This lecture will describe the formation, remodeling, maintenance, and function of the immune landscape of cancer. Specifically, the formation of the tumor-immune environment at the earliest stages of tumor development, its heterogeneity and constantly evolving phenotypes, the physiological processes that regulate innate and adaptive immune responses, and the role of adaptive evolution within the tumor will be discussed in the context of how they determine the duration and efficacy of anti-tumor immune responses. This presentation is organized in three topics. The first topic covers the formation of the tumor immune environment and is subdivided into three sections that will focus on (1) inflammation and cancer, (2) the immune response to cancer, and (3) the development of the tumor-immune environment. The second topic describes a cross sectional view of the tumor-immune landscape and is also subdivided into three sections that will focus on (1) the definition of the tumor-immune landscape, (2) the composition and complexity of the tumor-immune landscape, and (3) the clinical significance of the tumor-immune landscape. The final topic describes the evolution of the tumor-immune landscape and is subdivided into four sections that will focus on (1) the innate response to tumor formation, (2), the dynamic interactions between the tumor and the immune system, (3) the role of mutational neoantigens in the anti-tumor immune response, and (4) immunoediting, or the success or failure of anti-tumor immunity. An important conclusion from this lecture is that breaking the tumor immunosuppressive barrier(s) is an absolute condition that must be achieved if cancer immunotherapies are to be successful.
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The cancer stem cell theory states that tumor growth is driven by a small number of dedicated cancer stem cells (CSCs). These cells are endowed with the ability to self-renew (leading to unlimited cell division and maintenance of the stem cell pool), differentiate into non-CSCs and are intrinsically resistant to conventional therapeutics. This theory explains the clinical observations of almost inevitable tumor relapse after initially successful chemo and/or radiotherapy, and metastasis. This course reviews the biology of CSCs and provides insights into CSC plasticity, interaction with the niche, tumor repopulation and clinical implications of therapeutic response.
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Cancer is a genetic disease. The genomics revolution of the past two decades has provided detailed maps of the underpinnings of many human cancers through the generation of hundreds of thousands of cancer genome sequences. These data are increasingly leveraged to guide development of new clinical diagnostics, prognostics, and targeted treatments that are improving outcomes for human cancer patients. The genomics revolution has now also crossed into veterinary oncology, particularly in pet dogs, where nearly two thousand cancer genomes have been sequenced and published in the past five years alone. Although the path from mapping cancer genome landscapes to clinical translation is still under development, the oncoming flood of genomic data stands poised to transform veterinary oncology. We and others are charting the genomic landscapes of naturally occurring canine cancers in order to develop new clinical tools for veterinary oncology and to establish comparative settings in which clinical hypotheses can be rapidly tested across species. Here we will review cancer's genetic basis across species, summarize the history of and recent developments in naturally occurring canine cancer genomics, and discuss implications of these emerging data for development of new clinical tools in veterinary oncology including opportunities and challenges in leveraging these data.
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Pharmaceuticals are an important tool in the treatment of cancer. This course gives a high level view of the history of anticancer drugs, a general idea of the current drug discovery process for both small and large molecule drugs, and what tools might be coming next for the veterinary oncologist.
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This lecture describes the common, currently understood epigenetic mechanisms of mammalian cells that contribute to carcinogenesis. It will explain an overall mechanism for each type of epigenetic modification, and give specifics in veterinary oncology where they have been published. The student should be able to describe the effects of these epigenetic modifications on gene expression and cell function after this lecture.
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Metastasis is a common cause of death in patients with solid tumors. Research in this area may lead to better identification of patients at risk of developing metastasis in addition to improved therapies for patients with metastatic disease. This lecture is intended to provide a basic overview of tumor invasion and metastasis. We will start with an introduction to the steps of the metastatic cascade, including a review of foundational experimental and clinical evidence that has led to our current understanding of this process. We will then cover the fundamentals of tumor progression, as it relates to metastatic heterogeneity, and review evidence supporting Stephen Paget’s original “seed and soil” hypothesis. With this knowledge we will move into examples of how stromal and immune cells may interact with tumor cells to regulate or facilitate individual steps of the metastatic cascade. Finally, we will review current concepts and trends in metastasis research including the potential fate of disseminated tumor cells, importance of the metastatic niche, reactivation of dormancy, and implications for the clinical therapy of metastasis.
In this course we discuss the early findings with regard to the kinetics of tumor cell death that lead to current approaches to the treatment of cancer. For the major classes of cytotoxic agents that are used in veterinary medicine we have a detailed discussion of the mechanisms of action and potential mechanisms leading to intrinsic and/or acquired resistance. We also discuss some of the concepts that underlie combination chemotherapy and finally, provide some examples of the link between pharmacokinetics and pharmacodynamics of some chemotherapy agents.
Immunotherapy is now recognized as the “fourth pillar” of cancer therapy. As immunological approaches are translated into the clinic for human and veterinary cancer patients, it is essential for oncologists and other health care professionals to have a thorough understanding of immunophysiology and immunopathology, as this will allow them to appreciate the balance between the potential benefits and the considerable risks of immunotherapy. This lecture will emphasize general principles of immunotherapy, describe several approaches that have been or are being translated from the laboratory to the clinic, and provide selected examples of how gains in immunotherapy are being translated to companion animals with cancer. The presentation is divided into five sections. The first section will present a brief primer of immunophysiology and immunopathology. The viewer is strongly encouraged to watch the previous lecture in this series entitled, “Building the Immune Environment of Cancer.” The second section will review mechanisms whereby the immunosuppressive barrier can be disrupted and through which the immune system can attack the tumor. The third section will cover a brief history of immunotherapy, illustrating the centuries-old interest in this field. The fourth section will review general approaches to immunotherapy with select examples of their application in companion animals. The fifth and final section will introduce the emerging area of cancer Immunoprophylaxis, which represents the next frontier for cancer immunotherapy.
This lecture will describe the tumor microenvironment, beginning with the mechanisms that lead to the creation of a tumor niche and continuing through the steps that allow it to evolve to favor tumor growth and dissemination. The tumor microenvironment refers to the complex ecosystem in which tumor cells reside and interact. The key take-home messages in this lecture are that (1) Tumors are tissues, and the temporal and spatial organization of those tissues is a critical determinant of tumor biological behavior. (2) Mutations of driver genes are essential events required to initiate tumors (and can be unique to tumors, individuals, and/or species), but ultimately, selective pressures to establish a niche and form a new, organized tissue within the constraints of its anatomical location are critical determinants of tumor progression. And finally, (3) strategies to detect and disrupt the formation of the tumor microenvironment provide a new frontier for safe and effective cancer treatment, control, and prevention.
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On-demand courses are hosted in ACVIM’s online learning system Elevate Learning Platform, powered by Forj.
Individual access has been provided to enrolled participants via email or log in using your ACVIM.org username and password. You will be taken to your Dashboard where any course you are enrolled in will show in the Current Learning section.
All ACVIM Oncology Diplomates and Candidates have complimentary access to each Science of Veterinary Oncology course
Questions? Contact
Learning@ACVIM.org.