A5002774365- Acute Myeloid Leukemia Research
- Immune cells in cancer
- interferon and immune responses
- Cancer, Lipids, and Metabolism
- Immune Cell Function and Interaction
- Peroxisome Proliferator-Activated Receptors
- Cancer, Hypoxia, and Metabolism
- Phagocytosis and Immune Regulation
- Chemokine receptors and signaling
- Hematopoietic Stem Cell Transplantation
- Chronic Lymphocytic Leukemia Research
- Acute Lymphoblastic Leukemia research
- Ubiquitin and proteasome pathways
- Liver Disease Diagnosis and Treatment
- Multiple Myeloma Research and Treatments
- Cytokine Signaling Pathways and Interactions
- Immunodeficiency and Autoimmune Disorders
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Neutropenia and Cancer Infections
- Blood disorders and treatments
- Metabolism and Genetic Disorders
- Cell death mechanisms and regulation
- Metabolomics and Mass Spectrometry Studies
University of East Anglia
2023-2024
Norwich Research Park
2023-2024
Mitochondrial damage-associated molecular patterns (mtDAMPs) include proteins, lipids, metabolites and DNA have various context specific immunoregulatory functions. Cell-free mitochondrial (mtDNA) is recognised via pattern recognition receptors a potent activator of the innate immune system. mtDNA elevated in circulation trauma cancer patients, however functional consequences are largely undefined. Multiple myeloma (MM) relies upon cellular interactions within bone marrow (BM)...
Background: The BH3 mimetic Venetoclax, in combination with low dose cytarabine, decitabine or azacitidine, has shown clinical efficacy newly diagnosed acute myeloid leukemia (AML) patients over 75 those ineligible for intensive induction chemotherapy. This been a significant advance, particularly the treatment of older AML who historically have difficult to treat. Venetoclax selectively inhibits BCL-2 protein which is overexpressed order reactivate intrinsic apoptosis. However, this regime...
Background: Acute myeloid leukaemia (AML) initiation, expansion and treatment resistance is regulated by interactions with the bone marrow (BM) microenvironment. Previous research our group has shown that AML activates macrophage phagocytosis via activation of stimulator interferon genes (STING) pathway. This in contrast to solid tumours where immunosuppressive signals are released infiltrating macrophages enhances tumour progression. Phagocytosis blasts can be mitigated interaction CD47, on...
Background: Acute myeloid leukemia (AML) is a highly proliferative disease, which requires high metabolic turnover to allow for constant expansion. We and others have previously shown that primary human AML blasts rely on fatty acid (FA)-oxidation survival proliferation. More recently, FA metabolism has been be upregulated in confers resistance treatments such as venetoclax with azacytidine. The liver key role lipid can receive dietary FA, free acids (FFA) from adipose tissue, are oxidised,...
Topic: 13. Myeloma and other monoclonal gammopathies - Biology & Translational Research Background: Fatty acid metabolism in cancer is altered to promote growth survival of cells. Multiple (MM) cells acquire free fatty acids (FFA) fuel ATP production by a process known as (FA) oxidation (1). Under normal circumstances, the liver processes large quantities FFA daily stores only small amounts triglycerides. This because when FFAs are taken up from plasma, they processed re-esterification...