Eric Padron
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View article: Post-transplant MRD Monitoring by TP53 Duplex Sequencing with APR-246 + Azacitidine Maintenance Predicts Outcomes
Post-transplant MRD Monitoring by TP53 Duplex Sequencing with APR-246 + Azacitidine Maintenance Predicts Outcomes Open
Outcomes are poor for TP53 mutant myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) patients who undergo allo-HSCT. Notably, minimal data exist on the impact of TP53 MRD monitoring post allo-HSCT. Thus, we completed duplex TP…
View article: Early real-world experience with revumenib outside of a clinical trial setting: A single center retrospective review of efficacy and tolerability
Early real-world experience with revumenib outside of a clinical trial setting: A single center retrospective review of efficacy and tolerability Open
Background: Revumenib was approved by the US Food and Drug Administration on 11/15/2024 as the first menin inhibitor for treatment of relapsed/refractory (R/R) acute leukemias with a KMT2A-translocation (KMT2Ar) based on data from the AUGM…
View article: NOXA modulates tipifarnib sensitivity in myeloid leukemia cells.
NOXA modulates tipifarnib sensitivity in myeloid leukemia cells. Open
Tipifarnib is a potent small-molecule farnesyltransferase inhibitor (FTI) that has demonstrated single-agent activity in acute myeloid leukemia (AML). Although not all patients responded to tipifarnib, those who did sustained durable, clin…
View article: Machine learning using bayesian networks to predict response in patients with newly diagnosed Acute Myeloid Leukemia
Machine learning using bayesian networks to predict response in patients with newly diagnosed Acute Myeloid Leukemia Open
Background: Acute myeloid leukemia (AML) is a hematopoietic stem cell malignancy characterized by clonal proliferation and reduced differentiation of myeloid progenitor cells. The complex interactions among clinical, cytogenetic, and molec…
View article: Impact of clonal hematopoiesis on hematologic recovery and outcomes following tumor-infiltrating lymphocyte therapy
Impact of clonal hematopoiesis on hematologic recovery and outcomes following tumor-infiltrating lymphocyte therapy Open
Introduction: Clonal hematopoiesis of indeterminate potential (CHIP) has emerged as a biomarker of adverse outcomes across oncology and immunology, including inferior overall survival (OS) and increased risks of cardiovascular events, dise…
View article: Refined elderly comorbidity index is highly predictive of post-transplant survival in older adults with Acute Myeloid Leukemia and myelodysplastic syndrome
Refined elderly comorbidity index is highly predictive of post-transplant survival in older adults with Acute Myeloid Leukemia and myelodysplastic syndrome Open
Background: Allogeneic hematopoietic cell transplantation (HCT) is the only curative option for most adults with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). Although older age increases the risk of non-relapse mortalit…
View article: Long‐term follow‐up and combined Phase 2 results of eprenetapopt and azacitidine in patients with <i>TP53</i> mutant MDS/AML
Long‐term follow‐up and combined Phase 2 results of eprenetapopt and azacitidine in patients with <i>TP53</i> mutant MDS/AML Open
TP53 gene mutations (m TP53 ) represent a distinct molecular cohort with poor outcomes. Eprenetapopt (APR‐246) is a novel, first‐in‐class small molecule that reactivates p53 and targets cellular redox balance, ultimately inducing apoptosis…
View article: Reducing clinical trial eligibility barriers for patients with MDS: an icMDS position statement
Reducing clinical trial eligibility barriers for patients with MDS: an icMDS position statement Open
Excessively restrictive inclusion and exclusion criteria in clinical trials are one of many barriers to clinical trial enrollment for patients with myelodysplastic syndromes/neoplasms (MDSs). Many organizations are developing efforts to in…
View article: Role of allo-HCT in “nonclassical” MPNs and MDS/MPNs: recommendations from the PH&G Committee and the CMWP of the EBMT
Role of allo-HCT in “nonclassical” MPNs and MDS/MPNs: recommendations from the PH&G Committee and the CMWP of the EBMT Open
“Nonclassical” myeloproliferative neoplasms (MPNs) and myelodysplastic/myeloproliferative neoplasms (MDS/MPNs) represent a heterogeneous group of malignancies characterized by a wide range of clinical manifestations. Unlike classical MPNs,…
View article: Haploinsufficiency of miR-143 and miR-145 reveal targetable dependencies in resistant del(5q) myelodysplastic neoplasm
Haploinsufficiency of miR-143 and miR-145 reveal targetable dependencies in resistant del(5q) myelodysplastic neoplasm Open
Myelodysplastic neoplasms (MDS) are stem cell disorders characterized by ineffective hematopoiesis and risk of transformation to acute myeloid leukemia (AML). Chromosomal alterations are frequent in MDS, with interstitial deletion of chrom…
View article: Response to luspatercept can be predicted and improves overall survival in the real‐life treatment of LR‐MDS
Response to luspatercept can be predicted and improves overall survival in the real‐life treatment of LR‐MDS Open
We explored the impact of luspatercept therapy on overall survival (OS) and possible predictors of response in low‐risk (LR) myelodysplastic syndrome (MDS) patients. We evaluated 331 anemic patients treated with luspatercept. Hematological…
View article: Figure S5 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Figure S5 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Contains data showing Malat1 depletion has no effect on myelopoiesis or self-renewal
View article: Figure S1 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Figure S1 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Contains data related to Figure 1 but which were not included in the main figure
View article: Table S1 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Table S1 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
gRNAs for generation of MALAT1 knockout THP-1 cells (related to Fig S7)
View article: Figure S3 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Figure S3 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Contains data related to Figure 3 but which were not included in the main figure
View article: Table S4 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Table S4 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Taqman assays for murine cytokine gene expression (related to Fig S6)
View article: Table S6 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Table S6 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
guide RNA for T7 knockdown of TET2 (related to Fig 1, Fig S1)
View article: Table S3 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Table S3 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
qRT-PCR primer sequences (related to Fig 1, Fig S3, Fig S7)
View article: Figure S6 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Figure S6 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Contains data related to Figure 5 but which were not included in the main figure
View article: Table S2 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Table S2 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
qRT-PCR primers for confirming MALAT1 knockout across transcript. (Related to Fig S7)
View article: Figure S7 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Figure S7 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Contains data related to Figure 6 but which were not included in the main figure
View article: Figure S2 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Figure S2 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Contains data related to Figure 2 but which were not included in the main figure
View article: Table S5 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Table S5 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
primer sequences for EGR1 Chromatin Immunoprecipitation (ChIP) (related to Fig S2)
View article: Data from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Data from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
TET2 mutations (mTET2) are common genetic events in myeloid malignancies and clonal hematopoiesis. These mutations arise in the founding clone and are implicated in many clinical sequelae associated with oncogenic feedforward inflammatory …
View article: Figure S4 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis
Figure S4 from RNA Shielding of p65 Is Required to Potentiate Oncogenic Inflammation in <i>TET2</i>-Mutated Clonal Hematopoiesis Open
Contains data related to Figure 4 but which was not included in the main figure