The American Association for Cancer Research (AACR) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education activities for physicians.
CREDIT DESIGNATION STATEMENT
The AACR has designated this live activity for a maximum of 18.0 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
CLAIMING (CME) CREDIT
Physicians and other health care professionals seeking AMA PRA Category 1 Credit(s)TM for this continuing medical education activity must complete the CME Request for Credit Survey below. Certificates will only be issued to those who complete the survey. CME certificates will be sent by email after the completion of the activity.
STATEMENT OF EDUCATIONAL NEED, TARGET AUDIENCE AND LEARNING OBJECTIVES
The field of cellular metabolism and how it applies to the persistence and survival of cancer cells is ever-expanding since the first description of metabolic discrepancies in cancer cells by Otto Warburg in 1956. Warburg observed that even in the presence of ample amounts of oxygen, cancer cells will metabolize glucose to produce ATP in the less-efficient process of glycolysis. The processing and intake of nutrients are often dysregulated in growing cancer cells and can lead to cellular stress and local hypoxia in the tumor microenvironment. Cellular responses to hypoxia and stress induce a wide variety of genetic responses, including the expression of the hypoxia-inducible factor (HIF) transcriptional program. One of the main needs in this field is to identify the many different downstream effects of these genetic responses. The activation of many cancer-associated oncogenic pathways, such as Ras or Myc, can promote glycolysis. The loss of tumor suppressor gene products, like p53, can interfere with aerobic respiration. Therefore, there is a need to understand how metabolism is affected when the most common cancer-associated mutations occur in the cell. The reprogramming of a cancer cell’s metabolic capabilities may also allow for tumor-promoting events such as some lipid biosynthesis, avoidance of apoptosis, and the use of certain metabolites for local signaling. There is a need to gather a range of basic/translational research scientists, physician-scientists and clinicians to assess the net result of altered cellular metabolism to fully understand all of the processes that may be contributing to the increased proliferation and survival of cancer cells in the patient. Finally, there is a need to understand the basic science of metabolism in cancer cells to find targets within that pathway that may have potential therapeutic benefit and advance patient outcomes.
After participating in this CME activity, physicians should be able to:
- Evaluate the pros and cons of using different model organisms to study altered metabolism in proliferating cancer cells
- Identify specific responses to cellular stress, the downstream effects these may have on cancer cells, and how to target these responses for therapeutic benefit
- Compare and contrast the different signaling pathways that are involved in the altered metabolism of cancer cells in processes such as cellular growth control (i.e. BRAF, mTOR)
- Articulate the emerging role that epigenetics has in the field of metabolism and cancer
- Explain how altered metabolism in cancer cells can affect cell survival and death and determine how alterations in these cellular processes can affect patient outcomes
- Utilize the knowledge obtained in these various learning objectives to evaluate current methods of drug development and therapeutics.
It is the policy of the AACR that the information presented at AACR CME activities will be unbiased and based on scientific evidence. To help participants make judgments about the presence of bias, the AACR will provide information that chairpersons and speakers have disclosed about financial relationships they have with commercial entities that produce or market products or services related to the content of this CME activity. This disclosure information will be made available in the Program/Proceedings of this conference.
QUESTIONS ABOUT CME?
Please contact the Office of CME at (215) 440-9300 or email@example.com.