Patricia Sancho

Differential effects of catalase on apoptosis induction in human promonocytic cells. Relationships with heat-shock protein expression.

12-O-tetradecanoylphorbol-13-acetate may both potentiate and decrease the generation of apoptosis by the antileukemic agent arsenic trioxide in human promonocytic cells. Regulation by extracellular signal-regulated protein kinases and glutathione.

Pharmacologic inhibitors of PI3K/Akt potentiate the apoptotic action of the antileukemic drug arsenic trioxide via glutathione depletion and increased peroxide accumulation in myeloid leukemia cells.

Pharmacological inhibitors of extracellular signal-regulated protein kinases attenuate the apoptotic action of cisplatin in human myeloid leukemia cells via glutathione-independent reduction in intracellular drug accumulation.

Drp1 mediates caspase-independent type III cell death in normal and leukemic cells.

Inhibition of the EGF receptor blocks autocrine growth and increases the cytotoxic effects of doxorubicin in rat hepatoma cells: role of reactive oxygen species production and glutathione depletion.

Upregulation of the NADPH oxidase NOX4 by TGF-beta in hepatocytes is required for its pro-apoptotic activity.

The inhibition of the epidermal growth factor (EGF) pathway enhances TGF-beta-induced apoptosis in rat hepatoma cells through inducing oxidative stress coincident with a change in the expression pattern of the NADPH oxidases (NOX) isoforms.

Caspase-independent type III programmed cell death in chronic lymphocytic leukemia: the key role of the F-actin cytoskeleton.

Role of CXCR4/SDF-1 alpha in the migratory phenotype of hepatoma cells that have undergone epithelial-mesenchymal transition in response to the transforming growth factor-beta.

Overactivation of the MEK/ERK pathway in liver tumor cells confers resistance to TGF-{beta}-induced cell death through impairing up-regulation of the NADPH oxidase NOX4.

NADPH oxidase NOX1 controls autocrine growth of liver tumor cells through up-regulation of the epidermal growth factor receptor pathway.

Snail1 suppresses TGF-beta-induced apoptosis and is sufficient to trigger EMT in hepatocytes.

Dissecting the effect of targeting the epidermal growth factor receptor on TGF-β-induced-apoptosis in human hepatocellular carcinoma cells.

The NADPH oxidase inhibitor VAS2870 impairs cell growth and enhances TGF-β-induced apoptosis of liver tumor cells.

Sorafenib sensitizes hepatocellular carcinoma cells to physiological apoptotic stimuli.

The tyrphostin AG1478 inhibits proliferation and induces death of liver tumor cells through EGF receptor-dependent and independent mechanisms.

Reciprocal regulation of NADPH oxidases and the cyclooxygenase-2 pathway.

Lack of amino acids in mouse hepatocytes in culture induces the selection of preneoplastic cells.

Resilience and coping as predictors of general well-being in the elderly: a structural equation modeling approach.

Protein-tyrosine phosphatase 1B (PTP1B) deficiency confers resistance to transforming growth factor-β (TGF-β)-induced suppressor effects in hepatocytes.

Predicting perceived health in Angolan elderly: the moderator effect of being oldest old.

NADPH oxidase NOX4 mediates stellate cell activation and hepatocyte cell death during liver fibrosis development.

Coping strategies: gender differences and development throughout life span.

ROS production is essential for the apoptotic function of E2F1 in pheochromocytoma and neuroblastoma cell lines.

Overactivation of the TGF-β pathway confers a mesenchymal-like phenotype and CXCR4-dependent migratory properties to liver tumor cells.

TGF-beta signaling in cancer treatment.

Metformin targets the metabolic achilles heel of human pancreatic cancer stem cells.

[Cost-consequence analysis of respiratory preventive intervention among institutionalized older people: randomized controlled trial].

The NADPH oxidase NOX4 inhibits hepatocyte proliferation and liver cancer progression.

A mesenchymal-like phenotype and expression of CD44 predict lack of apoptotic response to sorafenib in liver tumor cells.

Nicotine Promotes Initiation and Progression of KRAS-Induced Pancreatic Cancer via Gata6-Dependent Dedifferentiation of Acinar Cells in Mice.

Microenvironmental hCAP-18/LL-37 promotes pancreatic ductal adenocarcinoma by activating its cancer stem cell compartment.