Understanding the Role of the TME

Reprogramming of Lung Tumor Microenvironment: A Path to Cancer Care for Better Therapeutic Benefit (B87)

2:15-4:15 p.m. Monday

Independence Ballroom Salon A-D (Level M4), Marriott Marquis Washington

Rajkumar Savai, PhD, spoke with the ATS Daily Bulletin about the Monday symposium he is co-moderating, which will explore what researchers have learned about the lung tumor microenvironment.

Dr. Savai leads the Molecular Mechanisms of Lung Cancer research group in the Department of Lung Development and Remodeling at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany. He is jointly appointed at the Department of Internal Medicine (pneumology/oncology) at the University Hospital Giessen. He is also project leader and member of the German Center for Lung Research and the Collaborative Research Center on Cardiopulmonary Systems.

Rajkumar Savai, PhD

Q: Why is this symposium important for ATS 2017 attendees?

A: Numerous cancer risk factors can be linked to chronic inflammation, which was recently recognized as a hallmark of cancer. The physiological microenvironment of any given organ is usually tumor-suppressive, yet the microenvironment is vulnerable to chronic inflammation caused by, for example, microbial infection. As a result, a tumor-promoting microenvironment can be established. Generated by tumor cells and surrounding stroma, the TME is composed of vascular and lymphatic endothelial cells, pericytes, fibroblasts, immune cells, and an altered extracellular matrix. In its early stages, it is restricted by a basement membrane.

The TME has a fundamental role in tumor progression, metastasis, and immunosuppression, and it also accounts for the resistance of tumor cells to drug treatment. Therefore, understanding the lung TME and the complex bidirectional interplay between the tumor and lung microenvironment in lung cancer is essential in designing effective therapies.

Q: What major topics will the session address?

A: We will be discussing five different TME topics, which will include TME cell types, such as tumor-associated fibroblasts and the role of tumor-associated macrophages in cancer development and metastasis. In addition, we will be talking about the TME cell secretory factors (cytokines and chemokines) and lymphatic vessel-microenvironmental cell interaction/involvement in cancer development. From the labs, we would like an update on the current work.

Q: Will groundbreaking research be a focal point?

A: Yes, presenters will be showing and discussing new or ongoing work from their labs. A better understanding of the TME and the complex bidirectional interplay between the tumor and lung microenvironment in lung cancer is needed to improve the efficacy of anticancer regimens in lung cancer.

The role of various tumor microenvironmental cells as well as mediators and molecular pathways regulated by these cells that contribute to lung tumor initiation, progression, and metastasis needs to be explored. Multiple TME-directed therapies are currently advancing through different clinical trials, necessitating an understanding of potential mechanisms of intrinsic or acquired resistance.

Q: What can attendees hope to take home from the session?

A: There will be three take-home messages. One, they will able to understand the
tumor-promoting/tumor-inhibitory properties of various tumor microenvironmental cells. Two, they will get an update on clinical trials targeting tumor microenvironments in lung cancer. Three, they will be introduced to novel therapeutic interventions aimed at treating lung cancer by reprogramming tumor microenvironmental cells.

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