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Evolution of 3D cell culture cancer models: Advances and future outlooks

This webinar is brought to you by the Science/AAAS Custom Publishing Office

Evolution of 3D cell culture cancer models: Advances and future outlooks

Recorded 16 May 2019


A growing body of evidence suggests that more relevant, translational observations can be made using 3D microtissues and organoids as compared to 2D monolayer cell culture. This is most notable in the fields of cancer biology, immuno-oncology, and hepatotoxicity. 2D models, though cost effective, fail to replicate the 3D complexity of an in vivo tumor and associated influences of the tumor microenvironment, such as that of cell-to-cell contact and the influence of the extracellular matrix. These complex interactions, in combination with the unique properties of a 3D structure, affect tumor cell properties and behavior, gene expression, distribution of proteins, and ultimately, response to anticancer drugs. Spheroid models have a layered structure with rapidly proliferating cells surrounding a more quiescent and hypoxic, necrotic core. This structure generates a gradient of nutrients, metabolites, and oxygen in the spheroid, important attributes for evaluation of drug resistance due to penetration effects in a heterogeneous tumor. Effective analysis of 3D tumor spheroids can be challenging, yet models are emerging that can overcome those limitations and drive future research.

During the webinar, viewers will:

  • Learn the two main approaches to generating 3D cancer models (liquid- and scaffold-based) and the limitations for assessing the growth and shrinkage of 3D tumor spheroids
  • Discover how live-cell analysis can be combined with advanced cell models for added insight and productivity
  • Glean what advances researchers can expect in the future
  • Have the opportunity to ask questions during the live broadcast.

This webinar will last for approximately 60 minutes.

Speaker bios

Keith L. Ligon, M.D., Ph.D.

Brigham and Women’s Hospital
Boston, MA

Keith Ligon is a principal investigator and board-certified Neuropathologist with expertise in glioma research. He holds joint appointments at the Dana-Farber Cancer Institute, Brigham and Women’s Hospital, Boston Children’s Hospital, and the Broad Institute. His early work demonstrated the essential role of OLIG2 in cancer stem-like cells of glioblastoma and medulloblastoma (Schuller U. et. Al. Cancer Cell 2008). His lab recently identified MYB-family transcription factors as new driver oncogenes in pediatric astrocytomas and elucidated their biological and epigenetic effects (Ramkissoon LA. et al PNAS 2013, Bandopadhayay P, et al Nat Gen 2016). He has made essential contributions in diagnostics and targeted therapy of gliomas (Francis J. et. Al. Cancer Discovery 2013). His lab has focused on generation and investigation of patient derived models of glioma and has generated more than 1000 patient models of brain cancers and has utilized these for preclinical studies of novel therapies. He serves as PI of one NCI R01 focused on glioma responses to therapy. He directs NCI P01 and P50 (SPORE) Pathology Cores and act as the PI of the unified Neurooncology Tissue and Data Bank across 4 member institutions of the P30 NCI designated Dana-Farber Harvard Cancer Center. He also has leadership roles and participation in pathology and biomarker research within several national NCI sponsored and private clinical trial consortia (DIPG-BATS, PNOC, COG, ABTC, Alliance, Ivy Foundation).

David Tuveson, M.D., Ph.D.

Cold Spring Harbor Laboratory
Cold Spring Harbor, NY

Dr. Tuveson serves as Director of the Cold Spring Harbor Laboratory Cancer Center and the Chief Scientist for the Lustgarten Foundation. His laboratory uses murine and human models of pancreatic cancer to explore the fundamental biology of malignancy and thereby identify new diagnostic and treatment strategies. The lab’s approaches run the gamut from designing new model systems of disease to developing new therapeutic and diagnostic approaches for rapid evaluation in preclinical and clinical settings. The lab’s studies make use of organoid cultures—three-dimensional cultures of normal or cancerous epithelia—as ex vivo models to probe cancer biology. Current projects in the lab explore changes in redox metabolism associated with pancreatic cancer tumorigenesis, dissect signaling by the Ras oncogene, discover new biomarkers of early pancreas cancer, and identify mechanisms of cross-talk between pancreatic cancer cells and the tumor stroma. Novel treatment approaches suggested by these studies are then tested by performing therapeutic experiments in mouse models. To dissect molecular changes associated with pancreatic tumorigenesis, the Tuveson lab has generated a large collection of human patient-derived organoid models. By measuring the therapeutic sensitivities of patient-derived organoids, the lab is working to identify novel strategies to treat patients as well as markers of therapeutic response. The Tuveson Laboratory maintains strong links to clinical research, and the ultimate goal is confirmation of preclinical findings in early-phase trials. Collectively, the lab’s bench-to-bedside approach is codified as the “Cancer Therapeutics Initiative,” and this initiative will provide these same approaches to the entire CSHL cancer community.

Jackie Oberst, Ph.D.

Washington, DC

Dr. Oberst did her undergraduate training at the University of Maryland, College Park, and her Ph.D. in Tumor Biology at Georgetown University, Washington D.C. She combined her interests in science and writing by pursuing an M.A. in Journalism from the Philip Merrill College of Journalism at the University of Maryland, College Park. Dr. Oberst joined Science/AAAS in 2016 as the Assistant Editor for Custom Publishing. Before then she worked at Nature magazine, the Howard Hughes Medical Institute, The Endocrine Society, and the National Institutes of Mental Health.

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