Helgi Kuzmychova

ORCID: 0009-0005-5260-349X
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About
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Research Areas
  • Cancer, Hypoxia, and Metabolism
  • Glioma Diagnosis and Treatment
  • Autophagy in Disease and Therapy
  • ATP Synthase and ATPases Research
  • RNA Interference and Gene Delivery
  • Cancer, Lipids, and Metabolism
  • Epigenetics and DNA Methylation
  • Nanoplatforms for cancer theranostics
  • Mitochondrial Function and Pathology
  • Diet and metabolism studies
  • Histone Deacetylase Inhibitors Research
  • Nanoparticle-Based Drug Delivery

University of Manitoba
2023-2025

Abstract Despite tremendous research efforts, successful targeting of aberrant tumor metabolism in clinical practice has remained elusive. Tumor heterogeneity and plasticity may play a role the failure metabolism-targeting interventions for treating cancer patients. Moreover, compensatory growth-related processes adaptive responses exhibited by heterogeneous subpopulations to metabolic inhibitors are poorly understood. Here, using clinically-relevant patient-derived glioblastoma (GBM) cell...

10.1186/s40478-023-01604-y article EN cc-by Acta Neuropathologica Communications 2023-07-07

Abstract Background The mitochondrial pyruvate carrier (MPC), a central metabolic conduit linking glycolysis and metabolism, is instrumental in energy production. However, the role of MPC cancer controversial. In particular, importance glioblastoma (GBM) disease progression following standard temozolomide (TMZ) radiation therapy (RT) remains unexplored. Methods Leveraging vitro vivo patient-derived models TMZ-RT treatment GBM, we characterize temporal dynamics abundance downstream...

10.1093/neuonc/noaf008 article EN cc-by-nc Neuro-Oncology 2025-01-11

Abstract Group 3 medulloblastoma (G3 MB) carries the worst prognosis of all MB subgroups. MYC oncoprotein is elevated in G3 tumors; however, mechanisms that support abundance remain unclear. Using metabolic and mechanistic profiling, we pinpoint a role for mitochondrial metabolism regulating MYC. Complex-I inhibition decreases MB, attenuates expression MYC-downstream targets, induces differentiation, prolongs male animal survival. Mechanistically, complex-I increases inactivating acetylation...

10.1038/s41467-023-38049-9 article EN cc-by Nature Communications 2023-05-02

Abstract Therapy resistance and tumor recurrence are barriers to achieving long-term survival in cancer patients, particularly evident glioblastoma (GBM), known for its dismal 5-year rate below 10%. Despite aggressive treatment regimens, including maximal resection, alkylating chemotherapy, radiation, the majority of GBM patients experience relapse within 7-9 months post-initial intervention. Recurrent poses surgical challenges resists subsequent treatments, leading an almost universally...

10.1093/neuonc/noae165.1162 article EN Neuro-Oncology 2024-11-01

Abstract BACKGROUND Despite tremendous research efforts, the successful targeting of aberrant tumor metabolism in clinical practice has remained elusive. Tumor heterogeneity and metabolic plasticity may play a role failure metabolism-targeting interventions for treating cancer patients. Moreover, compensatory growth-related processes adaptive responses exhibited by heterogeneous subpopulations to inhibitors are poorly understood. Hence, deeper understanding cellular adaptations response is...

10.1093/neuonc/noad137.101 article EN Neuro-Oncology 2023-09-01

Abstract BACKGROUND Glioblastoma (GBM) is the most common malignant brain tumour in adults. The current standard of care for GBM patients consists maximal surgical resection followed by chemotherapy and radiation. Despite such an aggressive treatment approach, average 5-year survival rate approximately 5%. One main reasons poor therapy response resistance to programmed cell death, otherwise known as apoptosis. mechanisms behind apoptosis relies on upregulation inhibitor proteins (IAPs) which...

10.1093/neuonc/noad137.220 article EN Neuro-Oncology 2023-09-01

Abstract BACKGROUND Brain tumors are the leading cause of cancer death in children, and medulloblastoma (MB) is one most common pediatric central nervous system malignancies. Amplification c-MYC oncogene frequently observed aggressive lethal subgroup this disease, group 3 (G3), but not other subgroups. Patients that have G3 MB with high abundance more likely to present as metastatic prone develop fatal recurrent tumors. Unfortunately, functional ubiquity disordered structure makes it...

10.1093/neuonc/noad137.003 article EN Neuro-Oncology 2023-09-01
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