Pamela Lockyer
Researcher
Also affiliated: University of North Carolina at Chapel Hill (2007–2021); NewYork–Presbyterian Hospital (2017); The University of Texas MD Anderson Cancer Center (2019–2024); North Carolina State University (2010); University of Freiburg (2010–2012); Baylor College of Medicine (2015–2017); Presbyterian Hospital (2017); Xenobe Research Institute (2014); Anna Needs Neuroblastoma Answers (2010); University of Education Freiburg (2010); Cardiovascular Research Center (2008); Mayo Clinic in Florida (2012); Hesco (United States) (2012); UNC Lineberger Comprehensive Cancer Center (2010); Indiana University School of Medicine (2020–2021)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Pamela Lockyer's research focuses on the molecular mechanisms underlying hematologic malignancies, particularly myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML). Her work investigates how alterations in stem cell architecture and signaling pathways contribute to disease progression and treatment response. Lockyer has published research on the role of specific genes and pathways, such as EIF2AK1, SF3B1, KDM6B, and TET2, in the pathogenesis of these conditions. Her studies have explored strategies to rescue red blood cell production in MDS and overcome metabolic reprogramming in multiple myeloma.
Her publications also address the transcriptomic signatures associated with treatment failure in MDS and CMML, suggesting potential biomarkers for predicting response to hypomethylating agents. Lockyer's group has examined hematopoiesis under telomere attrition at the single-cell level. She is a Co-PI on a grant from the NIH/National Cancer Institute for the drug development of Skp2 PROTACs in cancer.
Metrics
- h-index: 19
- Publications: 80
- Citations: 1,441
Selected Publications
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Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia (2025)
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Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia (2025)
Federal Grants 1 $1 total
Collaboration Network
Top Collaborators
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia
- Epigenetic Dysregulation and Therapeutic Targeting of RET Receptor Tyrosine Kinase in High-Risk KMT2A-Rearranged Pediatric Acute Myeloid Leukemia
- Epigenetic dysregulation and therapeutic targeting of <scp>RET</scp> receptor tyrosine kinase in high‐risk <scp> <i>KMT2A</i> </scp> ‐rearranged acute myeloid leukaemia
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