Fellows
Dan Chen, a Salk postdoctoral fellow, was born and raised in China, and obtained her BS in Cellular and Molecular Biology from Nantong University and her PhD from Nanjing University. During her undergraduate and graduate training, she received numerous awards, including the College Outstanding Students Fellowship, Innovation Project of Jiangsu Province Postgraduate Training Fellowship, and Outstanding Graduate Student of Nanjing University Award. During her doctoral studies, Chen investigated how non-small cell lung cancer (NSCLC) can develop resistance to a class of anti-cancer drugs, known as tyrosine kinase inhibitors (TKIs).
As a NOMIS Fellow, Chen will direct her expertise in cancer research toward understanding the anti-tumor immune response to one of the deadliest forms of cancer: glioblastoma. Glioblastoma affects cells in the brain and nervous system, which makes it extremely difficult to treat with typical approaches such as chemotherapy. Using an animal model, she found that a treatment known as an anti-CTLA-4 checkpoint inhibitor monotherapy—which activates the host’s immune cells to attack cancer cells—extended the lifetimes of glioblastoma bearing mice. Further experiments showed that the effectiveness of this treatment was dependent on the presence of a type of immune cells called CD4+ T-cells, which are supported, in turn, by other immune cells called microglia. She has made multiple discoveries indicating that microglia have the potential to activate CD4+ T cells in glioblastoma to maintain their anti-tumor function, but they often lose this function during tumor progression. Currently, Chen is investigating the mechanisms and strategies to reprogram and rejuvenate microglias’ anti-tumor activity, with the ultimate goal of developing an effective combination therapy to treat this often fatal disease.
Fun fact: Chen likes yoga and Totoro.
Lidia Jiménez, a Salk postdoctoral fellow, was born in Spain, and obtained a BS in Pharmaceutical Sciences in 2010 and a MSc in Regenerative Biomedicine in 2012 from the University of Granada in Spain. She obtained a PhD in Molecular Biosciences from the Autonomous University of Madrid in 2016 before joining the Salk Institute in 2017. She received multiple awards during her research including a doctoral research fellowship from the Carlos III Health Institute and a postdoctoral fellowship from the Martin Escudero Foundation. During her PhD, she focused on the role of macrophages, which are important sentinel cells of the immune system, in maintaining the homeostasis of different tissues, both under normal and pathological conditions, as well as their role in tumors.
As a NOMIS fellow, Jiménez will be studying TAM receptors on macrophages in the thymus and the spleen. Both tissues have a high ratio of cell death due to normal physiological processes occurring within the tissue itself, and TAM receptors are known to play a crucial role in clearing dead cells and controlling immune homeostasis. In the thymus, around 95% of the developing T cells need to be cleared by thymic macrophages, while in the spleen, around two million senescent (deteriorating) red blood cells are cleared per second. The clearance of dead cells by macrophages is critical to maintain tissue homeostasis, avoid autoimmunity and, in the case of the red blood cells, to recycle their iron content. Jiménez will be deciphering the consequences of macrophage TAM receptor signaling dysregulation in the thymus and the spleen, as well as some of the associated pathological scenarios that could be associated with it, such as autoimmunity and hematological problems.
Fun fact: Jiménez is part of La Jolla Symphony & Chorus. She loves those moments in a concert where she is on stage singing fortissimo in a big choir with a symphonic orchestra.
Andre Mu, a postdoctoral fellow, was born in Australia, and obtained his doctoral degree from the University of Melbourne in interdisciplinary sciences. There, he was awarded a competitive fellowship from the Natural Sciences and Engineering Research Council of Canada to establish an international collaboration with the University of Calgary. Mu conducted his postdoctoral research at the Peter Doherty Institute for Infection and Immunity at the University of Melbourne. Supported by the prestigious Australian Endeavour Research Fellowship, he collaborated with Professor Rob Knight at UC San Diego to investigate how the trillions of microbes in our gut, known as the gut microbiome, interact with drug-resistant bacterial pathogens.
Mu’s NOMIS research project will address why some patients develop severe illness while others seem to have no symptoms of disease despite the pathogens’ ability to infect, replicate and transmit. Using his expertise as a microbial ecologist and computational biologist, he aims to determine the compositional structure of gut microbiomes before and during infectious diseases in order to identify signature microbiome-markers that may predispose a person for acquiring infections. Such markers could help predict someone’s health outcomes after infection and help scientists engineer the gut microbiome toward cooperative host defense mechanisms during infection. Ultimately, Andre hopes to translate these observations from the bench to invent novel therapeutic applications for human diseases.
Fun fact: Mu loves cycling, live music, photography, and has a second-degree black belt in Tae Kwon Do.
Jan Pencik, a Salk postdoctoral fellow, is originally from Brno, Czech Republic—the city where Gregor Mendel, the father of modern genetics, invented his famous “Mendelian laws.” He obtained his master’s degree in biochemistry from the Palacky University, Olomouc, Czech Republic, before being accepted as a doctoral student in the Molecular Signal Transduction Program at the Medical University of Vienna, Austria. There, he joined the Ludwig Boltzmann Institute for Cancer Research, where he completed his PhD dissertation research focusing on development of novel prostate cancer models. His dissertation study has led to the seminal discovery of IL-6/STAT3 signaling as a major pathway that regulates senescence and tumor growth in prostate cancer.
As a NOMIS Fellow, Pencik is focusing on non-small cell lung cancer, the most common type of lung cancer. He is investigating a gene called STK11 (also known as LKB1) that is mutated or deleted in more than a third of patients. Recent work has shown that STK11 alterations are primarily responsible for loss of response to immunotherapy, which is a pivotal form of cancer therapy that is aimed at stimulating a person’s natural anti-tumor immunity. Importantly, Pencik’s work will serve to identify some of the most critical proteins linked to LKB1 that regulate a loss of therapeutic efficacy, providing valuable insights for designing optimal therapeutic strategies tailored toward hard-to-treat non-small cell lung tumors.
Fun fact: Pencik loves singing American country karaoke songs to his young daughter.
Katia Troha, a Salk postdoctoral fellow, received a BA in molecular and cell biology from the University of California, Berkeley and a PhD in immunology and infectious disease from Cornell University. During her PhD, she was awarded a Biological and Biomedical Sciences Fellowship and Diversity Fellowship from Cornell University and as a postdoctoral fellow, she was awarded the Eddie Méndez Scholar Award. Troha’s research approaches the study of infection in way that’s unique from the traditional perspective, which focuses on mechanisms of pathogen killing. Instead, Troha seeks to characterize the cooperative defense system: mechanisms that, independent of pathogen killing, promote health and survival by preventing and/or alleviating physiological damage during infection. During her PhD studies, Troha led projects that identified core components of the cooperative defense system and characterized the contribution of non-immune organs to the defense response against infection.
As a NOMIS fellow at Salk, Troha worked to elucidate the contribution of physiological renal adaptations to the cooperative defense system. Specifically, she focuses on how metabolic adaptations in the kidney can promote health and survival during sepsis. Her research has clinical implications in that it may provide new physiologies to target during infections.
Fun fact: Outside of the lab, Troha enjoys spooky movies and kayaking.
Siva Karthik Varanasi was born in India and received his bachelor’s degree in biotechnology at Osmania University in India in 2009 and a master’s degree in biotechnology at VIT University in India in 2011. Varanasi completed his PhD at the University of Tennessee, Knoxville in 2018. He received numerous awards during his PhD, including the Graduate Student Senate Research Award, Carolyn Fite Award, Yates dissertation Fellowship and Student/Faculty Research Grant for advancements in the field of biology. Varanasi’s dissertation investigated the reasons why virus infections lead to chronic inflammatory lesions and how immune cells and the metabolic state of the host plays a central role determining the outcome of virus infections.
As a NOMIS Fellow, Varanasi evaluated how immune cells called CD8+ T cells metabolically adapt to different tissues especially within liver. He focused on understanding the impacts the microenvironment on CD8+ T cell infiltration and function especially within liver tumors. In liver cancer, despite being infiltrated by T cells, adoptive immunotherapy is usually unsuccessful in controlling tumor progression as is the response to immune-checkpoint blockade. Often liver cancers are presented with elevated levels of bile acids (BAs) that are primarily synthesized within livers. Varanasi evaluated if these BAs contribute to tumor progression by modulating CD8+ T cell function and survival. The results from these studies will uncover novel forms of T cell immunosuppression in tumors and also provide new therapeutic options targeting BA signaling to enhance anti-tumor immune responses in combination with immunotherapy.
Fun fact: Varanasi loves hiking, snorkeling and cooking.
Qiyuan Yang, a Salk postdoctoral fellow, received his PhD in biochemistry and molecular biology in 2017 from Shanghai Institute of Biochemistry and Cell Biology, CAS, China. His doctoral studies focused on NGS technology development and application, especially for small RNA identification and their dynamic and modification in murine early embryonic development. Yang further developed single cell sequencing method as an approach for small RNA profiling of single human oocytes or embryos. Yang identified novel groups of oocyte specific piRNA, providing invaluable insights that expand scientists’ understanding of early stage embryonic development.
As a NOMIS fellow, Yang shifted his research direction to study the function of regulatory T cells, a subset of immune cells that play a pivotal role in tumor progression. He developed the ribosome profiling system for primary CD4+ T cells to reveal differential translated genes and utilized high-throughput CRISPR screening method to characterize underestimated but critical genes in T help cell differentiation and function. Taking advantage of his biochemistry background, he is exploring technologies for low-input or in vivo translatome analysis on T cells in the tumor microenvironment. Using these methods, Yang aims to identify novel genes and pathways that can enhance T cells’ activity and translate these findings for the treatment of cancer.
Fun fact: Yang enjoys surfing and snowboarding in southern California.
Kaisa Happonen, a Salk postdoctoral fellow, was born in Finland, and obtained her master’s degree in biochemistry from the University of Helsinki in 2007. She received her PhD in medical protein chemistry in 2011 at Lund University in Sweden. Her graduate studies focused on investigating how molecules released from the cartilage in rheumatoid arthritis cause inflammation, and how cartilage breakdown itself therefore may be a driving force behind the disease. As a postdoctoral fellow she studied the function of cell surface receptors called TAM receptor tyrosine kinases in endothelial cells, which form the inner lining of blood vessels. She received many research grants and awards, including grants from the Alfred Österlund’s Foundation, the Crafoord Foundation and Greta and Johan Kock’s Foundation, as well as the Young Investigator Award from the International Society of Thrombosis and Haemostasis, the Pioneer Fund Postdoctoral Scholar Award and the Sweden-America Foundation Postdoctoral Fellowship.
As a NOMIS fellow, Happonen continued pursuing her interest in the functions of TAM receptors in blood vessels, with a focus on the highly specialized vessels in the brain. She demonstrated that TAM receptors are crucial for brain endothelial cell movement and proliferation, two key features in the formation of new blood vessels, a process also known as angiogenesis. She is currently investigating how TAMs work in different models of angiogenesis in adult tissues in vivo, and how TAM receptors communicate with other angiogenic receptors in the endothelium. A deeper understanding of how angiogenesis is regulated is essential for the development of targeted therapeutics in diseases such as cancer and stroke.
Fun fact: Happonen likes dancing Cuban salsa so much that she has traveled to Cuba a couple of times just to be able to take dance classes with her favorite teachers.
Zhi Liu, a Salk postdoctoral fellow, was born in China, and received a BS in biology in 2009 from Anhui Normal University in China. He obtained a PhD in cell biology in 2016 from the University of Chinese Academy of Sciences in China. Liu’s doctoral studies focused on the epigenetic regulation, specifically processes that control T cell differentiation and thymic epithelial cell development.
As a NOMIS Fellow, Liu extends his research to understanding regulatory T cells, which serve to suppress immune responses to keep the immune system from attacking healthy cells in the body. The breakdown of regulatory T cell function is a common underlying condition for autoimmune diseases, such as type-1 diabetes, rheumatoid arthritis and multiple sclerosis. By taking advantage of the power of CRISPR technology, Liu is seeking a genetic switch that can turn regulatory T cell’s function on or off. Liu is also investigating how the three-dimensional configuration of the genome is transformed during regulatory T cell differentiation. The novel insights gained from Liu’s work will help researchers to develop potential treatment for autoimmune diseases.
Fun fact: Liu enjoys hiking, playing table tennis with friends and family during his spare time.
Lucie Novotna, a Salk postdoctoral researcher, was born and raised in a small village in central Czech Republic. She obtained her BS in 2008 in biology and clinical biology at the University of South Bohemia, Faculty of Science in Ceske Budejovice. Faculty of Science closely collaborates with the Academy of Science of Czech Republic, where she first discovered her passion for science and new discoveries. She joined the Molecular Biology of Protists laboratory in the first semester of her bachelor’s studies. In 2005 and 2006 she received Student Grant Agency Awards, internal awards for young students. She completed her master’s degree in 2010 from University of South Bohemia, Faculty of Science in Ceske Budejovice. She did her doctoral studies at University of California Riverside, focusing on Trypanosoma brucei, the causative agent of sleeping sickness.
As a NOMIS fellow, Novotna used multi-disciplinary approaches to elucidate structure-functional relations and the molecular underpinnings of T cell signaling mechanisms to identify novel targets for immunotherapies for cancer. In particular, she investigated immune checkpoint called programmed cell death protein 1 (PD1) and its interaction with a protein called SHP2. By combining in vivo and in vitro studies, she uncovered details into how SHP2’s enzymatic activity is regulated. This deeper understanding of protein-protein communication will help researchers uncover new possibilities to find better targets or improve current immunotherapies.
Fun fact: Novotna is an adrenaline enthusiast who loves mountain biking and rock climbing.
Sheila Rao received her PhD in immunology in 2013 from the University of Pennsylvania in Philadelphia. There, she worked on innate immune cell receptor signaling to identify the mechanisms by which the immune system recognizes foreign microbes.
As a NOMIS Fellow, she investigated host-microbe interactions in the context of gastrointestinal infection, using the bacterium Salmonella as a model. Sheila discovered that Salmonella, a microbe that causes disease, has actually evolved a strategy to promote host health during infection. Salmonella does this by manipulating signaling from the gut to the brain, which results in a decreased host anorexic (lack of appetite) response and improved host metabolic function. By inhibiting host anorexia, Salmonella improves the health of the host, which results in increased fitness of the microbe. Thus, by promoting host health, Salmonella ensures its own survival. This work helps to clarify the role of sickness-induced behaviors (like anorexia) and demonstrates that microbes have evolved strategies to maintain or even improve health of their hosts. Investigating how we have co-evolved with microbes will enable us to learn more about our own physiology and to better understand how to promote health during disease as a therapeutic strategy. Rao, Ayres and colleagues published this work in the journal Cell in 2017.
Fun fact: Rao loves to trail-run in the mountains, and participates (and sometimes wins!) ultramarathon races of 50 miles or 100 miles.
