Evaluating the Quality of Real-World Data on Adherence to Oral Endocrine Therapy in Breast Cancer Patients: How Real Is Real-World Data?

Purpose: The aim of this study was to compare estimates of adherence to oral endocrine therapy (OET) based on real-world data (RWD) and on clinical evaluation in people diagnosed with breast cancer in the public healthcare system in Catalonia (Spain).

Methods: We conducted two retrospective cohort studies. Cohort 1 (RWD) consisted of women diagnosed with breast cancer in 2021 in the public healthcare system of Catalonia (Spain).

The Impact of the COVID-19 Pandemic on Adherence to Endocrine Therapy for Breast Cancer in Catalonia (Spain).

. To assess the impact of the COVID-19 pandemic on adherence to oral endocrine therapy in patients diagnosed with breast cancer in the public healthcare system in Catalonia (Spain). .

BRAF activation by metabolic stress promotes glycolysis sensitizing NRAS-mutated melanomas to targeted therapy.

NRAS-mutated melanoma lacks a specific line of treatment. Metabolic reprogramming is considered a novel target to control cancer; however, NRAS-oncogene contribution to this cancer hallmark is mostly unknown. Here, we show that NRAS-mutated melanomas specific metabolic settings mediate cell sensitivity to sorafenib upon metabolic stress.

The Expression of TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Can Be Controlled by the Antioxidant Orchestrator NRF2 in Human Carcinoma Cells.

Hyperactivation of the KEAP1-NRF2 axis is a common molecular trait in carcinomas from different origin. The transcriptional program induced by NRF2 involves antioxidant and metabolic genes that render cancer cells more capable of dealing with oxidative stress. The TP53-Induced Glycolysis and Apoptosis Regulator () is an important regulator of glycolysis and the pentose phosphate pathway that was described as a p53 response gene, yet expression is detected in p53-null tumors.

TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Is Upregulated in Lymphocytes Stimulated with Concanavalin A.

The glycolytic modulator TP53-Inducible Glycolysis and Apoptosis Regulator (TIGAR) is overexpressed in several types of cancer and has a role in metabolic rewiring during tumor development. However, little is known about the role of this enzyme in proliferative tissues under physiological conditions. In the current work, we analysed the role of TIGAR in primary human lymphocytes stimulated with the mitotic agent Concanavalin A (ConA).