|
Pancreatic carcinoma
|
|
0.050 |
GeneticVariation
|
BEFREE |
Using the whole-cell recording mode of the patch-clamp technique, functional ion channels were electrophysiologically characterized in PANC-1 (K-ras G12D (+/-), p53 R273C, Deltap16), BxPC-3 (smad4-, p53 Y220C, Deltap16), and MiaPaCa-2 [transforming growth factor-beta receptor type II defect, K-ras G12C(-/-), p53 R248W, Deltap16] human pancreatic cancer cell lines.
|
14978241 |
2004 |
|
Malignant neoplasm of pancreas
|
|
0.040 |
GeneticVariation
|
BEFREE |
Using the whole-cell recording mode of the patch-clamp technique, functional ion channels were electrophysiologically characterized in PANC-1 (K-ras G12D (+/-), p53 R273C, Deltap16), BxPC-3 (smad4-, p53 Y220C, Deltap16), and MiaPaCa-2 [transforming growth factor-beta receptor type II defect, K-ras G12C(-/-), p53 R248W, Deltap16] human pancreatic cancer cell lines.
|
14978241 |
2004 |
|
Immunologic Deficiency Syndromes
|
|
0.020 |
GeneticVariation
|
BEFREE |
We show here that the expression of K-ras(G12V) oncogene in a near diploid HPV16-E6E7 gene immortalized human pancreatic duct epithelial cell line originally derived from normal pancreas induced the formation of carcinoma in 50% of severe combined immunodeficient mice implanted with these cells.
|
15958547 |
2005 |
|
Malignant tumor of colon
|
|
0.010 |
GeneticVariation
|
BEFREE |
The GR/RR IRS1 genotypes were associated with an increased risk of colon cancers with the KRAS2 G12D mutation (OR 2.3, 95% CI 1.5, 3.5 versus controls, OR 1.7, 95% CI 1.1, 2.6 versus KRAS2 wild type), the "no 192" IGFI genotype increased the risk of the KRAS2 G13D mutation (OR 2.3, 95% CI 1.2, 4.2 versus controls, OR 2.1, 95% CI 1.1, 4.0 versus wild type), and the DD IRS2 genotype increased the risk of the G12V KRAS2 mutation (OR 1.8, 95% CI 0.9, 3.5 versus controls, OR 2.0, 95% CI 1.0, 4.0 versus wild type).
|
16448675 |
2006 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Kras(G12D) and Smad4/Dpc4 haploinsufficiency cooperate to induce mucinous cystic neoplasms and invasive adenocarcinoma of the pancreas.
|
17349581 |
2007 |
|
Adenocarcinoma
|
|
0.080 |
GeneticVariation
|
BEFREE |
We show here that concomitant expression of Kras(G12D) and haploinsufficiency of the Smad4/Dpc4 tumor suppressor gene engenders a distinct class of pancreatic tumors, mucinous cystic neoplasms (MCNs), which culminate in invasive ductal adenocarcinomas.
|
17349581 |
2007 |
|
Pancreatic Neoplasm
|
|
0.010 |
GeneticVariation
|
BEFREE |
We show here that concomitant expression of Kras(G12D) and haploinsufficiency of the Smad4/Dpc4 tumor suppressor gene engenders a distinct class of pancreatic tumors, mucinous cystic neoplasms (MCNs), which culminate in invasive ductal adenocarcinomas.
|
17349581 |
2007 |
|
Adenocarcinoma of pancreas
|
|
0.010 |
GeneticVariation
|
BEFREE |
Kras(G12D) and Smad4/Dpc4 haploinsufficiency cooperate to induce mucinous cystic neoplasms and invasive adenocarcinoma of the pancreas.
|
17349581 |
2007 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Introduction of an RCAS vector with Bryan-RSV polymerase and subgroup A envelope [RCASBP(A)] carrying oncogenic Kras(G12D) induced focal ductal pancreatic lesions that recapitulate human pancreatic intraepithelial neoplasias that progress to pancreatic ductal adenocarcinomas.
|
18621715 |
2008 |
|
Adenocarcinoma
|
|
0.080 |
GeneticVariation
|
BEFREE |
TVA-mediated infection of genetically engineered mice with endogenous expression of Kras(G12D) in pancreatic progenitor cells by using RCASBP(A) virus carrying a short hairpin RNA directed against murine TP53, resulted in dramatically enhanced progression to invasive adenocarcinomas.
|
18621715 |
2008 |
|
Malignant neoplasm of breast
|
|
0.010 |
GeneticVariation
|
BEFREE |
The D153G substitution only partially segregated with breast cancer in the family and was not identified on additional 680 chromosomes screened.
|
18279506 |
2008 |
|
Breast Carcinoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
The D153G substitution only partially segregated with breast cancer in the family and was not identified on additional 680 chromosomes screened.
|
18279506 |
2008 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here, we have developed an inducible oral-specific animal tumor model system, which consists in the expression of a tamoxifen-inducible Cre recombinase (CreER(tam)) under the control of the cytokeratin 14 (K14) promoter (K14-CreER(tam)) and mice in which the endogenous K-ras locus is targeted (LSL-K-ras(G12D)), thereby causing the expression of endogenous levels of oncogenic K-ras(G12D) following removal of a stop element.
|
19435901 |
2009 |
|
Lung Neoplasms
|
|
0.030 |
GeneticVariation
|
BEFREE |
Conversely, in lung tumour cell lines expressing Kras(G12D) and lacking p53, p53 restoration led to NF-kappaB inhibition.
|
19847165 |
2009 |
|
Sarcoma
|
|
0.020 |
GeneticVariation
|
BEFREE |
These results suggest that genomic alterations present in human MFH are conserved in the LSL-Kras(G12D); p53(Flox/Flox) mouse model of soft tissue sarcoma and demonstrate the utility of this pre-clinical model.
|
19956606 |
2009 |
|
melanoma
|
|
0.020 |
GeneticVariation
|
BEFREE |
We detected the p.Gly23Asp missense mutation in one of the two tested melanoma patients of a family with three melanoma cases.
|
19712690 |
2009 |
|
Adult Soft Tissue Sarcoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
These results suggest that genomic alterations present in human MFH are conserved in the LSL-Kras(G12D); p53(Flox/Flox) mouse model of soft tissue sarcoma and demonstrate the utility of this pre-clinical model.
|
19956606 |
2009 |
|
Papilloma
|
|
0.010 |
GeneticVariation
|
BEFREE |
Surprisingly, whereas K14-CreER(tam) can also target the skin, K14-CreER(tam)/LSL-K-ras(G12D) mice developed papillomas exclusively in the oral mucosa within 1 month after tamoxifen treatment.
|
19435901 |
2009 |
|
Sarcoma of soft tissue
|
|
0.010 |
GeneticVariation
|
BEFREE |
These results suggest that genomic alterations present in human MFH are conserved in the LSL-Kras(G12D); p53(Flox/Flox) mouse model of soft tissue sarcoma and demonstrate the utility of this pre-clinical model.
|
19956606 |
2009 |
|
Childhood Soft Tissue Sarcoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
These results suggest that genomic alterations present in human MFH are conserved in the LSL-Kras(G12D); p53(Flox/Flox) mouse model of soft tissue sarcoma and demonstrate the utility of this pre-clinical model.
|
19956606 |
2009 |
|
Non-Metastatic Childhood Soft Tissue Sarcoma
|
|
0.010 |
GeneticVariation
|
BEFREE |
These results suggest that genomic alterations present in human MFH are conserved in the LSL-Kras(G12D); p53(Flox/Flox) mouse model of soft tissue sarcoma and demonstrate the utility of this pre-clinical model.
|
19956606 |
2009 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In contrast, the combination of p53 RNAi knockdown with expression of oncogenic H-Ras(G12V) transformed the p16-deficient BAR-T cells, as evidenced by their loss of contact inhibition, by their formation of colonies in soft agar, and by their generation of tumors in immunodeficient mice.
|
20927195 |
2010 |
|
Neoplasm Metastasis
|
|
0.040 |
GeneticVariation
|
BEFREE |
In summary, by using 'knock-in' mutations of Trp53 we have identified two critical acquired functions of a stably expressed mutant form of p53 that drive PDAC; first, an escape from Kras(G12D)-induced senescence/growth arrest and second, the promotion of metastasis.
|
20018721 |
2010 |
|
Immunologic Deficiency Syndromes
|
|
0.020 |
GeneticVariation
|
BEFREE |
In contrast, the combination of p53 RNAi knockdown with expression of oncogenic H-Ras(G12V) transformed the p16-deficient BAR-T cells, as evidenced by their loss of contact inhibition, by their formation of colonies in soft agar, and by their generation of tumors in immunodeficient mice.
|
20927195 |
2010 |
|
Precancerous Conditions
|
|
0.010 |
GeneticVariation
|
BEFREE |
Loss, or mutation, of Trp53 allows retention of the Kras(G12D)-expressing cells and drives rapid progression of these premalignant lesions to PDAC.
|
20018721 |
2010 |