Strategies for modulating the conversation between tumor cells and their stroma.

During my career I have worked with many different cell types in different contexts. I worked with vascular smooth muscle cells in the context of hypertension and atherosclerosis. I have worked on Macrophages in the context of tumor biology. And finally, I have worked on endothelial cells in the context of endothelial dysfunction and tumor biology. I have contributed to describe how tumor cells alter the membrane composition of the macrophages, inducing a dysregulation in the signaling pathways transducing inflammatory signaling, and eventually leading to immune suppression; I have also contributed to show how tumor cells induce endothelial cell senescence, rendering the endothelium more permeable and potentiating metastasis. These two works are the foundation of my line of research, which is focused on how tumor cells and their stroma communicate with each other, and how this interaction can influence tumor development. Although the group will initially focus on pancreatic and ovarian cancer, we believe that some of our discoveries would be important for many other tumors where stroma is a major driver of progression. We will employ different tools to modulate the communication between tumor cells and their stroma in order to identify potential therapeutic targets, and design strategies to regulate them.


Get to know us better

Research Staff

The people who make it all possible

Juan Rodriguez Vita

Francesca De Angelis Rigotti

Cristina Fandos Ramo


Our scientific contributions

Intraperitoneal Oil Application Causes Local Inflammation with Depletion of Resident Peritoneal Macrophages.
Alsina-Sanchis E, Mülfarth R, Moll I, Mogler C, Rodriguez-Vita J and Fischer A
MOLECULAR CANCER RESEARCH, 2021 Feb,  DOI:  10.1158/1541-7786.MCR-20-0650,  Vol. 19,  pag. 288-300

Membrane Cholesterol Efflux Drives Tumor-Associated Macrophage Reprogramming and Tumor Progression.
Goossens P, Rodriguez-Vita J, Etzerodt A, Masse M, Rastoin O, Gouirand V, Ulas T, Papantonopoulou O, Van Eck M, Auphan-Anezin N, Bebien M, Verthuy C, Vu Manh TP, Turner M, Dalod M, Schultze JL and Lawrence T
Cell Metabolism, 2019 Jun,  DOI:  10.1016/j.cmet.2019.02.016,  Vol. 29,  pag. 

Endothelial Notch1 Activity Facilitates Metastasis.
Wieland E, Rodriguez-Vita J, Liebler SS, Mogler C, Moll I, Herberich SE, Espinet E, Herpel E, Menuchin A, Chang-Claude J, Hoffmeister M, Gebhardt C, Brenner H, Trumpp A, Siebel CW, Hecker M, Utikal J, Sprinzak D and Fischer A
CANCER CELL, 2017 Mar,  DOI:  10.1016/j.ccell.2017.01.007,  Vol. 31,  pag. 355-367

Endothelin-1, via ETA receptor and independently of transforming growth factor-beta, increases the connective tissue growth factor in vascular smooth muscle cells.
Rodriguez-Vita J, Ruiz-Ortega M, Rupérez M, Esteban V, Sanchez-López E, Plaza JJ and Egido J
CIRCULATION RESEARCH, 2005 Jul,  DOI:  10.1161/01.RES.0000174614.74469.83,  Vol. 97,  pag. 125-134

Angiotensin II activates the Smad pathway in vascular smooth muscle cells by a transforming growth factor-beta-independent mechanism.
Rodríguez-Vita J, Sánchez-López E, Esteban V, Rupérez M, Egido J and Ruiz-Ortega M
CIRCULATION, 2005 May,  DOI:  10.1161/01.CIR.0000165133.84978.E2,  Vol. 111,  pag. 2509-2517


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