scholarly journals Absence of Germline Mutations in Genes within the MAP Kinase Pathway in Familial Nonmedullary Thyroid Cancer

Cell Cycle ◽  
2006 ◽  
Vol 5 (17) ◽  
pp. 2036-2039 ◽  
Author(s):  
Peng Hou ◽  
Mingzhao Xing
Keyword(s):  
Thyroid Cancer ◽  
Map Kinase ◽  
Germline Mutations ◽  
Map Kinase Pathway ◽  
Kinase Pathway

scholarly journals Redifferentiation-facilitated radioiodine therapy in thyroid cancer

2021 ◽  
Author(s):  
Livia Lamartina ◽  
Nadège Anizan ◽  
Corinne Dupuy ◽  
Sophie Leboulleux ◽  
Martin Schlumberger
Keyword(s):  
Experimental Data ◽  
Thyroid Cancer ◽  
Map Kinase ◽  
Alternative Treatment ◽  
Preliminary Data ◽  
Radioiodine Therapy ◽  
Small Series ◽  
Map Kinase Pathway ◽  
Kinase Pathway ◽  
Stimulation Of

Based on experimental data, the inhibition of the MAPkinase pathway in patients with radioiodine refractory thyroid cancer was capable to induce a redifferentiation. Preliminary data obtained on small series of patients are encouraging and this strategy might become an alternative treatment in those patients with a druggable mutation that induces a stimulation of the MAP kinase pathway. This is an active field of research to answer many still unresolved questions.

scholarly journals PIK3CAH1047R-induced paradoxical ERK activation results in resistance to BRAFV600E specific inhibitors in BRAFV600E PIK3CAH1047R double mutant thyroid tumors

2017 ◽  
Author(s):  
Matthias A. Roelli ◽  
Dorothée Ruffieux-Daidié ◽  
Amandine Stooss ◽  
Oussama ElMokh ◽  
Wayne A. Phillips ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Mouse Model ◽  
Map Kinase ◽  
Double Mutant ◽  
Great Success ◽  
Thyroid Carcinomas ◽  
Map Kinase Pathway ◽  
Phosphoinositide 3 Kinase ◽  
Kinase Pathway ◽  
Specific Inhibitors

AbstractThyroid carcinomas are the most prevalent endocrine cancers. The BRAFV600E mutation is found in 40% of the papillary type and 25% of the anaplastic type. BRAFV600E inhibitors have shown great success in melanoma but, they have been, to date, less successful in thyroid cancer. About 50% of anaplastic thyroid carcinomas present mutations/amplification of the phosphatidylinositol 3’ kinase. Here we propose to investigate if the hyper activation of that pathway could influence the response to BRAFV600E specific inhibitors.To test this, we used two mouse models of thyroid cancer. Single mutant (BRAFV600E) mice responded to BRAFV600E-specific inhibition (PLX-4720), while double mutant mice (BRAFV600E; PIK3CAH1047R) showed resistance and even signs of aggravation. This resistance was abrogated by combination with a phosphoinositide 3-kinase inhibitor. At the molecular level, we could show that this resistance was concomitant to a paradoxical activation of the MAP-Kinase pathway, which could be overturned by phosphoinositide 3-kinase inhibition in vivo in our mouse model and in vitro in human double mutant cell lines.In conclusion, we reveal a phosphoinositide 3-kinase driven, paradoxical MAP-Kinase pathway activation as mechanism for resistance to BRAFV600E specific inhibitors in a clinically relevant mouse model of thyroid cancer.

577: The RAF/MAP Kinase Pathway Influences Survival in Androgen-Insensitive Prostate Cancer

2005 ◽  
Vol 173 (4S) ◽  
pp. 157-158
Author(s):  
Rono Mukherjee ◽  
Sarath K. Nalagatla ◽  
Mark A. Undenvood ◽  
John M.S. Bartlett ◽  
Joanne Edwards
Keyword(s):  
Prostate Cancer ◽  
Map Kinase ◽  
Map Kinase Pathway ◽  
Kinase Pathway

scholarly journals Development of anticancer drugs targeting the MAP kinase pathway

Oncogene ◽  
2000 ◽  
Vol 19 (56) ◽  
pp. 6594-6599 ◽  
Author(s):  
Judith S Sebolt-Leopold
Keyword(s):  
Map Kinase ◽  
Anticancer Drugs ◽  
Map Kinase Pathway ◽  
Kinase Pathway

scholarly journals The MADD-3 LAMMER Kinase Interacts with a p38 MAP Kinase Pathway to Regulate the Display of the EVA-1 Guidance Receptor in Caenorhabditis elegans

PLoS Genetics ◽  
2016 ◽  
Vol 12 (4) ◽  
pp. e1006010 ◽  
Author(s):  
Serena A. D’Souza ◽  
Luckshi Rajendran ◽  
Rachel Bagg ◽  
Louis Barbier ◽  
Derek M. van Pel ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Caenorhabditis Elegans ◽  
Map Kinase ◽  
Motor Neurons ◽  
Leading Edge ◽  
P38 Map Kinase ◽  
Endosomal Trafficking ◽  
Guidance Cue ◽  
Map Kinase Pathway ◽  
Kinase Pathway

The proper display of transmembrane receptors on the leading edge of migrating cells and cell extensions is essential for their response to guidance cues. We previously discovered that MADD-4, which is an ADAMTSL secreted by motor neurons in Caenorhabditis elegans, interacts with an UNC-40/EVA-1 co-receptor complex on muscles to attract plasma membrane extensions called muscle arms. In nematodes, the muscle arm termini harbor the post-synaptic elements of the neuromuscular junction. Through a forward genetic screen for mutants with disrupted muscle arm extension, we discovered that a LAMMER kinase, which we call MADD-3, is required for the proper display of the EVA-1 receptor on the muscle’s plasma membrane. Without MADD-3, EVA-1 levels decrease concomitantly with a reduction of the late-endosomal marker RAB-7. Through a genetic suppressor screen, we found that the levels of EVA-1 and RAB-7 can be restored in madd-3 mutants by eliminating the function of a p38 MAP kinase pathway. We also found that EVA-1 and RAB-7 will accumulate in madd-3 mutants upon disrupting CUP-5, which is a mucolipin ortholog required for proper lysosome function. Together, our data suggests that the MADD-3 LAMMER kinase antagonizes the p38-mediated endosomal trafficking of EVA-1 to the lysosome. In this way, MADD-3 ensures that sufficient levels of EVA-1 are present to guide muscle arm extension towards the source of the MADD-4 guidance cue.

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