Results 111 to 120 of about 15,123,411 (350)

Special Treatment Everywhere, Special Treatment Nowhere

open access: yes, 2015
This symposium essay disputes the conventional wisdom that “special treatment” mandates are exceptional within employment discrimination jurisprudence. To the contrary, they are endemic, and necessarily so. This is true even within disparate treatment jurisprudence. The reasons are twofold.
openaire   +2 more sources

Aberrant expression of nuclear prothymosin α contributes to epithelial‐mesenchymal transition in lung cancer

open access: yesMolecular Oncology, EarlyView.
Nuclear prothymosin α inhibits epithelial‐mesenchymal transition (EMT) in lung cancer by increasing Smad7 acetylation and competing with Smad2 for binding to SNAI1, TWIST1, and ZEB1 promoters. In early‐stage cancer, ProT suppresses TGF‐β‐induced EMT, while its loss in the nucleus in late‐stage cancer leads to enhanced EMT and poor prognosis.
Liyun Chen   +12 more
wiley   +1 more source

Detecting homologous recombination deficiency for breast cancer through integrative analysis of genomic data

open access: yesMolecular Oncology, EarlyView.
This study develops a semi‐supervised classifier integrating multi‐genomic data (1404 training/5893 validation samples) to improve homologous recombination deficiency (HRD) detection in breast cancer. Our method demonstrates prognostic value and predicts chemotherapy/PARP inhibitor sensitivity in HRD+ tumours.
Rong Zhu   +12 more
wiley   +1 more source

Loss of proton‐sensing GPR4 reduces tumor progression in mouse models of colon cancer

open access: yesMolecular Oncology, EarlyView.
G protein‐coupled receptor 4 (GPR4) is a pH‐sensing receptor activated by acidic pH. GPR4 expression is increased in patients with inflammatory bowel disease who are at high risk of developing colorectal cancer. In mouse models, loss of GPR4 attenuated tumor progression. This correlated with increased IL2 and natural killer cell activity.
Leonie Perren   +16 more
wiley   +1 more source

The anticancer effect of the HDAC inhibitor belinostat is enhanced by inhibitors of Bcl‐xL or Mcl‐1 in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
The pan‐HDAC inhibitor belinostat increases the expression of the pro‐apoptotic proteins Bim, Puma, and Noxa and induces apoptosis in ovarian cancer cell lines and patient‐derived tumor organoids when used at high concentrations. Moreover, inhibiting the anti‐apoptotic proteins Bcl‐xL or Mcl‐1 sensitizes these preclinical models to the cytotoxic effect
Cécilia Thomine   +10 more
wiley   +1 more source

Systematic profiling of cancer‐fibroblast interactions reveals drug combinations in ovarian cancer

open access: yesMolecular Oncology, EarlyView.
Fibroblasts, cells in the tumor environment, support ovarian cancer cell growth and alter morphology and drug response. We used fibroblast and cancer cell co‐culture models to test 528 drugs and discovered new drugs for combination treatment. We showed that adding Vorinostat or Birinapant to standard chemotherapy may improve drug response, suggesting ...
Greta Gudoityte   +10 more
wiley   +1 more source

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