|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Western blot analysis of blast cells from patients with C-RAF germline mutations revealed loss of the tumor and metastasis suppressor RAF kinase inhibitor protein (RKIP).
|
19357705 |
2009 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Western blot analysis of tumor biopsies showed an increase in hsp70 and a decrease in cyclin D1 expression in the posttreatment biopsies but no significant effect on RAF kinases or phospho-extracellular signal-regulated kinase expression.
|
19088048 |
2008 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We have found that two solid tumors, peripheral neuroepithelioma and Ewing's sarcoma of bone, which share a common cytogenetic rearrangement, are characterized by an indistinguishable and highly reproducible pattern of protooncogene expression. c-myc, N-myc, c-myb, and c-mil/raf-1 are all expressed at similar levels in these tumors. c-fes and c-sis expression was not detected in any specimens of either tumor.
|
3390826 |
1988 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We found that EGFR-mediated MAPK pathway reactivation leads to resistance to vemurafenib in BRAF-mutant colorectal cancers and that combined RAF and EGFR inhibition can lead to sustained MAPK pathway suppression and improved efficacy in vitro and in tumor xenografts.
|
22448344 |
2012 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We demonstrate that CDK10 is an important determinant of resistance to endocrine therapies and show that CDK10 silencing increases ETS2-driven transcription of c-RAF, resulting in MAPK pathway activation and loss of tumor cell reliance upon estrogen signaling.
|
18242510 |
2008 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Vemurafenib, a selective inhibitor of RAF kinases, has clinical utility restricted to BRAF-mutant tumors.
|
24576830 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Vemurafenib and dabrafenib block MEK-ERK1/2 signaling and cause tumor regression in the majority of advanced-stage BRAF(V600E) melanoma patients; however, acquired resistance and paradoxical signaling have driven efforts for more potent and selective RAF inhibitors.
|
24422853 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Twenty-four (12.3 %) CRC cases carried mutations in the PIK3CA, and 18 of these tumors also contained activating alteration in the RAS/RAF genes (p = 0.007).
|
23943423 |
2013 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Tumours with EGFR GCN below 4.0 appear to be as refractory to anti-EGFR treatment as tumours with mutation in any of the RAS/RAF/PIK3CA pathway genes.
|
27879995 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
TTP defined as ≥50% increase in the sum of tumor diameters or appearance of new tumors was more strongly associated with OS than early tumor shrinkage in melanoma patients treated with RAF inhibitor.
|
26490313 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Treatment with RAF/MEK targeting agents (Hazard ratio (HR) = 0.16, 95%CI: 0.03-0.89, p = 0.037) and any decrease in tumor size after referral (HR = 0.07, 95%CI: 0.015-0.35, p = 0.001) correlated with longer survival in mutBRAF patients.
|
22039425 |
2011 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
To the standard prognostic features, only six markers added independent prognostic information including receptor for hyaluronic acid mediated motility (RHAMM) (HR = 2.39 (1.88 to 3.05)), epidermal growth factor receptor (HR = 1.65 (1.31 to 2.09)), tumour infiltrating lymphocytes (HR = 0.7 (0.54 to 0.92)), urokinase plasminogen activator (HR = 1.38 (1.09 to 1.75)), Raf-1 kinase inhibitor protein (HR = 0.75 (0.58 to 0.96)) and mammalian sterile 20-like kinase 1 (MST1) (HR = 0.75 (0.58 to 0.95).
|
18436576 |
2008 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To identify downstream targets of the metastasis suppressor Raf-1 kinase inhibitory protein (RKIP/PEBP1), we utilized an integrated approach based upon statistical analysis of tumor gene expression data combined with experimental validation.
|
23975428 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
To better understand the role of RAF→MEK→ERK signaling on PDA cell proliferation, we assessed the consequences of MEK inhibition on global patterns of mRNA expression and tumor cell proliferation in a panel of human PDA-derived cell lines.
|
22833572 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, expression of miR-195 or knockdown of Raf-1 can similarly reduce tumor cell survival but increase apoptosis through downregulation of Raf-1 and Bcl-2 and P-glycoprotein expression.
|
23760062 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Three loci, DNF 15S2, RAF1, and D3S18, were homozygous in all tumors in the SCLC panel.
|
1982064 |
1990 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This review will discuss the development of a potential treatment algorithm for acromegaly addressing the biochemical control of the disease as well of its associated comorbidities, under a personalized approach based upon markers of prognostic and predictive significance, such as tumour size, MRI adenoma signal, GH value after acute octreotide test, granular adenoma pattern, Ki-67, somatostatin receptor phenotype, aryl hydrocarbon-interacting protein expression, gsp mutations, RAF kinase activity, E-cadherin and beta-arrestin-1.
|
25640882 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This review article will address: (a) preclinical data on the antitumor activity of BRAF inhibitors in cell lines/ in vivo models and their opposing functions as inhibitors or activators of the MAPK pathway, depending on the cellular context; (b) drug development from non-selective RAF inhibitors to selective BRAF inhibitors, such as PLX4032 and GSK2118436, with emphasis in the clinical efficacy and toxicity of these agents; and (c) possible mechanisms of resistance to BRAF inhibitors and strategies to overcome its development in BRAF mutant tumors.
|
21426297 |
2011 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This is a highly relevant therapeutic issue that needs to be addressed to combat tumours that rely on constitutively active RAF and RAS mutants and the MAPK pathway.
|
31126017 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
This tumor displayed rearrangements of chromosome 3 and no LOH at the c-RAF-1 (close to the Von Hippel Lindau gene) locus.
|
9844606 |
1998 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Thirty fresh tumor specimens were analyzed for the presence of raf gene activation using Southern blot analysis.
|
8421418 |
1993 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These results suggest that normal human cells have redundant arrest pathways, which can be activated by Raf-1, and that even tumors that have dismantled p16(Ink4a)-dependent growth arrest pathways are potentially regulated by a second p21(Cip1)-dependent growth arrest pathway.
|
11278920 |
2001 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These data suggest that the therapeutic efficacy of paclitaxel in ovarian cancer patient whose tumors have TP53mut might be increased if it is administered in combination with Raf-1 kinase inhibitors, e.g., ISIS 5132.
|
10854551 |
2000 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These data suggest that the clinical effectiveness of paclitaxel could be substantially improved by the use of Raf-1 kinase inhibitors, provided that a similar relationship between Raf-1 kinase activity and paclitaxel cytotoxicity exists in the clinic, especially in those tumor sites where paclitaxel is the current treatment of choice e.g., ovarian and breast cancer.
|
9607567 |
1998 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These data suggest that mutational activation of the RAS/RAF/MAPK pathway in nevi is a critical step in the initiation of melanocytic neoplasia but alone is insufficient for melanoma tumorigenesis.
|
12447372 |
2003 |