Funded Research

  • Novel Drug Targets for High Grade Serous Ovarian Cancer identified through Induced Pluripotent Stem Cell Modeling of Disease
    $500,000 Tower Senior Investigator Grant

    Faults in high risk genes cause high grade serous ovarian cancer (HGSOC). This cancer is often lethal in patients. Novel drugs are needed to improve treatment and patient outcomes. We plan to use cells from individuals carrying high risk genes to develop precision models of their disease and then cutting edge methods in genomics and functional screens to identify novel therapeutic targets that can be tested for their potential to treat patients with HGSOC. Ultimately we expected these studies will improve survival rates in patients that get HGSOC because they carry faulty genes.

    Simon Gayther, PhD
    Cedars-Sinai Medical Center
  • Cold Atmospheric Plasma for the Treatment of NF1-related Peripheral Nerve Sheath Tumors
    $100,000 Angie and Michael David Career Development Grant

    Malignant peripheral nerve sheath tumors (MPNSTs) are aggressive soft-tissue sarcomas for which the only effective therapy is surgery and NF1 patients have a greater risk of developing these tumors from plexiform neurofibromas. These tumors are collectively known as Peripheral Nerve Sheath Tumors (PNSTs). One area of active research in plasma medicine is the use of cold atmospheric plasma (CAP) in treating tumors. In this proposal, we want to investigate the role of CAP in treating NF1-related PNSTs.

    Brian Na, MD
    University of California, Los Angeles
  • Epigenetic control of stem cell plasticity in colorectal cancer development and recurrence
    $100,000 Tower Career Development Grant

    Colorectal cancer (CRC) is the second-most lethal cancer in the United States causing 50,000 deaths annually. Cancer is caused by alterations in genetic material called mutations, however correcting such changes remains unfeasible. Additionally, non-genetic structural and chemical changes are essential for cancer to gain aggressive growth potential and evading therapy. Although such non-genetic changes are essentially reversible using therapeutic drugs, details of how and when they occur during CRC progression remains unknown. Using cutting-edge human CRC and mouse model systems, we will characterize the non-genetic changes during CRC growth and identify novel factors that can be targeted for innovative therapies.

    Unmesh Jadhav, PhD
    University of Southern California
  • Single Cell Spatial Analysis of DLBCL to Develop Biomarkers and Optimize CAR T Therapy
    $100,000 Tower Career Development Grant

    Recently we have discovered ways to reinvigorate the immune system to fight cancer. However, in immune cancers such as lymphoma, the line between cancer and the immune system is blurred. This presents an opportunity to learn how immune cells attack cancer under complex conditions, which is called the tumor microenvironment. I propose to use a spatial protein analysis technology to identify clues, not just in cancer cells but also in the embedded immune cells, that predict cancer outcomes. Further, I will study how genetically engineered anti-tumor immune cells operate in the tumor microenvironment to improve their efficacy.

    Alexander Xu, PhD
    Cedars-Sinai Medical Center
  • The impact of alpha catenin loss on DNA repair defects in triple negative breast cancer
    $500.000 Barry Rosenbloom, MD Senior Investigator Grant

    Triple negative breast cancer (TNBC) is an aggressive and has a high death rate, especially in black women. We have found a gene marker that may make these tumors escape chemotherapy. Our research also shows that when this marker is not present, the tumor cells respond to a very specific type of cancer therapy. Also, there might be more immune cells that come into the tumor. Therefore, we wish to expand our research help better understand the role of this marker in breast cancer growth to improve treatment of this hard to treat form of cancer.

    John Carpten, PhD
    University of Southern California
  • Targeting Monoamine Oxidase A to Expand Cancer Immune Checkpoint Blockade Therapy
    $500,000 Magnolia Council Senior Investigator Grant

    Immune checkpoint blockade (ICB) therapies have revolutionized the treatment of many cancers; however, the existing ICB therapies can only benefit a small fraction of cancer patients, demanding an expansion of ICB therapies. Monoamine oxidase A (MAO-A) is an enzyme best known for its function in the brain; small molecule MAO inhibitors (MOIs) have been developed and are clinically used for treating depression. This proposal aims to study MAO-A regulation of antitumor immunity and evaluate MAO-A blockade for cancer immunotherapy. The project has the potential to identify MAO-A as a new immune checkpoint and support repurposing MAOI antidepressants for cancer immunotherapy.

    Lili Yang, PhD
    University of California, Los Angeles
  • Performance of hypermethylated circulating tumor DNA’s in colorectal cancer
    $100,000 Rosen Cherney Tower Golf Tournament Research Grant

    Measuring DNA produced by colorectal cancer (CRC) in blood (ctDNA) is a new method to detect return (recurrence) of CRC. We developed an in-house, blood-based ctDNA test that is less costly and easier to apply in practice. We will compare our ctDNA test’s performance to a commercial ctDNA test for detecting recurrence in patients who no longer have CRC and tumor growth or spread in patients with existing CRC. We will also analyze our test’s potential to predict recurrence in localized rectal cancer, which can be helpful to identify candidates who can be spared from unnecessary surgery (ostomy bags).

    Jun Gong, MD
    Cedars-Sinai Medical Center
  • Sensitizing the tumor immune microenvironment of breast cancer
    $100,000 Howard and Reva Colover Trust Career Development Research Grant

    Breast cancer is the second leading cause of cancer-related death in women. Immunotherapies harness the body’s immune system to fight cancer, holding great promise to prevent recurrence and prolong survival. Immunotherapies have been less effective in patient’s with breast cancer in part, due to the recruitment of suppressive cells that prevent an anti-tumor effect. We will investigate strategies to decrease suppressive signals within the tumor, allowing anti-tumor signals to successfully eliminate tumor growth. We will also determine differences in suppressive signals between early versus metastatic breast cancers to improve response to immunotherapy for patients with all stages of disease.

    Evanthia Roussos-Torres, MD, PhD
    University of Southern California
  • Harnessing the Hippo signaling pathway to counteract chemoresistance
    $100,000 Cancer Free Generation Career Development Research Grant

    Cisplatin-based chemotherapy has been widely used for treating a variety of solid tumors including breast, lung and ovarian cancers. Although initial therapeutic success is achieved, a number of tumors are found to be intrinsically resistant or gradually develop resistance to cisplatin treatment, which greatly limits its therapeutic potential. Notably, cisplatin belongs to the platinum compound family, which are known as the only heavy metal containing drugs used for chemotherapy. Our proposed research will focus on a growth-related signaling pathway, named the Hippo pathway in regulating heavy metal-induced stress response, which results in a unique mechanism accounting for the cisplatin-based chemo-resistance.

    Wenqi Wang, PhD
    University of California, Irvine
  • Identifying novel therapeutic targets in circular RNAs that bolster the sarcoma-protective microenvironment
    $100,000 Tower Career Development Grant

    To identify circular RNAs abundantly expressed in Undifferentianted Pleiomorphic Sarcoma and illuminate how circRNAs catalyze cancer-promoting and drug-resisting conditions in the microenvironment surrounding tumor cells. In particular, we will study how circRNAs merge with RNAbinding proteins to powerfully modulate tumor cell secretions, which in turn forge a tumor-protective niche that renders many existing therapies ineffective against UPS. Finally, we will use newly developed molecular techniques to manipulate circRNAs in tumor cells, paving the way to design transcriptional therapies against UPS, and to use circRNAs to refashion the tumor microenvironment, rendering this intractable disease newly vulnerable to previously failed therapies.

    Jlenia Guarnerio, PhD
    Cedars-Sinai Medical Center

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