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.

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.

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.

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.

The 2018 Forum on Metabolic Signaling and the Epigenome will bring together current and emerging leaders whose work bridges the metabolism-epigenetics interface to discuss their work and to explore its potential as a novel area for therapeutic intervention.

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.

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.

Most cancer deaths are due to metastasis – the spread of cancer from its site of origin to distant, vital organs, and the physiological damage caused by tumor growth in those organs. While the broad outlines of the process of metastatic spread are known, much of the details of the process remain poorly understood. 

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.

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. 

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. 

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. 

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. 

The immune system in our bodies keeps us safe from our environment that is full of bacteria and viruses. When we catch a cold it is our immune system that fights the infection. When we cut ourselves our immune system ensures that foreign invaders do not take over our bodies. 

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. 

The focus of this meeting will be on tumor stem cells; how they arise and how they differ from the progeny that originate from these stem cells. Until 1998, stem cell biology was a field of narrow interest to developmental biologists with a single point of contact to adult human medicine: bone marrow transplantation. 

The diagnosis and treatment of cancer has changed dramatically in the past two decades as advances in medical science have revealed the causes of cancer at the molecular level. This understanding has provided new targets for drug discovery, new approaches to evaluation of high-risk patients, and methods for early detection of cancer. 

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. 

The important role that DNA damage plays in cancer development is illustrated by the clear connections between exposures to certain types of DNA damaging agents in the environment and the development of cancer, such as the links between cigarette smoking and lung cancer or sunlight exposure and skin cancer.