Reprogramming Tumor-Immune Cell Interface in Solid and Hematological Malignancies to Enhance Response to Therapy

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Publisher: BioMed Central Ltd.
Document Type: Conference news
Length: 5,890 words
Lexile Measure: 1670L

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Author(s): Maria Teresa Di Martino1 , Francesca Zazzeroni2 , Massimo Donadelli3 , Claudia Chiodoni4 , Michele Caraglia5 , Katia Scotlandi6 , Stefania Meschini7 and Carlo Leonetti8

Presentation of the conference

The 30th Annual Conference of Italian Association of Cell Cultures (AICC) was held at Fondazione IRCCS Istituto Nazionale dei Tumori, in Milan, on November 27-28, 2017, with the Scientific Coordination of Claudia Chiodoni and Mario Paolo Colombo, from the same Institute. The conference was opened by Katia Scotlandi, President of the Italian Association of Cell Cultures. The main objective of the conference was to discuss the present knowledge on the role of immune cells in the tumor microenvironment, shaped by cells promoting tumor survival that could be reeducated to treat cancer. The meeting was organized in two days with 5 thematic sessions, an opening and a closing lecture, with national and international speakers. The organizers truly thank those who took part in the conference and made the Conference a success.

Opening lecture

Michele De Palma, from École Polytechnique Fñdñrale de Lausanne, Swiss Institute for Experimental Cancer Research, in Lausanne, Switzerland, opened the 30th Annual Conference of AICC with the lecture "Reprogramming the tumor immune microenvironment". His lecture revised the role of the tumor microenvironment (TME) in the regulation of angiogenesis highlighting the potential vulnerabilities that could be targeted to improve the efficacy of anti-angiogenic cancer therapies (Fig. 1).The TME represents the primary location where tumor cells and the host immune system interact. Through interactions between chemokines and chemokine receptors, different immune cells are recruited into the TME where they influence tumor progression and therapeutic outcome. De Palma reported important findings suggesting that the manipulation of chemokine-chemokine receptor signaling pathways could reshape the immune and biological phenotypes of a tumor in a manner that increases effectiveness of immunotherapy. Based on recent findings, it is predicted that targeting both pro-tumor and anti-tumor chemokine-chemokine receptor signaling pathways, in combination with other immunotherapies, such as programmed cell death-protein 1 (PD-1) and ligand 1 (PD-L1) blockade, could give clinical benefit in cancer patients. In this context, De Palma addressed the extrinsic regulation of angiogenesis by TME. Pathological angiogenesis is a hallmark of cancer and a therapeutic target. The angiogenic programming of a tumor tissue is a process regulated by many players such as tumor cells together with different tumor-associated stromal cells and their bioactive products, including cytokines/chemokines or growth factors, the extracellular matrix and secreted microvesicles. De Palma and coworkers demonstrated that the combination of angiopoietin-2 (ANGPT2) and vascular endothelial growth factor A (VEGFA) blockade by a bi-specific antibody (A2V) provided therapeutic benefits, as compared to the single agents, in both genetically-engineered and transplantable tumor models, including metastatic breast cancer, pancreatic neuroendocrine tumor and melanoma. He reported that A2V promoted vascular regression, tumor necrosis, and antigen presentation by intratumoral phagocytes. A2V also normalized the remaining blood vessels and facilitated the extravasation and perivascular accumulation of activated, interferon-[gamma] (IFN[gamma])-expressing CD8+ cytotoxic T lymphocytes (CTLs). Whereas the anti-cancer activity of A2V was, at least...

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Gale Document Number: GALE|A546089662