TCRF
Funded Research

  • Functional Epigenomics of Transgenic Cellular Immunotherapies for Cancer
    $100,000 Tower Career Development Grant

    Cellular immunotherapies, in which a patient’s immune system is genetically engineered to target cancer cells, are revolutionizing cancer treatment. However, these engineered cells do not always persist long-term in patients, which can lead to disease relapse. I propose that the DNA structure of these engineered immune cells changes over time, ultimately impairing the expression of receptors which target the cancer cells, and that these changes can lead to treatment failure. I will examine genetically engineered immune cells from patients receiving them for cancer treatment for this phenomenon, and correlate the DNA structural changes with engineered receptor expression and therapeutic response.

    Theodore Scott Nowicki, MD, PhD
    University of California, Los Angeles
  • Use of Metformin for Prevention of Clonal Progression to Therapy-Related MDS/AML
    $100,000 Tower Career Development Grant

    Clonal hematopoiesis describes a common pre-cancerous condition where blood stem cells gain mutations in cancer-associated genes that allow them to grow and expand abnormally. This condition occurs more frequently with increasing age and after chemotherapy for solid tumors where it is a strong risk factor for developing secondary blood cancers. Inflammation after chemotherapy exposure is known to favor proliferation of mutant blood stem cells. We are investigating the anti-inflammatory effects of metformin on mutant blood stem cell behavior and how the presence of clonal hematopoiesis impacts clinical outcomes in women who received curative-intent chemotherapy after surgery for advanced breast cancer.

    Soo Park, MD
    University of California, San Diego
  • Nanosystems to accelerate clinical translation and generation of cellular immunotherapies
    $100,000 Randi and Warren Grant Research Grant

    For these patients, new treatments are being developed that recruit cells of the immune system to attack the cancer. To turn on these defenses, we need to deliver genetic instructions to about two hundred million immune cells, efficiently and safely. Unlike other strategies, these cells no longer need to come from the patients, who are already weakened. We have invented an engineering solution to do so and we are testing and optimizing it so that we can make this treatment widely available to patients and their doctors soon.

    Steven Jonas, MD, PhD
    University of California, Los Angeles
  • Predicting the metastatic risk of bladder cancer by cell-free DNA methylation sequencing
    $50,000 Jessica M. Berman Memorial Fund Career Development Grant

    Bladder cancer continues to cause significant mortality in the US due to the lack of reliable methods to identify high-risk patients who benefit from chemotherapy. We propose a study to characterize cell-free circulating DNA in the plasma for the purpose of creating a new noninvasive biomarker to identify patients with high-risk of recurrence. First, we will perform whole genome bisulfite sequencing to compare the methylation signatures between the patients who developed recurrence and those who did not. The identified differential methylation loci will be refined and then validated in a separate group of patients.

    Yi-Tsung Lu, MD
    University of Southern California
  • Targeting AML Stem Cells using Novel Small Molecule Inhibitors of RNA Regulatory Proteins
    $50,000 Cancer Free Generation Research Grant

    Acute myeloid leukemia (AML) is a devastating blood cancer were blood producing stem cells are damaged and become abnormally functioning leukemic stem cells (LSCs). To date, there is still no curative treatment targeting these aggressive LSCs. We identified novel compounds that inhibit important growth mechanisms of LSCs. In AML animal models and patient samples, these compounds decrease AML and improve survival. We will use rigorous experimental approaches to better understand the mechanism how these novel compounds kill LSCs. This project has a high potential to develop a new class of drugs for precision AML therapy.

    Martina Roos, PhD, PharmD
    University of California, Los Angeles
  • Using Oxaliplatin to improve the response to PD-1/PD-L1 blockade
    $500.000 Tower Senior Investigator Grant

    Immune checkpoint inhibitors had revolutionized cancer treatment. The most versatile such drugs are antibodies that target a receptor molecule called PD-1 or its ligand PD-L1. Although effective in many cancer types, response rates to these drugs rarely exceed 20-30%, necessitating the search for agents that synergize with PD-1/PD-L1 blockers. Using mouse models, we found that the conventional chemotherapeutic drug oxaliplatin has the unique ability to greatly enhance the response to PD-1/PD-L1 blocking antibodies. We will investigate how oxaliplatin increases the effectiveness of PD-1/PD-L1 blockers and will validate these findings in human lung cancer through a Phase I/II clinical study.

    Michael Karin, PhD
    University of California, San Diego
  • Eph/Ephrin Signaling Regulates Multiple Myeloma in the Bone Marrow Vascular Niche
    $100,000 Tower Career Development Grant

    Multiple Myeloma is the second most common blood cancer. It arises out of plasma cells, whose normal function is to make antibodies to fight infections. Although in recent years the treatment has become more effective, it remains essentially incurable. One unique aspect of the disease is the close ties to the normal bone marrow cells, specifically the blood vessel cells. Without signals from these cells the cancer dies. We don’t know which signals are the most relevant; our experiments are designed to discover that. This could form the basis for new treatments designed to disrupt these pathways to benefit patients.

    Sponsor: John Chute, MD

    Joshua P. Sasine, MD, PhD
    University of California, Los Angeles
  • Synthetic Lethal Networks to Guide Precision Oncology in GI Tumors
    $100,000 Cancer Free Generation Career Development Research Grant

    Cancer cells have many mutations- that is what makes them cancer. Recently it has become clear every cancer patient’s tumor is unique; like snowflakes, cancer cells appear similar from a distance, but when inspected closely no two are exactly the same. This research proposal attempts to better understand how each tumor is different, so that in the future oncologists will be able to pick the right drugs for each unique patient and tumor. Specifically, I am looking to find weaknesses in the cancer cell, so that newer drugs will be able to kill cancer cells while sparing heathy cells.

    Sponsor: Trey Ideker, PhD

    John Paul Shen, MD
    University of California, San Diego
  • Developing a Neoadjuvant Platform to Study Macrophage-Driven Resistance
    $50,000 Tower Career Development Grant

    Immunotherapy is an exciting development in cancer treatment, but has not yet made its mark in sarcoma. The resistance of sarcoma to immunotherapy might be related to the presence of macrophages –a type of immune cell. Here, we aim to understand why sarcomas are full of macrophages, and how macrophages impede the immune system. We will determine how radiation therapy, which is commonly used for patients before surgery, affects these phenomena. Our ultimate goal is to design clinical trials to test drugs targeting macrophages in combination with radiation to make immunotherapy relevant for sarcoma.

    Sponsor: Antoni Ribas, MD, PhD

    Anusha Kalbasi, MD
    University of California, Los Angeles
  • Modeling Super-Enhancers in Barrett’s esophagus-associated neoplastic evolution
    $50,000 Tower Career Development Grant

    With the help of medical research, the incidences and mortalities of many common cancers (e.g., those from breast, lung and colon cancers) are dropping significantly in US. However, as one of the deadliest malignancies, esophageal carcinoma (EAC) has strikingly risen in incidence (> 600% during the last four decades in USA), with the five-year survival of only 16%. Although Barrett’s esophagus (BE) has long been regarded as a precursor lesion of EAC, no effective preventive strategies is available. Better characterization of EAC pathogenesis and its evolution from BE is greatly needed to decrease the impact of this deadly cancer.

    Sponsor: H. Phillip Koeffler, MD, PhD

    Dechen Lin, PhD
    Cedars-Sinai Medical Center

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