Very High Very High
Angina 1 92.28 High High
Chronic pancreatitis 5 89.48 High High
cINOD 5 83.64 Quite High
aspirin 1 82.00 Quite High
fibrosis 3 52.72 Quite High
COX2 1 25.00 Low Low
Bile 12 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Sarcoma 3 100.00 Very High Very High Very High
Colorectal Cancer 55 99.84 Very High Very High Very High
Hyperplasia 10 99.36 Very High Very High Very High
Cancer 339 99.24 Very High Very High Very High
Apoptosis 47 99.24 Very High Very High Very High
Colon Cancer 34 98.86 Very High Very High Very High
Pancreatic Cancer 28 98.40 Very High Very High Very High
Adenocarcinoma 74 98.18 Very High Very High Very High
Pancreatitis 12 97.88 Very High Very High Very High
Reprotox - General 3 2 97.64 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We now report that in a mouse model where oncogenic Kras is activated in all pancreatic cell types, two brief episodes of acute pancreatitis caused rapid PanIN progression and accelerated pancreatic cancer development.
Positive_regulation (activated) of Kras associated with pancreatic cancer and pancreatitis
1) Confidence 0.67 Published 2009 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 19292977 Disease Relevance 0.80 Pain Relevance 0.13
This evidence suggests that in HuH28, OZ and TFK-1 no constitutive activation of the KRAS gene is present (data not shown).
Neg (no) Positive_regulation (activation) of KRAS in TFK-1
2) Confidence 0.58 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2896958 Disease Relevance 0.32 Pain Relevance 0
We evaluated the effects of the major sulfide and sulfone metabolites of sulindac and DFMO alone, or in combinations, on the growth and survival of Caco-2 colon cancer-derived cells and in clones of these cells transfected with an activated K-ras oncogene.
Positive_regulation (activated) of K-ras oncogene in colon associated with colon cancer
3) Confidence 0.51 Published 2000 Journal Cancer Epidemiol. Biomarkers Prev. Section Abstract Doc Link 11097222 Disease Relevance 0.61 Pain Relevance 0.08
Expression of an activated K-ras oncogene caused cells treated with either sulindac sulfide or sulfone to undergo apoptosis earlier than nontransfected controls.
Positive_regulation (activated) of K-ras oncogene associated with apoptosis
4) Confidence 0.51 Published 2000 Journal Cancer Epidemiol. Biomarkers Prev. Section Abstract Doc Link 11097222 Disease Relevance 0.65 Pain Relevance 0.07
Activation of an oncogenic allele of Kirsten rat sarcoma viral oncogene homologue (KRAS) in the reproductive tract of mice resulted in the development of endometriosis.
Positive_regulation (Activation) of KRAS in reproductive tract associated with endometriosis and sarcoma
5) Confidence 0.45 Published 2006 Journal Mol. Hum. Reprod. Section Abstract Doc Link 16973828 Disease Relevance 0.89 Pain Relevance 0.35
In order to scrutinize the possible significance of (nonatypical) mucous cell hyperplasia of the pancreas to neoplasia, we analyzed these lesions in terms of c-Ki-ras activation, which is known to be very frequent in pancreatic carcinomas.
Spec (analyzed) Positive_regulation (activation) of c-Ki-ras in mucous cell associated with cancer, pancreatic cancer and hyperplasia
6) Confidence 0.45 Published 1993 Journal Cancer Res. Section Abstract Doc Link 8439969 Disease Relevance 0.69 Pain Relevance 0.13
Frequent c-Ki-ras oncogene activation in mucous cell hyperplasias of pancreas suffering from chronic inflammation.
Positive_regulation (activation) of c-Ki-ras in mucous cell associated with inflammation and hyperplasia
7) Confidence 0.45 Published 1993 Journal Cancer Res. Section Title Doc Link 8439969 Disease Relevance 0.71 Pain Relevance 0.13
However, among women, those with a larger BMI were more likely to have a Ki-ras mutation in their tumor.
Spec (likely) Positive_regulation (have) of Ki-ras associated with cancer
8) Confidence 0.45 Published 2001 Journal Mutat. Res. Section Abstract Doc Link 11600135 Disease Relevance 0.90 Pain Relevance 0.12
Another study evaluating KRAS/BRAF mutation status in 80 patients receiving cetuximab as single-agent found only 3 KRAS mutated tumors out of 27 patients who experienced a clinical benefit, but 27 out of 53 nonresponding patients [15].
Positive_regulation (evaluating) of KRAS associated with cancer
9) Confidence 0.43 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2432064 Disease Relevance 0.39 Pain Relevance 0
While there was a trend for an increased KRAS mutation frequency in nonresponder patients (12 mutations out of 23, 52%) as compared to responder patients (2 out of 9, 22%), authentic tumor response or long-term disease stabilization was found in KRAS mutated patients.


Positive_regulation (increased) of KRAS associated with cancer and disease
10) Confidence 0.40 Published 2008 Journal BMC Cancer Section Abstract Doc Link PMC2432064 Disease Relevance 0.64 Pain Relevance 0
Amado et al evaluated KRAS mutational status on patients treated in a randomized, trial evaluating panitumumab vs best supportive care.60 KRAS mutational status was obtained on 427 (92%) of 463 patients (208 panitumumab arm, 219 BSC).
Positive_regulation (supportive) of KRAS in arm
11) Confidence 0.40 Published 2009 Journal OncoTargets and therapy Section Body Doc Link PMC2886332 Disease Relevance 0.51 Pain Relevance 0
Codon 12 mutations usually lead to KRAS activation in colorectal cancer cell lines, but the activation status was not formally tested in EGI-1 [19].
Positive_regulation (activation) of KRAS in EGI-1 associated with colorectal cancer
12) Confidence 0.34 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2896958 Disease Relevance 0.33 Pain Relevance 0
Interestingly, none of 9 patients in the erlotinib arm had an EGFR mutation, whereas, 3 of 11 had the KRAS mutation.
Positive_regulation (had) of KRAS mutation in arm
13) Confidence 0.26 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721286 Disease Relevance 0.54 Pain Relevance 0.09
The mRNA levels of the foxes resulting from the crosses did not provide any strong evidence for a composite dominance effect (p-values > 0.13 for all genes, Table 3), and thus the major variation in mRNA levels between S and NS foxes appears to be due to a composite additive genetic effect.
Positive_regulation (variation) of NS
14) Confidence 0.18 Published 2007 Journal Behav Brain Funct Section Body Doc Link PMC1858698 Disease Relevance 0 Pain Relevance 0
We studied the effects of these sulindac metabolites in human colon cancer-derived Caco-2 cells that have been transfected with an activated K-ras oncogene.
Positive_regulation (activated) of K-ras oncogene in Caco-2 associated with colon cancer
15) Confidence 0.17 Published 2000 Journal Cancer Res. Section Abstract Doc Link 11118042 Disease Relevance 0.53 Pain Relevance 0.08
CEGG carried out the RT-PCR assays using RNA isolates from passages 1, 2 and 3 to determine serotype and to amplify the NS5 and NS3 genes for genotyping, and co-wrote the manuscript.
Positive_regulation (amplify) of NS3
16) Confidence 0.10 Published 2008 Journal BMC Microbiol Section Body Doc Link PMC2515156 Disease Relevance 0 Pain Relevance 0
For genotype 1a, there were significantly more unique variations in the SVR group compared to the NR sequences for the polyprotein, core, E1, p7, NS3/4A and NS5A in the CA patients, whereas no significant differences were observed for AA patients (Figure 6A).
Positive_regulation (sequences) of NS3 in SVR
17) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2815788 Disease Relevance 0.46 Pain Relevance 0
When each gene was analyzed separately, core, E1, E2, NS3/4A, NS4B, NS5A and NS5B were significant in genotype 1a, and core, E2, NS2 and NS3/4A were significant for genotype 1b, with up to a 28% increase in the probability of achieving SVR per additional unique variation (genotype 1b core, Table 3).


Positive_regulation (increase) of NS3 in SVR
18) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2815788 Disease Relevance 0.26 Pain Relevance 0
The resulting conversion of G-C base pairs to T-A leads to activation of the K-ras oncogene and inactivation of the p53 tumor suppressor gene [32].
Positive_regulation (activation) of K-ras oncogene associated with cancer
19) Confidence 0.05 Published 2003 Journal Respir Res Section Body Doc Link PMC314397 Disease Relevance 1.12 Pain Relevance 0
Important insights into the mechanisms of pancreatic adenocarcinoma pathogenesis have been gained from the use of genetically engineered mice that express an activating mutation in the Kras gene (KrasG12D) targeted to the pancreas [21], [24].
Positive_regulation (activating) of Kras gene in pancreas associated with adenocarcinoma
20) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2859948 Disease Relevance 1.34 Pain Relevance 0.03

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