Lorenzo Brunetti
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View article: Correction: Real-world multicenter analysis of CPX-351 efficacy in patients aged less than 60 years with secondary acute myeloid leukemia
Correction: Real-world multicenter analysis of CPX-351 efficacy in patients aged less than 60 years with secondary acute myeloid leukemia Open
View article: Real-world multicenter analysis of CPX-351 efficacy in patients aged less than 60 years with secondary acute myeloid leukemia
Real-world multicenter analysis of CPX-351 efficacy in patients aged less than 60 years with secondary acute myeloid leukemia Open
View article: Real World Study on the Best <scp>CPX</scp> ‐351 Treatment Duration and Timing for Allogeneic Stem Cell Transplantation
Real World Study on the Best <span>CPX</span> ‐351 Treatment Duration and Timing for Allogeneic Stem Cell Transplantation Open
In the registration clinical trial 301 (NCT01696084), CPX‐351 has shown to be superior to conventional 3 + 7 in secondary AML (s‐AML). However, the optimal duration of treatment, the best timing for allogeneic stem cell transplantation (al…
View article: Nuclear Phase Separation Drives NPM1-mutant Acute Myeloid Leukemia
Nuclear Phase Separation Drives NPM1-mutant Acute Myeloid Leukemia Open
During cancer development, mutations promote gene expression changes that cause transformation. Leukemia is frequently associated with aberrant HOXA expression driven by translocations in nucleoporin genes or KMT2A, and mutations in NPM1. …
View article: Mutant NPM1 marginally impacts ribosome footprint in acute myeloid leukemia cells
Mutant NPM1 marginally impacts ribosome footprint in acute myeloid leukemia cells Open
Background NPM1 ‐mutated acute myeloid leukemia (AML) is the most frequent AML subtype. As wild‐type NPM1 is known to orchestrate ribosome biogenesis, it has been hypothesized that altered translation may contribute to leukemogenesis and l…
View article: Breast Cancer With Release of Tumor Cells in Peripheral Blood Mimicking Acute Myeloid Leukemia
Breast Cancer With Release of Tumor Cells in Peripheral Blood Mimicking Acute Myeloid Leukemia Open
A 75-year-old woman with a history of lobular breast adenocarcinoma treated with mastectomy and radiotherapy in 2021 and on maintenance hormone therapy, presented with asthenia and tremors. Laboratory tests showed leucocytosis, anemia and …
View article: An atypical GABARAP binding module drives the pro-autophagic potential of the AML-associated NPM1c variant
An atypical GABARAP binding module drives the pro-autophagic potential of the AML-associated NPM1c variant Open
View article: PB1762: A NEW MONOCLONAL ANTIBODY PROVIDES INSIGHTS ON NPM1 MUTANT SUBCELLULAR EXPRESSION, INTRACLONAL CELL DIFFERENTIATION AND MRD IN NPM1-MUTATED AML
PB1762: A NEW MONOCLONAL ANTIBODY PROVIDES INSIGHTS ON NPM1 MUTANT SUBCELLULAR EXPRESSION, INTRACLONAL CELL DIFFERENTIATION AND MRD IN NPM1-MUTATED AML Open
Topic: 3. Acute myeloid leukemia - Biology & Translational Research Background:NPM1-mutated AML is a distinct WHO and ICC entity characterized by unique clinical and molecular features, including the aberrant cytoplasmic dislocation of the…
View article: <scp><i>NPM1</i></scp>‐mutated <scp>AML</scp> with starry sky pattern
<span><i>NPM1</i></span>‐mutated <span>AML</span> with starry sky pattern Open
A 52-year-old women presented with fever, sore throat, white blood cells 181 × 109/L (>80% blasts), Hb 91 g/L, platelets 175 × 109/L. LDH was 1152 U/L. The bone marrow was diffusely infiltrated by blast cells with starry sky pattern due to…
View article: The <scp>NPM1</scp> mutant defines <scp>AML</scp> irrespective of blast count
The <span>NPM1</span> mutant defines <span>AML</span> irrespective of blast count Open
NPM1-mutated acute myeloid leukemia (AML) accounts for about 30%–35% of newly diagnosed cases in adults (50%–60% of all AML with normal karyotype1) and it is characterized by distinctive clinico-pathological and molecular features.2 For th…
View article: Data from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia
Data from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia Open
The dysregulation of developmental and stem cell–associated genes is a common phenomenon during cancer development. Around half of patients with acute myeloid leukemia (AML) express high levels of HOXA cluster genes and MEIS1…
View article: Supplementary Figures S1-S12 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia
Supplementary Figures S1-S12 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia Open
Supplementary Figure 1. NPM1c degradation leads to differentiation of OCI-AML3 cells.Supplementary Figure 2. NPM1c chromatin targets identified in OCI-AML3-NPM1c-FKBP12 cells and validated by targeted degradation.Supplementary Figure 3. Mo…
View article: Supplementary Tables S1-S14 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia
Supplementary Tables S1-S14 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia Open
Table S1. Read normalized ratios of ChIPseq signal of untreated versus dTAG-13 treated OCI-AML3-NPM1c-FKBP12 cells.Table S2. Summary of NPM1c and NPM1 Chromatin Binding Targets.Table S3. Patient info for patient derived xenograft (PDX) mod…
View article: Data from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia
Data from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia Open
The dysregulation of developmental and stem cell–associated genes is a common phenomenon during cancer development. Around half of patients with acute myeloid leukemia (AML) express high levels of HOXA cluster genes and MEIS1…
View article: Supplementary Figures S1-S12 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia
Supplementary Figures S1-S12 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia Open
Supplementary Figure 1. NPM1c degradation leads to differentiation of OCI-AML3 cells.Supplementary Figure 2. NPM1c chromatin targets identified in OCI-AML3-NPM1c-FKBP12 cells and validated by targeted degradation.Supplementary Figure 3. Mo…
View article: Supplementary Tables S1-S14 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia
Supplementary Tables S1-S14 from Mutant NPM1 Directly Regulates Oncogenic Transcription in Acute Myeloid Leukemia Open
Table S1. Read normalized ratios of ChIPseq signal of untreated versus dTAG-13 treated OCI-AML3-NPM1c-FKBP12 cells.Table S2. Summary of NPM1c and NPM1 Chromatin Binding Targets.Table S3. Patient info for patient derived xenograft (PDX) mod…
View article: Data from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Data from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Acute myeloid leukemia (AML) pathogenesis often involves a mutation in the NPM1 nucleolar chaperone, but the bases for its transforming properties and overall association with favorable therapeutic responses remain incompletely understood.…
View article: Key Resources Table from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Key Resources Table from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Key resource table with RRID
View article: Supplementary Table from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
Supplementary Table from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor Open
Supplementary Table from Systematic Profiling of DNMT3A Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
View article: Supplementary Table from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
Supplementary Table from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor Open
Supplementary Table from Systematic Profiling of DNMT3A Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
View article: Supplementary Figures and Methods from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Supplementary Figures and Methods from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Supplementary figures and methods
View article: Table S2 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Table S2 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Supplementary table S2
View article: Data from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Data from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Acute myeloid leukemia (AML) pathogenesis often involves a mutation in the NPM1 nucleolar chaperone, but the bases for its transforming properties and overall association with favorable therapeutic responses remain incompletely understood.…
View article: Table S1 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Table S1 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Supplementary table S1
View article: Supplementary Table from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
Supplementary Table from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor Open
Supplementary Table from Systematic Profiling of DNMT3A Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
View article: Data from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
Data from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor Open
Clonal hematopoiesis is a prevalent age-related condition associated with a greatly increased risk of hematologic disease; mutations in DNA methyltransferase 3A (DNMT3A) are the most common driver of this state. DNMT3A varian…
View article: Data from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor
Data from Systematic Profiling of <i>DNMT3A</i> Variants Reveals Protein Instability Mediated by the DCAF8 E3 Ubiquitin Ligase Adaptor Open
Clonal hematopoiesis is a prevalent age-related condition associated with a greatly increased risk of hematologic disease; mutations in DNA methyltransferase 3A (DNMT3A) are the most common driver of this state. DNMT3A varian…
View article: Supplementary Figures and Methods from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Supplementary Figures and Methods from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Supplementary figures and methods
View article: Table S2 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Table S2 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Supplementary table S2
View article: Table S1 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy
Table S1 from Actinomycin D Targets NPM1c-Primed Mitochondria to Restore PML-Driven Senescence in AML Therapy Open
Supplementary table S1