A5016973815- Fibroblast Growth Factor Research
- PI3K/AKT/mTOR signaling in cancer
- Neuroendocrine Tumor Research Advances
- Angiogenesis and VEGF in Cancer
- Lung Cancer Research Studies
- Axon Guidance and Neuronal Signaling
- Testicular diseases and treatments
- Neuroblastoma Research and Treatments
- Vascular Malformations and Hemangiomas
- Pancreatic and Hepatic Oncology Research
- Kruppel-like factors research
- Prostate Cancer Treatment and Research
- Epigenetics and DNA Methylation
- Cancer, Hypoxia, and Metabolism
- Vascular Tumors and Angiosarcomas
- Liver Disease Diagnosis and Treatment
- Vascular Anomalies and Treatments
- Liver Disease and Transplantation
- Ovarian cancer diagnosis and treatment
- Chemokine receptors and signaling
- Vascular Malformations Diagnosis and Treatment
- Cancer-related Molecular Pathways
- Immune cells in cancer
- Cancer, Lipids, and Metabolism
- Cell Adhesion Molecules Research
Josep Carreras Leukaemia Research Institute
2021-2025
Institució Catalana de Recerca i Estudis Avançats
2013-2024
Centro de Investigación Biomédica en Red de Cáncer
2018-2024
Instituto de Salud Carlos III
2018-2024
Institut d'Investigació Biomédica de Bellvitge
2013-2023
Centro de Investigación Biomédica en Red
2020-2021
Institut Català d'Oncologia
2013-2018
Duran i Reynals Hospital
2017
Ajuntament de L’Hospitalet
2015
University College London
2015
Pathological lymphatic diseases mostly affect vessels in specific tissues, yet little is known about organ-specific regulation of the vasculature. Here, we show that vascular endothelial growth factor receptor 3 (VEGFR-3)/p110α PI3-kinase signaling pathway selectively required for formation mesenteric Using genetic lineage tracing, demonstrate part vasculature develops from cKit cells hemogenic origin through a process define as lymphvasculogenesis. This contrary to current dogma all...
Mutant Pik3ca gives rise to venous malformations.
Activin receptor-like kinase 1 (ALK1) is an endothelial serine-threonine receptor for bone morphogenetic proteins (BMPs) 9 and 10. Inactivating mutations in the ALK1 gene cause hereditary haemorrhagic telangiectasia type 2 (HHT2), a disabling disease characterized by excessive angiogenesis with arteriovenous malformations (AVMs). Here we show that inducible, endothelial-specific homozygous Alk1 inactivation BMP9/10 ligand blockade both lead to AVM formation postnatal retinal vessels internal...
Fibronectin (FN) is a major component of the extracellular matrix and functions in cell adhesion, spreading migration. In retina, FN transiently expressed assembled on astrocytes (ACs), which guide sprouting tip cells deposit provisional for angiogenesis. The precise function retinal angiogenesis largely unknown. Using genetic tools, we show that are source cellular during mouse retina. Deletion astrocytic reduces radial endothelial migration vascular plexus formation gene dose-dependent...
Highlights•Resistance to antiangiogenic therapy involves metabolic symbiosis patterning in RCC•mTOR pathway mediates this resistance and mTOR inhibition blocks symbiosis•In patients, antiangiogenics induce symbiotic mostly resistant tumors•mTOR implication is also suggested patients treated with antiangiogenicsSummaryAntiangiogenic drugs are used clinically for treatment of renal cell carcinoma (RCC) as a standard first-line treatment. Nevertheless, these agents primarily serve stabilize...
Abstract Coordinated activity of VEGF and Notch signals guides the endothelial cell (EC) specification into tip stalk cells during angiogenesis. activation in leads to proliferation arrest via an unknown mechanism. By using gain- loss-of-function gene-targeting approaches, here we show that PTEN is crucial for blocking downstream Notch, this critical mouse vessel development. Endothelial deletion results vascular hyperplasia due a failure mediate Notch-induced arrest. Conversely,...
Objective— ALK1 (activin-receptor like kinase 1) is an endothelial cell-restricted receptor with high affinity for BMP (bone morphogenetic protein) 9 TGF-β (transforming growth factor-β) family member. Loss-of-function mutations in cause a subtype of hereditary hemorrhagic telangiectasia—a rare disease characterized by vasculature malformations. Therapeutic strategies are aimed at reducing potential complications because vascular malformations, but currently, there no curative treatment...
Abstract Lymphatic malformations (LMs) are debilitating vascular anomalies presenting with large cysts (macrocystic) or lesions that infiltrate tissues (microcystic). Cellular mechanisms underlying LM pathology poorly understood. Here we show the somatic PIK3CA H1047R mutation, resulting in constitutive activation of p110α PI3K, underlies both macrocystic and microcystic LMs human. Using a mouse model -driven LM, demonstrate types arise due to lymphatic endothelial cell (LEC)-autonomous...
Oncogenic mutations in PIK3CA, encoding p110α-PI3K, are a common cause of venous and lymphatic malformations. Vessel type-specific disease pathogenesis is poorly understood, hampering development efficient therapies. Here, we reveal new immune-interacting subtype Ptx3-positive dermal capillary endothelial cells (iLECs) that recruit pro-lymphangiogenic macrophages to promote progressive overgrowth. Mouse model Pik3caH1047R-driven vascular malformations showed proliferation was induced both...
Vascular networks form, remodel and mature under the influence of both fluid shear stress (FSS) soluble factors. Physiological FSS promotes maintains vascular stability via synergy with Bone Morphogenic Protein 9 (BMP9) BMP10. Conversely, mutation BMP receptors ALK1, Endoglin or downstream effector SMAD4 leads to Hereditary Hemorrhagic Telangiectasia (HHT), characterized by fragile leaky arterial-venous malformations (AVMs). But how endothelial cells (EC) integrate signals in development...
Abstract Activation of the p53 tumor suppressor triggers a transcriptional program to control cellular response stress. However, molecular mechanisms by which controls gene transcription are not completely understood. Here, we uncover critical role spatio-temporal genome architecture in this process. We demonstrate that drives direct and indirect changes compartments, topologically associating domains, DNA loops prior one hour its activation, escort program. Focusing on p53-bound enhancers,...
In cirrhotic livers, increased resistance to portal flow, in part due an exaggerated response vasoconstrictors, is the primary factor pathophysiology of hypertension. Our aim was evaluate intrahepatic circulation rat livers α 1 -adrenergic vasoconstrictor methoxamine and mechanisms involved its regulation. A perfusion pressure dose-response curve performed control preincubated with vehicle, nitric oxide synthase blocker NG -nitro-l-arginine (l-NNA), indomethacin cyclooxygenase (COX)...