Presentación
MECHANISMS OF TUMOUR PROGRESSION

mecanismosdeprogresiontumoral@idipaz.es
Excellence Group
Composition
Name
Position
Institution
José Manuel González Sancho
Profesor Titular 
Universidad Autónoma de Madrid
David Albandea Rodríguez
Investigador Predoctoral
IIB "Sols Morreale"
Antonio Barbachano Becerril
Investigador Postdoctoral
IIB "Sols Morreale"
Aurora Burgos García
Jefe de Sección Unidad de Endoscopias
Hospital Universitario La Paz
Pilar de la Paz Bustamante Madrid
Investigador Predoctoral
Universidad Autónoma de Madrid
Gemma Domínguez Muñoz
Profesora contratada
Universidad Autónoma de Madrid
Asunción Fernández Barral
Investigadora Postdoctoral
IIB "Sols Morreale"
Arturo González de Aleja Molina
Investigadora Postdoctoral
IIB "Sols Morreale"
María Jesús Larriba Muñoz
Investigadora Postdoctoral
IIB "Sols Morreale"
Esther Martín Villar
Investigadora Postdoctoral
Universidad Autónoma de Madrid
Alberto Muñoz Terol
Profesor de Investigación
IIB "Sols Morreale"
José Luis Orgaz Bueno
Jefe de Laboratorio de Citoesqueleto y Metástasis
IIB "Sols Morreale"
Francisco Portillo Pérez
Catedrático. Departamento de Bioquímica
Facultad de Medicina
Universidad Autónoma de Madrid
Silvia Rodríguez Marrero
Investigador predoctoral
IIB "Sols Morreale"
Johana Alexandra Troya Balseca 
Lab Manager
FIBHULP
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
• Study of vitamin D effects on patient-derived colon normal and cancer-associated fibroblasts and organoids
• Comparative study of early onset colorectal cancer (EOCRC) vs. late onset colorectal cancer (LOCRC): Effects of vitamin D.
• Identification of early diagnostic biomarkers in liquid biopsy in colorectal cancer.
• Cell plasticity and tumor metastasis. 
• Mechanisms of tumor resistance.