Scholar Retreat

Each year, 16 Forbeck Scholars are invited to Lake Geneva, Wisconsin for a scientific gathering. Here, the Scholars share their research with the other Scholars and Mentors. Each Scholar will participate in four sequential retreats, with all expenses paid by WGFRF. The opportunity for Scholars to connect and form relationships with researchers from completely different areas of cancer research and to have a sort of peer review is one of the most valuable roles of the Retreat. Through the Mentors, the Retreat offers Scholars guidance on practical career issues such as writing grants and preparing successful scientific publications.

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Cancer Predisposition

The 2018 Forum on Cancer Predisposition will be chaired by Dr. John Maris from the Children's Hospital of Philadelphia and the University of Pennsylvania, and Dr. Judy Garber from the Dana Farber Cancer Institute and Harvard Medical School. While we expect to explore mechanisms of cancer initiation in great depth, the meeting will also seek to focus on how research in the field of cancer predisposition should impact patient care now and in the future.

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Tumor Microenvironment

The 2018 Forum on Tumor Microenvironment will be chaired by Dr. Rakesh K. Jain of Massachusetts General Hospital and Harvard Medical School, and Dr. Lisa M Coussens from the Knight Cancer Institute at Oregon Health & Science University. The goal will be not only to discuss the current state of the tumor microenvironment field, but also discuss approaches towards applying that knowledge to the development of effective and broadly applicable anti- cancer therapies for long-term management of disease.

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Epigenetic Therapy

The 2018 Forum on Epigenetic Therapy will be co-chaired by Dr. Jean-Pierre Issa of Temple University, Dr. Stephen Baylin of Johns Hopkins University and Dr. Peter Jones of Van Andel Research Institute. It will bring together investigators with expertise in diverse areas (different epigenetic targets, immunotherapy, basic investigators, clinical-translational investigators) to discuss how synergies across different fields can help move epigenetic therapy forward to improve cancer outcomes.

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Annual Forum 2017 - Convergence of Myc and Ras in Cancer

Myc and Ras are two of the most commonly deregulated genes in human cancer. Nonetheless, we still lack a clear understanding of how these cancer-causing genes work, how they cooperate during tumor development, or how we may convert our biological insights into therapies. This Forbeck Foundation Forum brought together thought leaders from both the Myc and Ras fields to address critical questions about these two cancer-causing genes and to think outside the conventional biopharmacological box.

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Annual Forum 2016 - Chromosomal Instability & Aneuploidy

The 2016 Forbeck Foundation meeting provided an exciting venue for researchers in different fields to come together, for the first time, to discuss new advances in understanding the structure of cancer genomes, with potentially important implications for novel therapeutic strategies in cancer. Much like the evolution of a new organism, cancer genomes evolve from normal ones by a series of DNA alterations, enabling all of the manifestations of the disease to develop. It is common to quote Shakespeare’s Tempest for the insight that “What’s past is prologue”; this insight was the theme of the 2016 Forbeck meeting.   Knowing the past history of a cancer genome can help us identify the “drivers” of uncontrolled cancer cell division.  Such drivers are important drug targets.  Knowledge of the evolutionary history can also tell us about trade-offs made during cancer evolution, trade-offs that could lead vulnerabilities that might also be “druggable”.  

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Annual Forum 2015 – Immunotherapy

Some of the most exciting results in cancer medicine, in the last decade, have come about by treating relapsed patients with B cell lymphoma with their own T cells that have been modified to attack the tumor cells.  T cells in the body form part of the cellular immune response and they normally carry out a very important role in killing cells that are infected with viruses.

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Annual Forum 2013 – Resistance Mechanisms

Cancer therapies that specifically target the genetic alterations associated with subsets of advanced cancers have shown impressive success in the clinic.  Examples include ABL inhibitors fro chronic myelogenous leukemia, RAF inhibitors for BRAF mutant melanomas, EGFR inhibitors for EGFR mutant lung cancers, and HER2 inhibitors for HER2 amplified breast cancers. In each of these cancer paradigms, the treatments are often highly effective, leading to remarkable remissions that have a profound beneficial impact on patients. These successes have changed the landscape of the diagnosis and treatment of cancer for the foreseeable future.

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Annual Forum 2012 – Tumor Metabolism

The focus of the 2012 Forbeck Foundation forum was on the role of tumor metabolism on oncogenesis. While it has been known for over 50 years that the metabolism of cancer cells is distinct from that or normal cells, the reasons for this have only been emerging recently. Now that we are beginning to understand how and why metabolic pathways are altered in cancer, there is the potential to make use of this knowledge to improve cancer treatment. 

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Annual Forum 2011 - Epigenetics & Drug Therapy

Cancer development is a multi-step process with mutations in proto-oncogenes and tumor suppressor genes playing a well-defined role. In this regard, cancer is a genetic disease. However, cellular mechanisms that control the differentiation state, survival and self-renewal of cancer cells are often independent of mutations in DNA sequence and are increasingly recognized as critical for tumor development and progression. These epigenetic mechanisms are largely a result of the multitude of chromatin modifications that control gene expression. Since epigenetic changes are largely reversible, there is significant hope that therapies targeting these modifications may be particularly effective anti-tumor agents. 

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Annual Forum 2010 – Cancer Genomics

Cancer is a genetic disease. Increased cancer susceptibility can result from inherited mutations in tumor suppressor genes and oncogenes as well other genes. In addition, in both inherited and the much more common sporadic cancers, mutations arise that drive the development and progression of the cancer. Decades of research have led to an understanding of the types of pathways that become genetically and epigenetically compromised in cancer; however, a comprehensive understanding of the genetics of all tumor types is not yet available. In recent years it has been possible to bring to the clinic therapies that are targeted to genetic defects found in cancer. 

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Annual Forum 2009 – The Biology and Treatment of Primary Brain Tumors

Primary tumors of the central nervous system are the leading cause of cancer death in children, and a tumor of growing incidence in adults, in whom it is equally difficult to treat. Only recently have researchers begun to understand the basic genetic derangements that play a central role in the growth of these tumors. In children, brain tumors are found in a variety of unusual types, some with unique and characteristic appearance on pathologic examination and in their clinical behavior. 

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Annual Forum 2007 – MicroRNA and Cancer

The 2007 Forbeck Foundation Forum will focus on the topic of microRNA. MicroRNA, as the name implies, are small RNA that have been identified in human cells. Despite their small sizes, microRNAs have big roles in human biology. Recently, scientists have discovered that microRNAs are involved in cancer, and that microRNA will be useful in the prediction, the diagnosis and the treatment of cancer. The Forbeck Forum on MicroRNA and Cancer will be a catalyst for expanding this forefront of cancer research. 

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Annual Forum 2004 – Molecular Targets in Pediatric Malignancies

This topic pertains to the new quest of utilizing molecular and genetic information about cancer to specifically design treatments which target functionally important molecular lesions. In the past several decades enormous quantities of information have accumulated regarding the precise mutations which either activate or disrupt genes in many human cancers. 

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