From the Duke Cancer Institute archives. Content may be out of date.
More than 3,000 Duke Cancer Institute community members came together virtually on Thursday, December 3, for the Nancy Weaver Emerson 30th Annual Tree of Hope Lighting Ceremony to honor loved ones and recognize those whose lives have been touched by cancer.
The lights on these beautiful trees at Duke Cancer and Duke Cancer Center Raleigh represent and illuminate HOPE that outshines the darkness it is surrounded by. This year we celebrated our healthcare heroes for their continued commitment to care for our patients, their loved ones and the community despite all the challenges and uncertainties during the COVID-19 pandemic.
Two patients and their families shared how they have been impacted by cancer and the remarkable services they received from our cancer support team that helped them find their place and made the journey easier for them.
Our Duke Cancer Institute team members expressed their gratitude to the patients for allowing them to be a part of their cancer journey. They also recognized the many heroes involved in the cancer process including those cleaning the rooms, making the meals, drawing blood and those who give life every day through medications and treatments. All of us work together as a team to care for the whole patient and help them get to the other side.
Please take a moment to enjoy the recording of the event.
We would like to extend our appreciation for all who joined us for the remarkable 30th Annual Tree of Hope Ceremony and thank those who purchased tribute cards and more 500 luminaries in honor of our healthcare heroes and support the Duke Cancer Patient Support Program - which provides critical services and support to patients at Duke Cancer Institute and in the community, who are battling cancer.
The luminaries were lit on December 3 and they will remain lit through December 31 in the Garden of Tranquility in front of the Duke Cancer Center and in the Duke Raleigh Garden adjacent to Duke Cancer Center Raleigh.
A Duke-led study published in iScience provides new insights into the tumor microenvironment of brain metastases, identifying distinct macrophage populations associated with patient survival and highlighting potential targets for future therapeutic intervention.Brain metastases remain a significant clinical challenge across multiple tumor types, including breast cancer, lung cancer, and melanoma. Despite advances in systemic therapies and local treatment approaches, outcomes remain poor for many patients, underscoring the need for a deeper understanding of the biological mechanisms driving disease progression.Using an integrated multi-omic approach, investigators analyzed 23 human brain metastasis specimens through single-nucleus RNA sequencing and spatial transcriptomic profiling. The study leveraged these complementary technologies to characterize cellular heterogeneity within the tumor microenvironment and define spatial relationships between immune and tumor cell populations.The analysis revealed substantial macrophage heterogeneity and demonstrated that macrophage-associated transcriptional programs differ significantly between patients with favorable and unfavorable survival outcomes. Specifically, inflammatory macrophage populations localized at the tumor boundary were associated with improved survival, while macrophage populations characterized by extracellular matrix remodeling signatures and TGFβ1 expression were associated with poorer outcomes.These findings suggest that distinct macrophage subtypes may play context-dependent roles in brain metastatic progression, functioning as either tumor-restrictive or tumor-supportive components of the microenvironment. The results further emphasize the importance of spatial cellular organization in shaping disease biology and clinical outcomes.Importantly, the study extends current understanding of immune-tumor interactions in brain metastases by linking specific macrophage subtypes and locations within the tumor ecosystem to survival-associated phenotypes. The identification of these distinct cellular programs may provide a framework for the development of novel therapeutic strategies aimed at modulating macrophage function or disrupting protumor signaling networks within the metastatic niche.As the incidence of brain metastases continues to increase and therapeutic resistance remains a critical barrier to long-term disease control, these findings represent an important step toward the development of more precise, microenvironment-directed treatment approaches. Further investigation will be needed to validate these observations and assess their translational potential in prospective clinical studies.This work was a joint research collaboration among Duke Center for Brain and Spine Metastasis (DCBSM) members: Dr. Ann Marie Pendergast (Department of Pharmacology and Cancer Biology, Duke University School of Medicine), Dr. Carey Anders (Department of Medicine, Division of Medical Oncology), and Dr. Simon Gregory (Department of Neurosurgery, and Duke Molecular Physiology Institute), and first-author Dr. Aaditya Khatri (Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Duke University School of Medicine).
A Duke-led study published in iScience provides new insights into the tumor microenvironment of brain metastases, identifying distinct macrophage populations associated with patient survival and highlighting potential targets for future therapeutic intervention.Brain metastases remain a significant clinical challenge across multiple tumor types, including breast cancer, lung cancer, and melanoma. Despite advances in systemic therapies and local treatment approaches, outcomes remain poor for many patients, underscoring the need for a deeper understanding of the biological mechanisms driving disease progression.Using an integrated multi-omic approach, investigators analyzed 23 human brain metastasis specimens through single-nucleus RNA sequencing and spatial transcriptomic profiling. The study leveraged these complementary technologies to characterize cellular heterogeneity within the tumor microenvironment and define spatial relationships between immune and tumor cell populations.The analysis revealed substantial macrophage heterogeneity and demonstrated that macrophage-associated transcriptional programs differ significantly between patients with favorable and unfavorable survival outcomes. Specifically, inflammatory macrophage populations localized at the tumor boundary were associated with improved survival, while macrophage populations characterized by extracellular matrix remodeling signatures and TGFβ1 expression were associated with poorer outcomes.These findings suggest that distinct macrophage subtypes may play context-dependent roles in brain metastatic progression, functioning as either tumor-restrictive or tumor-supportive components of the microenvironment. The results further emphasize the importance of spatial cellular organization in shaping disease biology and clinical outcomes.Importantly, the study extends current understanding of immune-tumor interactions in brain metastases by linking specific macrophage subtypes and locations within the tumor ecosystem to survival-associated phenotypes. The identification of these distinct cellular programs may provide a framework for the development of novel therapeutic strategies aimed at modulating macrophage function or disrupting protumor signaling networks within the metastatic niche.As the incidence of brain metastases continues to increase and therapeutic resistance remains a critical barrier to long-term disease control, these findings represent an important step toward the development of more precise, microenvironment-directed treatment approaches. Further investigation will be needed to validate these observations and assess their translational potential in prospective clinical studies.This work was a joint research collaboration among Duke Center for Brain and Spine Metastasis (DCBSM) members: Dr. Ann Marie Pendergast (Department of Pharmacology and Cancer Biology, Duke University School of Medicine), Dr. Carey Anders (Department of Medicine, Division of Medical Oncology), and Dr. Simon Gregory (Department of Neurosurgery, and Duke Molecular Physiology Institute), and first-author Dr. Aaditya Khatri (Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, Duke University School of Medicine).
