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One of the revised hallmarks of cancer is dysregulated energy metabolism. This session will cover the historical and modern concepts of glucose utilization and energy generation in cancer, how it may affect tumor cell behavior, and strategies for intervention.

Learning Objectives

  • Compare the historical and modern concepts in cancer of glucose utilization and energy generation
  • Discuss how glucose utilization and energy generation affects tumor cell behavior
  • Identify strategies for intervention in cancer bioenergetics

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 module reviews the biology of CSCs and provides insights into CSC plasticity, interaction with the niche, tumor repopulation and clinical implications of therapeutic response. 

Learning Objectives

  • Explain the difference between the clonal evolution model and the CSC model 
  • Define a stem cell
  • List the key characteristics of a CSCs 
  • Define cellular plasticity and explain why it is important within the tumor 
  • Describe the epithelial-to-mesenchymal transition 
  • Explain the Warburg effect 

The objective of this module is to provide an overview of signal transduction in both normal and neoplastic cells, how dysregulated signaling contributes to tumor growth and methods used to target aberrant signaling in cancer cells. This module covers the following subjects: 

  • Normal signal transduction and cellular homeostasis
  • Major signal transduction pathways in cells (PI3 kinase, MAP Kinase, etc.)
  • Causes of dysregulated signaling in cancer cells (e.g., mutations, etc.)
  • Role of dysregulated signaling in supporting cancer cell growth/survival
  • Methods and mechanisms to aberrant signal transduction in cancer (e.g., small molecular inhibitors)
  • Resistance to small molecule inhibitors
  • Application of small molecule inhibitors to veterinary cancers  

Pharmaceuticals are an important tool in the treatment of cancer. This module 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.

Learning Objectives

  • Gain a general knowledge of how a target-based drug discovery program works 
  • Gain a general knowledge of how a mAb-based drug is found 
  • Become familiar with some of the tools used to evaluate anticancer drugs during drug discovery 
  • Gain a general knowledge about the relationship between human drug discovery and how these drugs become available for veterinary use 
Speakers CE Credit Hours Duration
0.530 minutes

This module 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.

Learning Objectives

  • How DNA methylation contributes to cancer 
  • How histone changes contribute to cancer 
  • How miRNAs and IncRNAs contribute to cancer 
  • The clinical impact of epigenetic changes 

DNA damage response mechanisms protect mammalian cells from genomic instability and phenotypes such as aging and cancer. In contrast to normal cells, tumors exhibit extreme genomic instability, which can occur at the level of DNA as well as at the chromosomal level. This course reviews the causes and consequences of genomic instability, including manifestations in DNA and chromosomes; the course also provides a thorough review of cellular DNA damage response mechanisms, including detection of damage, checkpoint signaling, and recruitment of repair factors.

Learning Objectives

  • List causes and consequences of genomic instability
  • Define the following and explain their significance in cancer: chromosomal deletion, chromosomal translocation, chromosomal inversion, aneuploidy, polyploidy, internal tandem duplication and provide key examples
  • Explain the difference between and the significance of somatic and germline mutations
  • Describe the differences between single strand and double strand DNA breaks in terms of impact on the cell and repair processes involved
  • Name the kinases involved in signaling for DNA damage
  • Explain the following: mismatch repair, nucleotide excision repair, base excision repair, microsatellite instability. Name cancers or cancer syndromes associated with deficiencies in these repair processes
  • Recognize the key players in checkpoint signaling and DNA repair including the DNA damage response pathway components that are currently undergoing evaluation as therapeutic targets  
Speakers CE Credit Hours Duration
1.060 minutes

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.  

Learning Objectives

  • Recall the steps of the metastatic cascade and the 'decathlon' analogy
  • Assimilate the fundamental experiments that have led to our understanding of the metastatic cascade
  • Provide an example of paracrine signaling or cross-talk between tumor tissues and stromal tissues/immune cells and explain how this might lead to tumor progression or metastasis
  • Recognize strengths and shortcomings of common in vitro and in vivo techniques capable of evaluating metastasis
  • Understand the clinical implications (and limitations) of detecting tumor cells within the circulation, regional nodes or distant tissues
  • Assimilate and discuss with clients, in lay terms, the metastatic cascade and how it relates to their pet's recommended treatment
  • Recognize and define the concepts of "seed and soil", "foraging", tumor heterogeneity, exosomes and tumor dormancy  

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.  

Learning Objectives

  • Describe the kinetic basis of cancer drug therapy 
  • Describe determinants of intrinsic tumor cell sensitivity, specifically related to drug class and cell-intrinsic factors 
  • Describe putative mechanisms of action for anti-cancer agents used in veterinary medicine 
  • Describe key components driving efficacy of combination chemotherapy: dose intensity and effect of schedule 
  • List and provide examples of tumor cell resistance mechanisms for anti-cancer agents used in veterinary medicine: intrinsic resistance, acquired resistance and pharmacokinetic factors influencing dose-response relationship 
  • Describe the pharmacokinetic-pharmacodynamic relationships driving efficacy and toxicity for select drugs: carboplatin and doxorubicin 

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. 

Learning Objectives

  • Learners will have an improved understanding of the formation of the tumor niche and the evolution of the tumor microenvironment. 
  • Learners will recognize that natural selection dictates the evolution towards convergent molecular programs, regardless of mutational drivers, to create predictable tumor phenotypes. 
  • Learners will appreciate opportunities for therapies directed towards the tumor microenvironment to more effectively manage malignant cancers. 

Angiogenesis

Cancer Etiology

Cancer Genome

Cancer Immunotherapy

Cell Death