Dr. Jamieson is a board-certified hematologist with broad clinical expertise in caring for patients with hematologic malignancies. As hematology team leader for the Division of Hematology/Oncology at UC San Diego Health Moores Cancer Center, Dr. Jamieson’s clinical interests include the treatment of myeloproliferative neoplasms including chronic myeloid leukemia (CML), polycythemia vera (PV), myelofibrosis and essential thrombocythemia. She is also the principal investigator on several clinical trials for the treatment of these and related bone marrow disorders.
As a physician-scientist, Dr. Jamieson completed her residency and clinical fellowships in bone marrow transplantation and hematology, as well as a postdoctoral research fellowship in the laboratory of Professor Irving Weissman at Stanford. Together with collaborators, she discovered in 2004 that chronic phase CML is initiated by blood-forming stem cells through expression of the BCR-ABL gene, but that a patient’s transition to the blast crisis stage of CML is driven by myeloid progenitors that have been reprogrammed to behave like leukemia stem cells (LSC) through aberrant activation of the gene beta-catenin (Jamieson et al., The New England Journal of Medicine 2004). In her own laboratory first at Moores Cancer Center, and now also at the Sanford Consortium for Regenerative Medicine, she has expanded this research to include analysis of the events involved in the initiation and progression of a variety of blood cancers.
As a principal investigator on several research grants funded by the California Institute for Regenerative Medicine (CIRM), Dr. Jamieson has a deep interest in understanding the mechanisms fueling the development, progression and therapeutic resistance of hematologic malignancies. Her translational research efforts have led to discovery of small molecule therapeutic inhibitors that are now being tested in two Phase 1 clinical trials for two different blood cancers. A successful, recently completed Phase l clinical trial showed promising results for myelofibrosis. The continued aims of her research group focus on developing novel therapeutic strategies for hematological malignancies that will improve the quality of life of people with these disorders, with the goal of developing curative therapies that will obviate therapeutic resistance and disease relapse.
Areas of Expertise (6)
Bone Marrow Transplantation
Chronic Myeloid Leukemia
Myelofibrosis and Essential Thrombocythemia
Stanford University: Fellowship, School of Medicine
University of British Columbia: M.D.
University of British Columbia: Residency
Media Appearances (5)
Daily Business Report-Aug. 28, 2018
San Diego Metropolitan online
Cirmtuzumab is a novel monoclonal antibody developed at UC San Diego, with support from the California Institute for Regenerative Medicine (CIRM) and the CIRM-funded Alpha Clinic at UC San Diego. It targets ROR1, a cell surface protein that is present on tumors, but not in normal adult tissues, making it “a vital opportunity for targeting cancer stem cells,” said Catriona Jamieson, Alpha Clinic director who also directs stem cell research at UC San Diego Moores Cancer Center.
Celgene to buy San Diego cancer-drug maker Impact for $1.1B
The San Diego Union-Tribune
Hood and Dr. Catriona Jamieson, a UC San Diego oncologist/researcher, have looked ever since for a way to bring back fedratinib, which led to the launch of Impact Biomedicines.
San Diego’s biggest biotech deal was in 2013 when Life Technologies agreed to be purchased for $13.6 billion by scientific instrumentation company Thermo Fisher, bringing to an end the independent existence of San Diego County's most highly valued biotech company.
San Diego stem cell scientists awarded $8.7M to research cancer, other diseases
The San Diego Union-Tribune online
The two biggest local grants went to Dan Kaufman, M.D., and Catriona Jamieson, M.D., of UC San Diego, both for ways to treat acute myelogenous leukemia (AML).
Kaufman was awarded $5.15 million to make “natural killer” immune cells from embryonic stem cells, for use in helping patients who aren’t responding to treatment.
Jamieson received $2.7 million to target cancer stem cells in AML. Cancer stem cells share many characteristics with normal stem cells, and are the hardest to eradicate of all malignant cells.
Cancer drug fedratinib attracts $90 million for Impact Biomedicines
The San Diego Union-Tribune online
Hood and Dr. Catriona Jamieson, a UC San Diego oncologist/researcher, have looked ever since for a way to bring back fedratinib. Efforts began almost immediately, but negotiating rights to the drug from Sanofi and getting the needed funding took time.
Jamieson said fedratinib produced durable remissions in some patients that no other drug could replicate. A number relapsed and died after the drug was no longer available, said Jamieson, the company’s interim chief medical officer.
Startup Impact Biomedicines Raises $22M to Bring Fedratinib to Myelofibrosis Patients
Dr. Catriona Jamieson serves as Interim Chief Medical Officer of Impact Biomedicines, and co-founder. Concurrently, Dr. Jamieson is a Professor of Medicine and Chief of Regenerative Medicine, Deputy Director of the Sanford Stem Cell Clinical Center, Co-leader of the Hematologic Malignancies Program, and Director of Stem Cell Research at the Moores UC San Diego Cancer Center. She specializes in myeloproliferative neoplasms and leukemia, and was the principal investigator on several fedratinib trials. Dr. Jamieson obtained an M.D., a Ph.D. in microbiology and a B.S. in Genetics from the University of British Columbia prior to completing fellowships in hematology and bone marrow transplantation at Stanford University and being recruited to UC San Diego.
Christopher DeBoever, Emanuela M Ghia, Peter J Shepard, Laura Rassenti, Christian L Barrett, Kristen Jepsen, Catriona HM Jamieson, Dennis Carson, Thomas J Kipps, Kelly A Frazer
Mutations in the splicing factor SF3B1 are found in several cancer types and have been associated with various splicing defects. Using transcriptome sequencing data from chronic lymphocytic leukemia, breast cancer and uveal melanoma tumor samples, we show that hundreds of cryptic 3’ splice sites (3’SSs) are used in cancers with SF3B1 mutations. We define the necessary sequence context for the observed cryptic 3’ SSs and propose that cryptic 3’SS selection is a result of SF3B1 mutations causing a shift in the sterically protected region downstream of the branch point.
Jamieson, et al.
Leukemia stem cells (LSCs) play a pivotal role in the resistance of chronic myeloid leukemia (CML) to tyrosine kinase inhibitors (TKIs) and its progression to blast crisis (BC), in part, through the alternative splicing of self-renewal and survival genes. To elucidate splice-isoform regulators of human BC LSC maintenance, we performed whole-transcriptome RNA sequencing, splice-isoform-specific quantitative RT-PCR (qRT-PCR), nanoproteomics, stromal coculture, and BC LSC xenotransplantation analyses.
Marc R Mansour, Takaomi Sanda, Lee N Lawton, Xiaoyu Li, Taras Kreslavsky, Carl D Novina, Marjorie Brand, Alejandro Gutierrez, Michelle A Kelliher, Catriona HM Jamieson, Harald von Boehmer, Richard A Young, A Thomas Look
The oncogenic transcription factor TAL1/SCL is aberrantly expressed in 60% of cases of human T cell acute lymphoblastic leukemia (T-ALL) and initiates T-ALL in mouse models. By performing global microRNA (miRNA) expression profiling after depletion of TAL1, together with genome-wide analysis of TAL1 occupancy by chromatin immunoprecipitation coupled to massively parallel DNA sequencing, we identified the miRNA genes directly controlled by TAL1 and its regulatory partners HEB, E2A, LMO1/2, GATA3, and RUNX1. The most dynamically regulated miRNA was miR-223, which is bound at its promoter and up-regulated by the TAL1 complex. miR-223 expression mirrors TAL1 levels during thymic development, with high expression in early thymocytes and marked down-regulation after the double-negative-2 stage of maturation.
Takaomi Sanda, Lee N Lawton, M Inmaculada Barrasa, Zi Peng Fan, Holger Kohlhammer, Alejandro Gutierrez, Wenxue Ma, Jessica Tatarek, Yebin Ahn, Michelle A Kelliher, Catriona HM Jamieson, Louis M Staudt, Richard A Young, A Thomas Look
The oncogenic transcription factor TAL1/SCL is aberrantly expressed in over 40% of cases of human T cell acute lymphoblastic leukemia (T-ALL), emphasizing its importance in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, LMO1/2, GATA3, and RUNX1. We show that TAL1 forms a positive interconnected autoregulatory loop with GATA3 and RUNX1 and that the TAL1 complex directly activates the MYB oncogene, forming a positive feed-forward regulatory loop that reinforces and stabilizes the TAL1-regulated oncogenic program.
Animesh Pardanani, Jason R. Gotlib, Catriona Jamieson, Jorge E. Cortes, Moshe Talpaz, Richard M. Stone, Michael H. Silverman, D. Gary Gilliland, Jolene Shorr, and Ayalew Tefferi
Fifty-nine patients were treated, including 28 in the dose-escalation phase. The maximum-tolerated dose was 680 mg/d, and dose-limiting toxicity was a reversible and asymptomatic increase in the serum amylase level. Forty-three patients (73%) continued treatment beyond six cycles; the median cumulative exposure to TG101348 was 380 days. Adverse events included nausea, vomiting, diarrhea, anemia, and thrombocytopenia; corresponding grades 3 to 4 incidence rates were 3%, 3%, 10%, 35%, and 24%. TG101348 treatment had modest effect on serum cytokine levels, but greater than half of the patients with early satiety, night sweats, fatigue, pruritus, and cough achieved rapid and durable improvement in these symptoms.