Cancer Metabolism: From molecules to medicine
Harvard Medical School・52 minutes read
Harvard Medical School's Mini-Med School program provides global students with science and health education from expert faculty, allowing attendees to learn about the latest research, ask questions, and participate in planning future programs. The evening's seminar focuses on cancer metabolism, exploring how cancer cells differ in fuel metabolism and macromolecule production from normal cells, with the goal of targeting cancer metabolism effectively through selective inhibition of specific pathways controlled by mTOR.
Insights
- The Mini-Med School program by Harvard Medical School offers global students the chance to engage with cutting-edge science and health information from expert faculty, focusing on cancer metabolism in a recent seminar.
- Understanding cancer metabolism, particularly in pancreatic cancer driven by KRAS mutations, is crucial for developing effective treatments, as targeting specific metabolic pathways can lead to tumor regression and cell death.
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Recent questions
What is the focus of the Harvard Medical School Mini-Med School program?
Cancer metabolism research
How can attendees participate in planning future Harvard Medical School programs?
Through crowdsourcing and surveys
What is the significance of inhibiting glutamate dehydrogenase in cancer growth?
Slows cancer growth in animal models
How do KRAS mutations impact pancreatic cancer growth?
Orchestrating nutrient acquisition
What challenges are associated with targeting cancer cell metabolism?
Robustness of metabolic pathways
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Summary
00:00
Harvard Mini-Med School: Global Health Education
- Gina Vild, Chief Communications Officer for Harvard Medical School, welcomes attendees to the 19th year of Harvard Medical School's Mini-Med School program.
- The program offers science and health education from Harvard's expert faculty to thousands of students globally.
- Attendees have the opportunity to learn and ask questions about the latest research and medical breakthroughs.
- Last year, over 120,000 students from 84 countries participated in Longwood seminars.
- Attendees are encouraged to participate in planning future programs through crowdsourcing and surveys.
- Topics for upcoming Longwood seminars are chosen based on attendee feedback.
- Participants are invited to join a Twitter conversation during the event using the hashtag #HMSMiniMed.
- Certificates and professional development points are offered to attendees who complete three or more seminars.
- Questions can be submitted by audience members via index cards or online for global viewers.
- The evening's seminar focuses on Cancer Metabolism, exploring how cancer cells differ from normal cells in fuel metabolism and macromolecule production.
18:39
Ammonia's Role in Cancer Metabolism Research
- Ammonia builds up in the tumor microenvironment, leading to two hypotheses: secretion as waste or utilization for cell growth.
- Ammonia accumulation in tumor microenvironments can be measured in mouse models.
- Addition of ammonia stimulates proliferation in estrogen receptor positive breast cancer cells.
- Inhibiting glutamate dehydrogenase, an enzyme crucial for ammonia recycling, slows cancer growth in animal models.
- Cancer cells recycle nitrogen waste products for growth, using ammonia to produce glutamate amino acids.
- Understanding metabolic signatures of specific tumor types is crucial for targeting cancer metabolism effectively.
- Combinations of metabolic inhibitors with approved drugs need to be studied for optimal treatment.
- Tumor metabolism varies with genotype and signaling, impacting sensitivity to metabolic inhibitors.
- Cancer metabolism research has expanded beyond cancer biology, influencing fields like immunology and stem cell biology.
- The mechanistic studies in cancer biology have led to technological advancements and further research opportunities.
36:20
Targeting Cancer Metabolism: A Promising Approach
- The analogy of building a house is used to explain the concept of creating an imbalanced setting to collapse a tumor.
- Targeting mTOR signaling in cancer cells can slow down tumor growth by affecting metabolic pathways.
- Resistance to targeted therapeutics can develop when other pathways are activated to counter the effects of mTOR inhibition.
- By selectively inhibiting a single metabolic pathway controlled by mTOR, it is possible to create a metabolic imbalance that leads to tumor cell death.
- Experimental data from cell culture and a mouse tumor model demonstrate the effectiveness of inhibiting specific metabolic pathways in causing tumor cell collapse.
- Dr. Sidney Farber's discovery of antimetabolite therapy targeting nucleotide synthesis paved the way for targeting cancer metabolism.
- Advances in technology and understanding of cancer biology have re-energized the field of targeting cancer metabolism.
- Pancreatic cancer, driven by mutated KRAS gene, presents challenges due to limited therapies and late detection.
- KRAS mutations in pancreatic cancer lead to abnormal cell growth and alterations in cell metabolism.
- The unique microenvironment of pancreatic cancer, characterized by dense fibrotic tissue and compressed blood vessels, limits nutrient availability and poses challenges for targeting cancer metabolism.
52:06
KRAS mutations drive cancer growth through nutrients.
- Cancer growth is facilitated by KRAS mutations orchestrating a balance between growth cues and nutrient acquisition.
- KRAS mutations play a crucial role in tumor growth by ensuring robust nutrient availability and enhanced nutrient acquisition despite limited supply.
- Genetic tools can be used to switch off KRAS in mouse or human cells, demonstrating its importance in tumor growth.
- Turning off KRAS genetically leads to tumor regression and cell death, primarily due to metabolic imbalances.
- Pancreatic cancers excel in taking up glucose, glutamine, and fats, essential for generating basic building blocks needed in cells.
- Specialized processes like macropinocytosis and autophagy are crucial in capturing extracellular nutrients and recycling damaged organelles in pancreatic cancer cells.
- Inhibiting cellular recycling programs in pancreatic cancer cells has shown promise in treatment by hindering growth.
- Understanding nutrient utilization in cancer cells is vital for exploiting metabolic reprogramming effectively.
- KRAS coordinates enhanced growth with increased antioxidant production to protect cancer cells from oxidative stress.
- Challenges in targeting cancer metabolism include the robustness of metabolic pathways, necessitating a deeper understanding to intervene effectively.
01:08:25
"Targeting Cancer Metabolism for Effective Therapy"
- The therapeutic window in cancer therapies is a crucial challenge, targeting normal cell functions while avoiding harm.
- Metabolic imbalance is key, with cancer cells driven to grow despite nutrient limitations.
- Genomic data mining is a powerful tool to identify unique pathways in tumor cells for targeted therapy.
- Different cancers have varying fuel preferences, such as sugars, amino acids, or fatty acids.
- Identifying which patients will respond best to specific metabolic pathway inhibitors is complex, considering genetic, anatomical, and dietary factors.
- Inhibiting specific metabolic pathways can trigger compensatory mechanisms like mTOR activation, impacting treatment effectiveness.
- Targeting cancer cell metabolism shows promise but may require combination therapies for optimal results.
- Dietary interventions can influence tumor growth in animal models, but their impact on human cancer treatment is less clear.
- Certain dietary interventions may enhance the efficacy of targeted metabolic therapies, while others may be harmful.
- Obesity and high-fat diets are statistically linked to increased cancer incidence in various types.
01:26:29
Diet's Impact on Cancer Incidence
- Experimental testing in laboratory models of cancer has shown that diets lacking specific amino acids or metabolites can impact the bloodstream and tumor metabolite profile, although the direct reflection in cancer cells is not always clear. Despite clear associations, the impact of diet on cancer incidence is generally much smaller compared to established risk factors like smoking or sunlight exposure.
