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Africa Fernandez-L

Researcher at Memorial Sloan Kettering Cancer Center

Publications -  19
Citations -  2258

Africa Fernandez-L is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: Endoglin & Sonic hedgehog. The author has an hindex of 19, co-authored 19 publications receiving 2051 citations. Previous affiliations of Africa Fernandez-L include Carlos III Health Institute & Spanish National Research Council.

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Subgroup-specific structural variation across 1,000 medulloblastoma genomes

Paul A. Northcott, +139 more
- 02 Aug 2012 - 
TL;DR: Somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas are reported, including recurrent events targeting TGF-β signalling in Group 3, and NF-κB signalling in Groups 4, which suggest future avenues for rational, targeted therapy.
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YAP1 is amplified and up-regulated in hedgehog-associated medulloblastomas and mediates Sonic hedgehog-driven neural precursor proliferation

TL;DR: Up-regulation of the oncogenic transcriptional coactivator yes-associated protein 1 (YAP1), which is negatively regulated by the Hippo pathway, is reported in human medulloblastomas with aberrant Shh signaling, implicate YAP1 as a new Shh effector that may be targeted by medullOBlastoma therapies aimed at eliminating medulloplastoma recurrence.
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Oncogenic YAP promotes radioresistance and genomic instability in medulloblastoma through IGF2-mediated Akt activation

TL;DR: It is reported that YAP accelerates tumor growth and confers radioresistance, promoting ongoing proliferation after radiation, and indicates the YAP/IGF2/Akt axis as a therapeutic target in medulloblastoma.
Journal ArticleDOI

Hereditary hemorrhagic telangiectasia, a vascular dysplasia affecting the TGF-beta signaling pathway.

TL;DR: The recent isolation and characterization of circulating endothelial cells from HHT patients has revealed a decreased endoglin expression, impaired ALK1- and ALK5-dependent TGF-beta signaling, disorganized cytoskeleton and the failure to form cord-like structures which may lead to the fragility of small vessels with bleeding characteristic of HHT vascular dysplasia.