Results 101 to 110 of about 902,007 (283)

Editorial from the New Co-Editors-in-Chief of ACM Transactions on Economics and Computation

open access: yes, 2023
Editorial from the New Co-Editors-in-Chief of ACM Transactions on Economics and ...
P Goldberg (13635205)   +1 more
core  

Differential expression of cancer‐related genes supports prediction of poor response to first‐line treatments in T‐ALL pediatric patients with high minimal residual disease

open access: yesMolecular Oncology, EarlyView.
In the present work, we have identified a transcriptional signature based on the differential expression of six genes (BCL2&MAST4, HSH2D&LAT2, METRN&PITPNM2) that would facilitate the early detection of T‐cell acute lymphoblastic leukemia (T‐ALL) patients prone to a poor treatment response and could be implemented at diagnosis, along with other risk ...
Antonio Lahera   +11 more
wiley   +1 more source

Letter from the Editors

open access: yes
This is a letter from the editors of the California Sociology Forum Student Journal of Sociology Volume 6 Spring ...
CSF Editors
core   +2 more sources

A word of thanks to our reviewers in 2017 and a call for new reviewers

open access: yesEuropean Journal of General Practice, 2018
Jelle Stoffers   +6 more
doaj   +1 more source

Beginnings: A Letter from the Editors

open access: yes, 2015
The editors would like to welcome you to the inaugural issue of ...
Akesis Editors
core  

CCDC80 suppresses high‐grade serous ovarian cancer migration via negative regulation of B7‐H3

open access: yesMolecular Oncology, EarlyView.
PAX8 is a lineage‐specific master regulator of transcription in high‐grade serous ovarian cancer (HGSC) progression. We show for the first time that PAX8 facilitates proliferation and metastasis by repressing the cell autonomous tumor suppressor CCDC80 and inducing B7‐H3 expression.
Aya Saleh   +12 more
wiley   +1 more source

E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer

open access: yesMolecular Oncology, EarlyView.
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov   +3 more
wiley   +1 more source

What did you do at work today?

open access: yesAustralian and New Zealand Journal of Public Health, 2014
John B. Lowe   +3 more
doaj   +1 more source

Foreword

open access: yesScientia Marina, 2014
Jordi Lleonart, Francesc Maynou
doaj   +1 more source

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