Progression of BRAF-induced thyroid cancer is associated with epithelial-mesenchymal transition requiring concomitant MAP kinase and TGFβ signaling. - Wikidata - awgldk - TriplyDB

Progression of BRAF-induced thyroid cancer is associated with epithelial-mesenchymal transition requiring concomitant MAP kinase and TGFβ signaling.

Progression of BRAF-induced thyroid cancer is associated with epithelial-mesenchymal transition requiring concomitant MAP kinase and TGFβ signaling.

http://www.wikidata.org/entity/Q33839230

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BRAF activates and physically interacts with PAK to regulate cell motility Oxidative stress: a new risk factor for thyroid cancer Oncogenic BRAF disrupts thyroid morphogenesis and function via twist expression.The role of podoplanin in the biology of differentiated thyroid cancers.Apigenin in combination with Akt inhibition significantly enhances thyrotropin-stimulated radioiodide accumulation in thyroid cells.BRAF-activated long non-coding RNA contributes to colorectal cancer migration by inducing epithelial-mesenchymal transition.Stemness is Derived from Thyroid Cancer Cells.S100-A10, thioredoxin, and S100-A6 as biomarkers of papillary thyroid carcinoma with lymph node metastasis identified by MALDI imaging.MicroRNA Deregulation in Anaplastic Thyroid Cancer Biology.Obatoclax overcomes resistance to cell death in aggressive thyroid carcinomas by countering Bcl2a1 and Mcl1 overexpression.Molecular pathogenesis and mechanisms of thyroid cancer Biotinidase is a novel marker for papillary thyroid cancer aggressiveness.An Ep-ICD based index is a marker of aggressiveness and poor prognosis in thyroid carcinoma.Genetic and pharmacological targeting of CSF-1/CSF-1R inhibits tumor-associated macrophages and impairs BRAF-induced thyroid cancer progression.Single live cell TGF-β signalling imaging: breast cancer cell motility and migration is driven by sub-populations of cells with dynamic TGF-β-Smad3 activity.Expression of cancer stem cell markers and epithelial-mesenchymal transition-related factors in anaplastic thyroid carcinoma.Late intervention with anti-BRAF(V600E) therapy induces tumor regression in an orthotopic mouse model of human anaplastic thyroid cancer.BRAFV600E-Associated Gene Expression Profile: Early Changes in the Transcriptome, Based on a Transgenic Mouse Model of Papillary Thyroid Carcinoma.GLI1 Transcription Factor Affects Tumor Aggressiveness in Patients With Papillary Thyroid Cancers.The Clinicopathological Features of BRAF Mutated Papillary Thyroid Cancers in Chinese Patients Epigenetics modifications and therapeutic prospects in human thyroid cancer.Mouse models of follicular and papillary thyroid cancer progression.Inflammatory mediators, tumor necrosis factor-α and interferon-γ, induce EMT in human PTC cell lines Expression of epithelial-mesenchymal transition regulators SNAI2 and TWIST1 in thyroid carcinomas.Evolving approaches to patients with advanced differentiated thyroid cancer The immune network in thyroid cancer Oncogenic B-RAF(V600E) signaling induces the T-Box3 transcriptional repressor to repress E-cadherin and enhance melanoma cell invasion.Obatoclax kills anaplastic thyroid cancer cells by inducing lysosome neutralization and necrosis The role of epithelial mesenchymal transition markers in thyroid carcinoma progression.BRAF and epithelial-mesenchymal transition in papillary thyroid carcinoma - challenging the roles of Snail and E-Cadherin?Fisetin inhibits human melanoma cell invasion through promotion of mesenchymal to epithelial transition and by targeting MAPK and NFκB signaling pathways Papillary thyroid carcinomas with cervical lymph node metastases can be stratified into clinically relevant prognostic categories using oncogenic BRAF, the number of nodal metastases, and extra-nodal extension.E-cadherin expression and cell proliferation in the primary tumor and metastatic lymph nodes of papillary thyroid microcarcinoma β-catenin signaling is required for RAS-driven thyroid cancer through PI3K activation.Thyrotropin signaling confers more aggressive features with higher genomic instability on BRAF(V600E)-induced thyroid tumors in a mouse model Down-regulation of 14q32-encoded miRNAs and tumor suppressor role for miR-654-3p in papillary thyroid cancer.p53 constrains progression to anaplastic thyroid carcinoma in a Braf-mutant mouse model of papillary thyroid cancer Cell Cycle M-Phase Genes Are Highly Upregulated in Anaplastic Thyroid Carcinoma.Effects of Curcumin on Tobacco Smoke-induced Hepatic MAPK Pathway Activation and Epithelial-Mesenchymal Transition In Vivo.NADPH Oxidase NOX4 Is a Critical Mediator of BRAFV600E-Induced Downregulation of the Sodium/Iodide Symporter in Papillary Thyroid Carcinomas.

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Progression of BRAF-induced thyroid cancer is associated with epithelial-mesenchymal transition requiring concomitant MAP kinase and TGFβ signaling.

http://www.wikidata.org/entity/Q33839230

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Progression of BRAF-induced th ...... MAP kinase and TGFβ signaling.

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P2860

Smurf2 is a ubiquitin E3 ligase mediating proteasome-dependent degradation of Smad2 in transforming growth factor-beta signaling

TGF beta signals through a heteromeric protein kinase receptor complex

Evolving gene/transcript definitions significantly alter the interpretation of GeneChip data.

The novel E3 ubiquitin ligase Tiul1 associates with TGIF to target Smad2 for degradation

ConceptGen: a gene set enrichment and gene set relation mapping tool

The basics of epithelial-mesenchymal transition

Fast-Find: a novel computational approach to analyzing combinatorial motifs.

Clinical implication of hot spot BRAF mutation, V599E, in papillary thyroid cancers

Smad-dependent and Smad-independent pathways in TGF-beta family signalling

The BRAFV600E oncogene induces transforming growth factor beta secretion leading to sodium iodide symporter repression and increased malignancy in thyroid cancer

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