Unbiased proteomics and molecular analysis revealed a new role for S6K1 in regulating DNA repair through the orchestrated phosphorylation of CDK1 and MSH6. The findings may explain why RPS6KB1 gene amplification contributed to breast cancer drug resistance.
Arnaud Carrier, Cécile Desjobert ... Paola B Arimondo
An original molecular multi-step approach integrating DNA methylome and chromosome-cluster localization cross-analysis identified a DNA methylation signature of patient outcome supporting that the core DNA methylation for a given trait is independent of the physiological context under which it arises.
Arbidol is a ATR inhibitor to reduce the phosphorylation and activation of MCM2 at Ser108, and innhibits the cell proliferation of ESCC in vitro and in vivo through the DNA replication and cell cycle pathway.
Amit Gutwillig, Nadine Santana-Magal ... Yaron Carmi
Tumors escape killing by the immune system through generating transient spatial cell-in-cell structures that are impenetrable to cytotoxic compounds including lytic granules and chemotherapy.
Nuria Vilaplana-Lopera, Vincent Cuminetti ... Paloma Garcia
Interplay between AML and stromal cells can initiate a mechanism involving gap junctions where ROS is transferred from cancer cells to stromal cells which then produce acetate which can in return be absorbed/utilised by the cancer cells.
Siavash Mansouri, Daniel Heylmann ... Rajkumar Savai
The crosstalk between cancer cell genomic features and the tumor microenvironment (TME) to reveal the impact of genetic alterations on the TME phenotype.
Detailed in vivo and in vitro experimental data in mice and human cell experimental data provide critical insight for understanding the role of the DC-based mechanical regulation of immunopathology in directing T cell lineage commitment in tumor microenvironments.
Özgün Le Roux, Nicole LK Pershing ... Christopher M Counter
Altering the level of different oncogenic mutants of Kras induces unique tumor patterns in mice, suggesting that tissue-specific responses mold the sensitivity of normal tissues to different oncogenic RAS mutations.
