rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
Mechanisms of Acquired Resistance to BRAF V600E Inhibition in Colon Cancers Converge on RAF Dimerization and Are Sensitive to Its Inhibition.
|
28951457 |
2017 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
Our data suggest that BRAF(V600E) mutant colon cancers (approximately 8-10% of all colon cancers), for which there are currently no targeted treatment options available, might benefit from combination therapy consisting of BRAF and EGFR inhibitors.
|
22281684 |
2012 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
In conclusion, our findings suggest that targeting ErbB-3 receptors could represent an effective therapeutic approach in BRAF-V600E mutant colon cancer.
|
26160848 |
2015 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
The results of these studies suggest that combined treatment of BRAF(V600E)-driven colon cancers with both vemurafenib and EGFR inhibitors is worth clinical evaluation.
|
23074264 |
2012 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
Colon cancers carrying BRAF V600E and β-catenin T41A activating mutations are resistant to numerous common anticancer drugs.
|
29541216 |
2018 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
Most BRAF (V600E) mutant melanomas are sensitive to selective BRAF inhibitors, but BRAF mutant colon cancers are intrinsically resistant to these drugs because of feedback activation of EGFR.
|
26365186 |
2015 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
Sorafenib and cetuximab therapy led to a mixed radiographic response with some areas showing dramatic improvement and other areas showing stable disease over a 7-month period which is a notably long period of progression-free survival for V600E BRAF mutated colon cancer.
|
23792568 |
2013 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
The clinical studies in the manuscript by Al-Marrawi et al. describe the rational combination of signaling inhibitors in a colon cancer patient whose tumor cells express a mutant active B-RAF V600E protein that signals into the MEK1/2-ERK1/2 pathway downstream of K-RAS; this is a particularly aggressive form of colon cancer for which few rational therapeutic interventions have been available until recent times.
|
24025253 |
2013 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
Colon cancers from 2008 to 2012 tested by pyrosequencing for BRAF V600E mutation were selected.
|
23650027 |
2013 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
Female patients and older group harbored a higher KRAS mutation (P = 0.018 and P = 0.031, respectively); BRAF (V600E) mutation showed a higher frequency in colon cancer and poor differentiation tumors (P = 0.020 and P = 0.030, respectively); proximal tumors appeared a higher PIK3CA mutation (P<0.001) and distant metastatic tumors shared a higher NRAS mutation (P = 0.010).
|
24339949 |
2013 |
rs397517132
|
|
Malignant tumor of colon
|
|
0.100 |
GeneticVariation
|
BEFREE |
In contrast, colon cancers that harbour the same BRAF(V600E) mutation are intrinsically resistant to BRAF inhibitors, due to feedback activation of the epidermal growth factor receptor (EGFR).
|
24670642 |
2014 |