mTOR Pathway Overactivation in BRAF Mutated Papillary Thyroid Carcinoma | Zendy

Alexandra Faustino | Zendy; Joana Couto | Zendy; Helena Pópulo | Zendy; Ana Sofia Rocha | Zendy; Fernando Pardal | Zendy; José CameselleTeijeiro | Zendy; José Manuel Lopes | Zendy; Manuel SobrinhoSimões | Zendy; Paula Soares | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

mTOR Pathway Overactivation in BRAF Mutated Papillary Thyroid Carcinoma

Author(s) -

Alexandra Faustino,

Joana Couto,

Helena Pópulo,

Ana Sofia Rocha,

Fernando Pardal,

José CameselleTeijeiro,

José Manuel Lopes,

Manuel SobrinhoSimões,

Paula Soares

Publication year - 2012

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.206

H-Index - 353

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2011-2748

Subject(s) - pi3k/akt/mtor pathway , cancer research , gene knockdown , thyroid cancer , thyroid carcinoma , rptor , mapk/erk pathway , biology , protein kinase b , thyroid , context (archaeology) , signal transduction , medicine , endocrinology , microbiology and biotechnology , cell culture , genetics , paleontology

There are several genetic and molecular evidences suggesting dysregulation of the mammalian target of rapamycin (mTOR) pathway in thyroid neoplasia. Activation of the phosphatidylinositol-3-kinase/AKT pathway by RET/PTC and mutant RAS has already been demonstrated, but no data have been reported for the BRAF(V600E) mutation.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research