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Biography and Research Information
OverviewAI-generated summary
Pamela Lockyer's research focuses on understanding the molecular mechanisms underlying hematologic malignancies, particularly myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML).
Her work investigates how cellular processes, such as stem cell architecture and gene expression, contribute to disease progression and treatment response. Lockyer has published research on the role of specific signaling pathways, including EIF2AK1, in rescuing red blood cell production in MDS with ringed sideroblasts, and the cooperation between KDM6B overexpression and TET2 deficiency in CMML pathogenesis. Her group also explores the impact of telomere attrition on hematopoiesis at the single-cell level and investigates strategies to overcome metabolic reprogramming in cancers, such as multiple myeloma, through targeting pathways like DNA2.
Lockyer's research group has also examined transcriptomic signatures associated with treatment failure in MDS and CMML patients treated with hypomethylating agents, and investigated the downregulation of UBA1 expression in myelodysplastic neoplasms. She is a Co-PI on an NIH/National Cancer Institute grant focused on the drug development of Skp2 PROTACs in cancer. Lockyer's scholarship metrics include an h-index of 19, 81 total publications, and 1,403 total citations.
Metrics
- h-index: 19
- Publications: 81
- Citations: 1,418
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
NIH/National Cancer Institute
Co-PI
May 2023 - Jul 2023
Collaboration Network
Top Collaborators
Irene Gañán‐Gómez
The University of Texas MD Anderson Cancer Center (US)
22 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting DNA2 overcomes metabolic reprogramming in multiple myeloma
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
Showing 5 of 22 shared publications
Natthakan Thongon
The University of Texas MD Anderson Cancer Center (US)
18 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting DNA2 overcomes metabolic reprogramming in multiple myeloma
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
Showing 5 of 18 shared publications
Feiyang Ma
Michigan Medicine (US)
18 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting DNA2 overcomes metabolic reprogramming in multiple myeloma
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
Showing 5 of 18 shared publications
Guillermo Garcia‐Manero
The University of Texas MD Anderson Cancer Center (US)
18 shared publications
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting DNA2 overcomes metabolic reprogramming in multiple myeloma
- Transcriptomic Signatures of Hypomethylating Agent Failure in Myelodysplastic Syndromes and Chronic Myelomonocytic Leukemia
- Downregulation of UBA1 expression in myelodysplastic neoplasm
Showing 5 of 18 shared publications
Rashmi Kanagal‐Shamanna
The University of Texas MD Anderson Cancer Center (US)
17 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Transcriptomic Signatures of Hypomethylating Agent Failure in Myelodysplastic Syndromes and Chronic Myelomonocytic Leukemia
- Downregulation of UBA1 expression in myelodysplastic neoplasm
Showing 5 of 17 shared publications
Guillermo Montalban‐Bravo
The University of Texas MD Anderson Cancer Center (US)
17 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Transcriptomic Signatures of Hypomethylating Agent Failure in Myelodysplastic Syndromes and Chronic Myelomonocytic Leukemia
Showing 5 of 17 shared publications
Vera Ademà
The University of Texas MD Anderson Cancer Center (US)
17 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting DNA2 overcomes metabolic reprogramming in multiple myeloma
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
Showing 5 of 17 shared publications
Hui Yang
The University of Texas MD Anderson Cancer Center (US)
13 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Transcriptomic Signatures of Hypomethylating Agent Failure in Myelodysplastic Syndromes and Chronic Myelomonocytic Leukemia
- Downregulation of UBA1 expression in myelodysplastic neoplasm
- Cooperation between KDM6B overexpression and TET2 deficiency in the pathogenesis of chronic myelomonocytic leukemia
Showing 5 of 13 shared publications
Caleb A. Class
Butler University (US)
11 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting DNA2 overcomes metabolic reprogramming in multiple myeloma
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Transcriptomic Signatures of Hypomethylating Agent Failure in Myelodysplastic Syndromes and Chronic Myelomonocytic Leukemia
Showing 5 of 11 shared publications
Matteo Pellegrini
11 shared publications
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in SF3B1 Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- P-106: Targeting DNA2 overcomes myeloma cells’ metabolic reprogramming in response to DNA damage
- Targeting DNA2 Overcomes Myeloma Cells' Metabolic Reprogramming in Response to DNA Damage
Showing 5 of 11 shared publications
Carlos E. Bueso‐Ramos
10 shared publications
- Hematopoiesis under telomere attrition at the single-cell resolution
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in SF3B1 Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting DNA2 Overcomes Metabolic Reprogramming in Multiple Myeloma
- Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
Showing 5 of 10 shared publications
Feng Wang
10 shared publications
- Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Author Correction: Stem cell architecture drives myelodysplastic syndrome progression and predicts response to venetoclax-based therapy
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in SF3B1 Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
Showing 5 of 10 shared publications
Scott A. Peslak
8 shared publications
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in SF3B1 Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Supplementary Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Supplementary Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
Showing 5 of 8 shared publications
Pamela Acha
8 shared publications
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in SF3B1 Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Supplementary Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Supplementary Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
Showing 5 of 8 shared publications
Françesc Solé
8 shared publications
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i> -Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in SF3B1 Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Supplementary Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
- Supplementary Data from Targeting the EIF2AK1 Signaling Pathway Rescues Red Blood Cell Production in <i>SF3B1</i>-Mutant Myelodysplastic Syndromes With Ringed Sideroblasts
Showing 5 of 8 shared publications
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