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Soengas M.S.,CSIC - National Center for Metallurgical Research
Pigment Cell and Melanoma Research

Proteins and pathways that control cell fate are placed under intense scrutiny. The same tight regulation applies to essential organelles that can both sustain cell survival or promote self-degradation programs. Mitochondria are perhaps the prime example of cellular machineries with split functions (personalities). As a main source of ATP, mitochondria represent the main powerhouse of eukaryotic cells. However, mitochondrial respiration has the hidden complication of the production of potentially harmful reactive oxygen species (ROS). Moreover, mitochondria holds an armamentarium of stress-response factors, which depending on the context, may lead to pro-inflammatory signals, and to various forms of cell death, ranging from apoptosis to necrosis. A main clearance mechanism to eliminate superfluous, damaged or hyperactive mitochondria is selective mitophagy. Mitophagy, in fact, is emerging as a key quality-control mechanism in cancer cells. Specifically, malignant transformation has been found to induce marked changes in mitochondrial dynamics and structure. Moreover, a key hallmark of tumor progression is metabolic reprogramming, which further deregulates ROS content and renders cells more susceptible to mitochondrial perturbations. Despite its increasing relevance in cancer biology, the field of mitophagy remains virtually unexplored in melanoma. However, given unique antioxidant mechanisms in melanocytic cells (e.g., linked to melanin) and the idiosyncratic interplay between ROS and hypoxia (both mitophagy inducers) in melanoma, this tumor type represents an ideal scenario for physiological studies of mitochondrial turnover. This perspective summarizes proof of concept for in-depth basic and translational studies of mitophagy in melanoma. Particular emphasis is dedicated to new opportunities for gene discovery and drug design in this still aggressive disease. © 2012 John Wiley & Sons A/S. Source

Manuel H.,CSIC - National Center for Metallurgical Research | Manuel H.,Johns Hopkins University
New England Journal of Medicine

Deaths from pancreatic ductal adenocarcinoma, also known as pancreatic cancer, rank fourth among cancer-related deaths in the United States, yet the causes of pancreatic cancer remain unknown. This review article summarizes recent progress in the understanding and management of pancreatic cancer. Copyright © 2010 Massachusetts Medical Society. Source

Sancho D.,CSIC - National Center for Metallurgical Research | Reis e Sousa C.,London Research Institute
Annual Review of Immunology

Myeloid cells are key drivers of physiological responses to pathogen invasion or tissue damage. Members of the C-type lectin receptor (CLR) family stand out among the specialized receptors utilized by myeloid cells to orchestrate these responses. CLR ligands include carbohydrate, protein, and lipid components of both pathogens and self, which variably trigger endocytic, phagocytic, proinflammatory, or anti-inflammatory reactions. These varied outcomes rely on a versatile system for CLR signaling that includes tyrosine-based motifs that recruit kinases, phosphatases, or endocytic adaptors as well as nontyrosine-based signals that modulate the activation of other pathways or couple to the uptake machinery. Here, we review the signaling properties of myeloid CLRs and how they impact the role of myeloid cells in innate and adaptive immunity. © 2012 by Annual Reviews. All rights reserved. Source

CSIC - National Center for Metallurgical Research | Date: 2010-12-31

There is provided compounds of formula (I), wherein R

CSIC - National Center for Metallurgical Research, Servicio Andaluz De Salud and Hospital Clinic De Barcelona | Date: 2010-10-22

The present invention relates to the use of at least one isolated multipotent stem cell for maintaining haematopoiesis in vitro, in which said multipotent stem cell is preferably a mesenchymal stem cell or, more preferably, said mesenchymal stem cell is a mesenchymal stem cell capable of expressing the nestin protein. The present invention also relates to an isolated cell population of adult nestin-positive mesenchymal cells from a mammal, including humans, to the use thereof for producing a drug for maintaining haematopoiesis in a mammal, for the prevention and/or treatment of at least one disease associated with a malfunction in maintaining haematopoiesis in a mammal, and for maintaining and expanding adult haematopoietic stem cells of said mammal, including a human. Furthermore, the present invention also relates to a method for maintaining haematopoiesis in vitro or to a method for evaluating the haematopoietic capacity of a mammal.

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