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Escobar-Hoyos Lab


Despite recent targeted- and immune-therapies that have benefitted other cancer types, pancreatic and lung tumors develop therapy resistance. Therefore, there is an urgent clinical need to better understand the molecular biology of this disease to enable the improvement of therapeutic strategies.Activating mutations in KRAS and p53 co-occur in 40% of pancreatic and lung and other tumors. We recelty addressed the long-standing question of how these most common co-occurring mutations in human cancers cooperate to cause tumors, hoping to identify a meaningful therapeutic opportunity. We demonstrated that altered RNA splicing by mutant p53 activates and maintains oncogenic KRAS signaling. These paradigm shifting studies led to discovering that oncogenic KRAS is susceptible to inactivation, a novel finding in the field, and suggested the likelihood that inhibiting RNA splicing represents a valuable therapeutic strategy for mutant KRAS/p53 tumors (Cancer Cell 2020).

Therefore, our research focuses on understanding how aberrant RNA splicing contributes to the maintenance, establishment, and impairment of anti-tumor immune response in tumors. Additionally, we aim to test our novel developed therapy, called Splicing-Hit Oligonucleotide Therapy (SHOT), which corrects the RNA splicing errors selectively killing PDAC and LUAD cells of our own genetically engineered mouse models (GEMM) to recapitulate the human PDAC background and to validate our findings. Compared to traditional targeted therapies where it takes years to generate a compound or antibody to inhibit mutant proteins, SHOT enables rapid and precise therapy development. SHOTs are adaptable and scalable, to be used against second-line therapy resistant cancers or to target more than one cancer type.

Our laboratory collaborates actively with laboratories at Yale University, Stony Brook University, and Memorial Sloan Kettering Cancer Center. Our team involves experts within backgrounds spanning oncology, immunology, bioinformatics, drug delivery, and microbiology. We believe that through this collaborative environment, we will achieve our ultimate goals in hopes of developing new efficient therapies that can ultimately lead to the cure of this devastating malignancy.

Research Interests

  • Pancreatic ductal adenocarcinoma,
  • lung adenocarcinoma,
  • neuroendocrine tumors,
  • RNA splicing,
  • cancer biology,
  • tumor immunology,
  • genetically engineered mouse models,
  • KRAS,
  • GTPases,
  • driver mutations,
  • p53, and
  • resistance to therapy.

Lab Members

  • Principal Investigator

    Assistant Professor of Therapeutic Radiology; Radiobiology Course Director, Therapeutic Radiology

    Dr. Escobar-Hoyos obtained her master’s degree in Biomedical Sciences at the Universidad del Valle in Cali, Colombia. As a Fulbright Scholar, she pursued a Ph.D. in Cancer Molecular and Cellular Pharmacology at Stony Brook University mentored by Dr. Kenneth Shroyer. She then completed her postdoctoral training at the Memorial Sloan Kettering Cancer Center co-mentored by Drs. Steven Leach and Omar Abdel-Wahab. In 2020, Dr. Escobar-Hoyos joined the Department of Therapeutic Radiology at Yale as an Assistant Professor.The overarching goal of Dr. Escobar-Hoyos' lab is to cure pancreatic and lung cancers. Specifically, the team seeks to understand and target somatic mutations, and aberrant RNA processing in these tumors to  develop of novel therapies.
  • Postdoctoral Associate

    My goal is to develop novel therapies for pancreatic cancer by understanding how alternative splicing drives antitumor immunity and serves as a potential therapeutic target. I earned my Ph.D. in Biomedical Sciences at the National Autonomous University of Mexico (UNAM). My research projects aimed to elucidate pathways and mechanisms associated with anti-inflammatory M2-macrophages to reduce the inflammatory process. During my Ph.D., I discovered that microRNAs are crucial to reducing the expression of inflammatory mediators in macrophages and inducing the expression of M2-associated molecules. This finding suggests reprogramming macrophages through the identified pathways can guide the development of new therapies across inflammatory pathologies in MS and diabetes type 1, among others. This understanding of post-transcriptional events' impact on cells motivated me to study the role of alternative splicing in one of the most aggressive and therapeutically resistant cancers: Pancreatic cancer. Understanding the microenvironment of the tumors, tumor cell interaction with the immune system, and the role of splicing in these contexts is crucial to developing better therapeutic approaches. Postdoctoral Fellowship: Leslie Warner, Yale Cancer Center.
  • Postdoctoral Associate

    I am a microbiologist/immunologist with background in host-pathogen interactions and in molecular immunology that spans over 10 years of training. My doctoral work led to the discovery of how virulence factors activate inflammation responses in macrophages, and these findings impact our understanding of how we can develop therapeutics suitable for auto-immune diseases. With my thorough understanding that the immune system is a principal site that determines disease prognosis, I became motivated to pursue the study of its molecular regulation in pancreatic cancer, based on its high resistant to the best standard-of-care therapeutics we have and very short survival. In addition, while immunotherapy has shown promise in many cancers, pancreatic cancer is refractory to the current best immunotherapies available, suggesting that additional work is required to understand what makes the immune system in pancreatic cancer different and whether these differences can reveal therapeutic opportunities.
  • Matthew is a first-year graduate student at Yale University in the Molecular Biophysics and Biochemistry department. His previous work focused on secondary structural modeling of long noncoding RNAs. Currently, he is investigating how alternative RNA splicing contributes to lung adenocarcinomas.
  • Postdoctoral Associate

    I started my Postdoctoral training as a Postdoctoral Associate in the laboratory of Dr. Luisa Escobar-Hoyos in the Department of Therapeutic Radiology at Yale University in 2021. As a scientist in the field of Cancer Biology and Chemotherapeutics, my research goal is to understand essential cellular mechanisms that can serve as targets and therapy resistance for the development of new and more effective therapies to prevent and fight cancer. I have trained as a Molecular Pharmacologist in the field of Cancer and Inflammatory diseases, and I am now expanding my scientific repertoire through my postdoctoral training to understand what non-mutational mechanisms are used by pancreatic ductal carcinoma (PDAC) to thrive and develop resistance to currently available therapies.
  • Associate Research Scientist

    Saúl Rojas Sánchez, Ph.D., is an Associate Research Scientist at the Yale School of Public Health in the Epidemiology of Microbial Diseases department. He received a Doctor of Philosophy degree in Experimental Biology and Biomedicine from the National Autonomous University of Mexico as part of the doctoral program of the Postgraduate School in Biological Sciences. During his undergraduate and graduate studies his research focused on the characterization of the specific DNA sequences responsible for promoting transcription of the U2 small nuclear RNA in the trypanosomatid parasite Leishmania major, which causes the disease known as leishmaniasis. The current studies of Dr. Saúl, conducted in the laboratory of Dr. Christian Tschudi, are focused toward understanding the molecular mechanisms causing gain of infectivity and quiescence in the protozoan parasite Trypanosoma brucei, the etiological agent of human and animal African trypanosomiasis.
  • Deanne Yugawa is currently pursuing an M.D./Ph.D. at the Yale School of Medicine. She graduated from the University of Utah with degrees in Biology (with Honors) and Economics. During her undergraduate career, Deanne completed internships at Memorial Sloan Kettering Cancer Center, Hawaii Pathologists' Laboratory, and the Office of the Assistant Secretary for Planning and Evaluation (ASPE) at HHS. Deanne's past research focused on the role of Ptf1a (p48) in pancreatic cancer initiation. She is currently a member of the lab of Luisa Escobar-Hoyos where she studies the role of RNA splicing in pancreatic cancer.  In her free time, she enjoys reading mystery novels, exploring Japan, and going home to Hawaii.Fun Fact About Me: I never saw snow until college, but ended up living in a city where the snow was often taller than me.