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Composition
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Name
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Position
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Institution
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José Manuel González Sancho
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Profesor Titular
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Universidad Autónoma de Madrid
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David Albandea Rodríguez
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Investigador Predoctoral
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IIB "Alberto Sols"
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Antonio Barbachano Becerril
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Investigador Postdoctoral
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IIB "Alberto Sols"
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Pilar de la Paz Bustamante Madrid
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Investigador Predoctoral
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Universidad Autónoma de Madrid
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Gemma Domínguez Muñoz
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Profesora contratada
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Universidad Autónoma de Madrid
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Asunción Fernández Barral
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Investigadora Postdoctoral
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IIB "Alberto Sols"
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Gemma Ferrer Mayorga
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Investigadora Predoctoral
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IIB "Alberto Sols"
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María Jesús Larriba Muñoz
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Investigadora Postdoctoral
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IIB "Alberto Sols"
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Esther Martín Villar
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Investigadora Postdoctoral
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Universidad Autónoma de Madrid
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Alberto Muñoz Terol
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Profesor de Investigación
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IIB "Alberto Sols"
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José Luis Orgaz Bueno
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Jefe de Laboratorio de Citoesqueleto y Metástasis
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IIB Alberto Sols
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Francisco Portillo Pérez
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Catedrático. Departamento de Bioquímica
Facultad de Medicina
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Universidad Autónoma de Madrid
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Javier Rodríguez Cobos
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Investigador Postdoctoral
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FIBHULP
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Strategic Objective
Metastasis represents the most life-threatening event for cancer patients. Invasion of tumour cells from the primary tumour to adjacent tissues represents the first step in the metastatic cascade for most solid tumours.
The carcinoma invasion process involves the loss of Ecadherin mediated cell-cell contacts and cell polarity, degradation of the basement membrane, and acquisition of migratory properties. These changes are collectively known as the epithelial-mesenchymal transition (EMT). Presently, EMT is considered a manifestation of the epithelial plasticity of carcinomas. One of the most significant contributions in the last decade has been the identification of mechanisms responsible for EMT induction.
Our previous studies, and those of other groups, led to the identification of several transcription factors from various families such as E-cadherin repressors and EMT inducers (EMT-TFs): Snail (Snail1, Snail2), bHLH (E47, E2-2, Twist) and Zeb (ZEB1/2). The EMT process is regulated by a plethora of signalling pathways at the transcriptional and posttranscriptional level, including TGF-b (one of the most potent EMT inducers), vitamin D (which antagonises Snail1 repression), phosphorylation events and lysyl oxidase-like 2 (LOXL2). EMT has been recently with stemness, opening new avenues for tumour initiation and metastatic dissemination.
The group is composed of several principal investigators leading specific research lines (see below) related to tumour progression and metastasis. The main objectives of the group are as follows:
1. Establish the role of various EMT-TFs in tumour progression and metastasis
2. Determine the role of LOXL2, LOXL3 and the microenvironment in epithelial plasticity and tumour progression
3. Determine the role of TGFb/endoglin and podoplanin in tumour progression
4. Determine the role of vitamin D in the regulation of EMT and stemness in colorectal tumours
5. Characterise stem cells and their niche in the epidermis and their influence on skin carcinogenesis.
Research Lines
• Regulation of cell plasticity and tumour metastasis by EMT factors and lysyl oxidase LOXL2:
Studies in mouse models of skin and breast tumorigenesis genetically modified for Loxl2, Snail and E47.
• LOXL3 involvement in melanomagenesis: Studies in melanoma cell lines and mouse models
genetically modified for Loxl3.
• Genetic and molecular studies in breast and gynaecological cancers: Identification of novel
predictive biomarkers.
• Characterization of novel resistance mechanisms in human cancer using high throughput
techniques.
• Study of podoplanin role in epidermal homeostasis and skin cancer.
• Study of vitamin D effect on normal and cancer-associated fibroblasts and on normal and colon cancer patient-derived tumour organoids.
• Determine ÄNp73 role in tumour progression.
• Identify molecular alterations responsible for progression of precancerous colorectal lesions.
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