Thanks to private funding, 100% of every dollar donated to The Lustgarten Foundation goes directly to pancreatic cancer research.

Current Research Investigator Award Recipients

Andrew Feinberg, M.D., Johns Hopkins University School of Medicine, Baltimore

$1 million over 3 years (2018-2020) | Project: Targeting the epigenomic-metabolomic foundation of PDAC metastasis

PDAC mortality usually results from the spread of the primary pancreatic cancer cells to distant organs such as the lung or liver. To address the causes of cancer in these metastatic cells, we have identified novel and surprising epigenetic defects (changes caused by modification of gene expression) in pancreatic cancer that occur during metastasis. These defects involve modifications to DNA and the proteins that package DNA (the chromatin), as well as a link to metabolism. By studying these mechanisms, Dr. Feinberg and his team can develop target compounds to prevent the tumor from spreading beyond the pancreas.

Tony Hunter, Ph.D., Salk Institute for Biological Studies, La Jolla, CA

$1 million over 3 years (2018-2020) | Project: Understanding the value of LIF (leukemia inhibitor factor) serum level as a biomarker of pancreatic cancer

Leukemia inhibitory factor (LIF) is a protein highly expressed in pancreatic cancer that helps sustain tumor growth and blunts the body’s immune response to the tumor. Dr. Hunter’s goal is to validate LIF as a biomarker and identify how it can influence the immune system.

Elizabeth Jaffee, M.D., Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore

$1 million over 3 years (2018-2020) | Project: A phase II study of HDAC inhibition to sensitize to immunotherapy in advanced pancreatic cancer

The immune system can unmask and destroy cancer cells. Dr. Jaffee’s lab has examined an important subset of immune cells that suppress the immune response. The drug entinostat can decrease these immunosuppressive cells and allow access to tumor-killing T cells. The goal is to enroll chemotherapy resistant pancreatic cancer patients into a Phase II clinical trial using entinostat given with the PD1-inhibitor nivolumab.

David Pellman, M.D., Dana-Farber Cancer Institute, Boston

$1 million over 3 years (2018-2020) | Project: Mechanisms and therapeutics for genome catastrophes that drive genome evolution in PDAC


Dr. Pellman will establish, for the first time, why genome catastrophes, a phenomenon by which up to thousands of clustered chromosomal rearrangements occur in a single event, are so common in pancreatic cancer and will define underlying mechanisms. He will also identify potential therapies for treating genome catastrophes to prevent pancreatic tumors from developing. Dr. Pellman and his team will use pancreatic organoid cultures to model the different stages in pancreatic cancer development.

Hidde Ploegh, Ph.D., Children’s Hospital Boston

$1 million over 3 years (2018-2020) | Project: New nanobodies for use in diagnosis and therapy of pancreatic cancer


When properly stimulated, the human immune system can kill cancer cells, which makes immunotherapy a promising option in the fight against cancer. For an immune response against cancer to be effective, cells of the immune system known as T cells must recognize the cancer by means of their T cell receptors. The human immune system is not always equipped with receptors up to the task. Dr. Ploegh therefore proposes genetically engineering T cells with new receptors that recognize targets on newly formed blood vessels in growing pancreatic cancers.
Furthermore, the team will produce biologically active molecules that can direct T cells toward the location of pancreatic tumors to increase their ability to kill cancer cells. In similar fashion, imaging agents will be developed, enabling us to monitor the effectiveness of therapy and to do so non-invasively, an aspect often lacking in cancer trials.

David Sabatini, M.D., Ph.D., Whitehead Institute for Biomedical Research, Boston

$1 million over 3 years (2018-2020) | Project: Locking away the lysosomal nutrient supply of pancreatic cancer cells


A new approach to fighting pancreatic cancer is to target cancer metabolism. In order to grow, cancer cells need to produce energy and build blocks for the generation of new cancer cells. To do that, cancer cells increase uptake of nutrients from their environment by overexpressing specific transporters. The Sabatini lab has recently discovered a molecular machine called SLC38A9 that acts as a gate through which those nutrients are released to cells. If SLC38A9 is removed from pancreatic cancer cells, the food is trapped inside, unable to fuel cancer growth.

Matthew Vander Heiden, M.D., Ph.D., Koch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Boston

$1,260,888.48 over 3 years (2016-2018) | Project: Understanding the metabolic interplay between tumor and host in pancreatic cancer


Changes in how nutrients are metabolized, or broken down for energy, contribute to both the development and progression of pancreatic cancer, but the complicated relationship between the cancer itself and a person’s body is not well understood. In previous work, Dr. Vander Heiden has shown that the breakdown of muscle tissue, which is common in pancreatic cancer patients, takes place early in their disease. Dr. Vander Heiden found that muscle breakdown releases branched chain amino acids (BCAAs), and he will test how the BCAAs affect the growth of the tumor and the patient’s metabolism. Through this research, Dr. Vander Heiden’s objectives are to identify targets for new therapies to stop the growth of the cancer and treat the effects of the disease that impact the use of existing therapies.

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