Lydia Visser
PhD
My research in the Pathology department is mainly focused on immunological aspects of B-cell lymphoma. I study interactions of tumor cells with the microenvironment, and signaling pathways in Hodgkin lymphoma and non-Hodgkin lymphomas.
CCR5 antagonism by maraviroc inhibits Hodgkin lymphoma microenvironment interactions and xenograft growth
Published in: Haematologica
Access to document
10.3324/haematol.2018.196725
document
Classic Hodgkin lymphoma tumor cells express a functional CCR5 receptor, and tumor tissues express high CCL5 levels, suggesting that CCL5-CCR5 signaling is involved in tumor-microenvironment formation and tumor growth. Using the CCR5 antagonist maraviroc and a neutralizing anti-CCL5 antibody, we found that CCL5 secreted by Classic Hodgkin lymphoma cells recruited Mesenchymal-stromal cells and monocytes. Education of Mesenchymal-stromal cells by tumor cell conditioned medium enhanced Mesenchymal-stromal cells proliferation and CCL5 secretion. In turn, educated Mesenchymal-stromal cell conditioned medium increased the clonogenic growth of tumor cells and monocyte migration, but...
Naike Casagrande, Cinzia Borghese, Lydia Visser, Maurizio Mongiat, Alfonso Colombatti, Donatella Aldinucci
Correction: miR-24-3p Is Overexpressed in Hodgkin Lymphoma and Protects Hodgkin and Reed Sternberg Cells from Apoptosis (vol 187, pg 1343, 2017)
Published in: American Journal of Pathology
Access to document
10.1016/j.ajpath.2018.12.002
document
Ye Yuan, Joost Kluiver, Jasper Koerts, Debora de Jong, Bea Rutgers, F. Reeny Abdul Razak, Martijn Terpstra, Boudewijn E. Plaat, Ilja M. Nolte, Arjan Diepstra, Lydia Visser, Klaas Kok, Anke van den Berg
Plasma cells in classical Hodgkin lymphoma: a new player in the microenvironment?
Published in: British Journal of Haematology
Access to document
10.1111/bjh.15704
document
The Microenvironment in Epstein-Barr Virus-Associated Malignancies
Published in: Pathogens
Access to document
10.3390/pathogens7020040
document
The Epstein-Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an aspecific reaction to the tumor cells. In fact, latent EBV-infected tumor cells utilize several specific mechanisms to form and shape the TME to their own benefit. These mechanisms have been studied largely in the context of EBV+ Hodgkin lymphoma, undifferentiated nasopharyngeal carcinoma, and EBV+ gastric...
Combined PD-1 and JAK1/2 inhibition in refractory primary mediastinal B-cell lymphoma
Published in: Annals of Hematology
Access to document
10.1007/s00277-018-3233-9
document
Marcel Nijland, Tom van Meerten, Annika Seitz, Gerwin Huls, Robby Kibbelaar, Lydia Visser, Anke van den Berg, Arjan Diepstra