By Shushan Rana, MD
Tremendous strides have been made in recent years to define the tumor microenvironment (TME) and to understand its role in tumorigenesis and cancer therapy. The TME is the local area surrounding the tumor that can include immune cells (T cells, B cells and others), the vasculature, fibroblasts and the extracellular matrix. This mix of tumor and healthy cells supports cancer cell growth while separating the tumor from the adjacent normal tissues. Clearly, as evidenced by the remarkable increase in the number of therapeutic targeted agents, including radiation, that target cells within the site, the TME holds significant biological importance. Understanding how cells within the TME, and treatments that target them interact, warrants consideration and discussion.
Today, there is a greater appreciation for the role of the TME in cancer cell growth and in its response to treatment. All aspects of the TME—from the immune cells within it, to the stroma that surrounds it, to the microbiome of the patient—can determine how a specific tumor responds to or can be altered by treatment. These treatments, including radiation, chemotherapy, surgery, immunotherapy and targeted therapies, all change the tumor microenvironment and, depending on the type, dose and timing, can either increase or decrease tumor growth. Evidence is emerging that radiation alone or in combination with other TME targeting agents can significantly alter the TME, such as through abscopal effects and altering tumor vasculature. In addition, a recent publication highlights the effects of clinical doses of radiation on tumor cells’ extracellular collagen matrix. These profound advances in knowledge of TME and treatment interactions have paved the way for more novel therapeutics to be developed over the coming years.
To explore the role of radiation therapy in the TME, ASTRO, in collaboration with the American Association for Cancer Research (AACR), is sponsoring “Targeting the Tumor Microenvironment in Radiation Oncology,” the 2018 ASTRO Research Workshop, taking place July 26 and 27 in Washington, D.C. This workshop has been developed under the leadership of Wendy Woodward, MD, PhD, and Amato Giaccia, PhD, program co-chairs and globally recognized experts in the field.
Dr. Woodward is an associate professor and director of clinical breast radiation research in the department of radiation oncology at The University of Texas MD Anderson Cancer Center. Her research focuses on breast cancer stem cell biology and progenitor cells interaction within the TME as part of the tissue remodeling process.
Co-chair Amato Giaccia, PhD, is a professor of radiation oncology, as well as associate chair for research and director of the division of radiation and cancer biology in the department of radiation oncology at Stanford University. Dr. Giaccia’s primary research focus is hypoxia-mediated therapeutic resistance, tumor invasiveness and metastases. Through synthetic lethality screening, he has identified many small molecules targeting Von Hippel Lindau (VHL)-deficient renal cancer cells. He has expanded targeting of hypoxia-induced genes that promote invasion and metastases to several other cancer types, including breast, ovarian and head and neck cancer.
The full agenda with speakers can be found here. Abstract submissions are currently being accepted for poster presentations. Your abstract may be selected for a short talk on day two. A small number of short oral presentations, chosen from those submitted by our trainees and early-career investigators, will be selected from those abstract submissions received by April 30. For more information on how to submit an abstract, view the abstraction submission guidelines.
Dr. Rana is an instructor and the Chief Resident in the Department of Radiation Medicine at Oregon Health & Science University and was the recipient of ASTRO’s Resident/Fellow in Radiation Oncology Seed Grant in 2017. His work focuses on how microRNA affects radiosensitivity, and he hopes to use this work to prevent the development of immune cell anergy and/or exhaustion, thereby improving tumor responses to treatment.
Tremendous strides have been made in recent years to define the tumor microenvironment (TME) and to understand its role in tumorigenesis and cancer therapy. The TME is the local area surrounding the tumor that can include immune cells (T cells, B cells and others), the vasculature, fibroblasts and the extracellular matrix. This mix of tumor and healthy cells supports cancer cell growth while separating the tumor from the adjacent normal tissues. Clearly, as evidenced by the remarkable increase in the number of therapeutic targeted agents, including radiation, that target cells within the site, the TME holds significant biological importance. Understanding how cells within the TME, and treatments that target them interact, warrants consideration and discussion.
Today, there is a greater appreciation for the role of the TME in cancer cell growth and in its response to treatment. All aspects of the TME—from the immune cells within it, to the stroma that surrounds it, to the microbiome of the patient—can determine how a specific tumor responds to or can be altered by treatment. These treatments, including radiation, chemotherapy, surgery, immunotherapy and targeted therapies, all change the tumor microenvironment and, depending on the type, dose and timing, can either increase or decrease tumor growth. Evidence is emerging that radiation alone or in combination with other TME targeting agents can significantly alter the TME, such as through abscopal effects and altering tumor vasculature. In addition, a recent publication highlights the effects of clinical doses of radiation on tumor cells’ extracellular collagen matrix. These profound advances in knowledge of TME and treatment interactions have paved the way for more novel therapeutics to be developed over the coming years.
To explore the role of radiation therapy in the TME, ASTRO, in collaboration with the American Association for Cancer Research (AACR), is sponsoring “Targeting the Tumor Microenvironment in Radiation Oncology,” the 2018 ASTRO Research Workshop, taking place July 26 and 27 in Washington, D.C. This workshop has been developed under the leadership of Wendy Woodward, MD, PhD, and Amato Giaccia, PhD, program co-chairs and globally recognized experts in the field.
Dr. Woodward is an associate professor and director of clinical breast radiation research in the department of radiation oncology at The University of Texas MD Anderson Cancer Center. Her research focuses on breast cancer stem cell biology and progenitor cells interaction within the TME as part of the tissue remodeling process.
Co-chair Amato Giaccia, PhD, is a professor of radiation oncology, as well as associate chair for research and director of the division of radiation and cancer biology in the department of radiation oncology at Stanford University. Dr. Giaccia’s primary research focus is hypoxia-mediated therapeutic resistance, tumor invasiveness and metastases. Through synthetic lethality screening, he has identified many small molecules targeting Von Hippel Lindau (VHL)-deficient renal cancer cells. He has expanded targeting of hypoxia-induced genes that promote invasion and metastases to several other cancer types, including breast, ovarian and head and neck cancer.
The full agenda with speakers can be found here. Abstract submissions are currently being accepted for poster presentations. Your abstract may be selected for a short talk on day two. A small number of short oral presentations, chosen from those submitted by our trainees and early-career investigators, will be selected from those abstract submissions received by April 30. For more information on how to submit an abstract, view the abstraction submission guidelines.
Dr. Rana is an instructor and the Chief Resident in the Department of Radiation Medicine at Oregon Health & Science University and was the recipient of ASTRO’s Resident/Fellow in Radiation Oncology Seed Grant in 2017. His work focuses on how microRNA affects radiosensitivity, and he hopes to use this work to prevent the development of immune cell anergy and/or exhaustion, thereby improving tumor responses to treatment.