September 28 - Oct 1, 2018
Marriott New York Brooklyn Bridge
New York, New York, USA
Abstract submission deadline: Wednesday, July 11
Advance registration deadline: Monday, August 13
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.
AACR has designated this live activity for a maximum of 18.5 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
Physicians and other health care professionals seeking AMA PRA Category 1 Credit(s)TM for this live continuing medical education activity must complete the CME Request for Credit Survey by Monday, November 12, 2018. Certificates will only be issued to those who complete the survey. The Request for Credit Survey will be available via a link on the website and via email.Your CME certificate will be sent to you via email after the completion of the activity.
The field of cellular metabolism and how it applies to the persistence and survival of cancer cells has expanded dramatically 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 (Warburg, 1956). Additionally, the processing and intake of nutrients are often dysregulated in growing cancer cells and can lead to alterations in metabolite-driven gene regulation, cellular stress, and local hypoxia in the tumor microenvironment (Pavlova and Thompson, 2016). Cancer cells have an increased rate of reactive oxygen species production, leading to activation of signaling pathways (such as PI3K and MAPK) and transcription factors (such as HIF and NF-κB) necessary for tumorigenesis (DeBerardinis and Chandel, 2016). Furthermore, metabolism is affected when the most common cancer-associated mutations occur in the cell, and cancer cells will exploit any mode (autophagy, micropinocytosis, lipid scavenging) to keep up with metabolic demands. The activation of many cancer-associated pathways, such as Ras or Myc, can promote glycolysis (Dang and Semenza, 1999). The loss of tumor suppressor gene products, like p53, can interfere with aerobic respiration (Matoba et al., 2006). Thus, the sum of metabolic changes involved cannot be captured by a single model, and it is important to understand the basis and downstream effects of this heterogeneity in order to develop and optimize therapeutic strategies (Cantor and Sabatini, 2012).
Of note, inhibition of some metabolic enzymes could be toxic because of their functions in normal tissues; new approaches need to be assessed to improve the understanding of how metabolic programming is regulated and which altered pathways hold promise as therapeutic targets. Cancer also alters immune cell metabolism, and a deeper understanding of the interplay between metabolism and immunity is needed to target the immune system for cancer therapy (Chandel and DeBerardinis).
Additionally, diet and other manipulations have the potential to reprogram a cancer cell’s metabolic capabilities to allow for tumor-promoting events based on alterations in stem cell function and cancer initiation (Mihaylova et al., 2014). Thus, understanding the impact and biologic significance of these manipulations may have implications for assessing cancer risk, developing cancer prevention strategies, and expanding potential therapeutic approaches for cancer patients.
There is a need to gather a range of basic/translational research scientists and clinicians to assess the result of altered cellular metabolism and its impact on the processes that contribute to the proliferation and survival of cancer cells in the patient. Bridging the gap between what basic and translational scientists understand about cancer metabolism biology and how physicians understand and apply this knowledge to clinical oncology is critical for the implementation of effective strategic approaches to aid in the diagnosis, treatment, and prevention of cancer. Furthermore, facilitating a dynamic interface between physicians and scientists at a conference targeted to both disciplines will increase knowledge of the current state of basic and translational research in the field of cancer metabolism and create a forum for discussion and collaboration to aid in the rapid translation of laboratory research findings to feasible “bench-to-bedside” treatment options based on the latest findings on metabolic pathways and cancer.
After participating in this CME activity, physicians should be able to:
1. Articulate the role of metabolism in tumor progression and survival.2. Distinguish among the different signaling pathways involved in the altered metabolism of cancer cells and the impact of these pathways on cell proliferation, cell survival, and cell death.3. Explain the development and relationship between systemic metabolic alterations and cancer.4. Identify approaches for exploiting cancer metabolism for cancer therapy and clinical applications.5. Assess how metabolism can change or control immune responses, and how this impacts protective immunity to cancer.6. Evaluate how metabolic signals can affect chromatin structure and regulate epigenetics.7. Explain redox metabolism and the metabolism of the tumor microenvironment.
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, AACR will provide information that Scientific Program Committee members 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.
This activity is supported by professional educational grants and will be disclosed at the activity.
Please contact the Office of CME at (215) 440-9300 or