Publications by authors named "Tamburini J"

Background: Tumor lysis syndrome (TLS) is a potentially life-threatening condition resulting from the rapid destruction of malignant cells, leading to electrolyte imbalances and severe complications, such as acute kidney injury, arrhythmias, and seizures. TLS can be managed through hyperhydration, urate-lowering treatments, and a steroid prophase strategy.

Aims: This study aims to explore the impact of fractionated rituximab, an anti-CD20 antibody, on the occurrence and severity of TLS during the initial cycle in patients with aggressive B-cell non-Hodgkin lymphoma (B-NHL).

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  • * Researchers excluded pregnancies that ended in termination or miscarriage and those with prior blood cancer histories, focusing on the survival rates and maternal health during these malignancies compared to healthy pregnancies.
  • * The study found that of nearly 10 million pregnancies analyzed, 1,366 were associated with haematological cancers, providing new insights into their incidence and effects on maternal morbidity and mortality.
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  • Identification of stearoyl-CoA desaturase (SCD) as a key therapeutic target in improving the outcomes of acute myeloid leukemia (AML) patients, showing its role across different mutational backgrounds.
  • Inhibition of SCD using the drug SSI-4 induces lipotoxicity, leading to cell death in AML models both in lab conditions and in living organisms.
  • The study suggests that combining SCD inhibition with standard chemotherapy enhances the effectiveness of treatment, emphasizing the need for predictive biomarkers and combination therapies for optimal results.
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  • Acute myeloid leukemia (AML) is a difficult-to-treat blood cancer, mainly due to the presence of leukemic stem cells (LSCs) that lead to treatment resistance and relapse.
  • This research focuses on how the quiescence (dormancy) of LSCs and related molecular mechanisms impact AML development, revealing that quiescent LSCs have a distinct gene signature and increased autophagic activity that helps them survive.
  • The study identifies nuclear receptor coactivator 4 (NCOA4) as a key player in iron metabolism for quiescent LSCs, showing that inhibiting NCOA4 can effectively target these cells without harming normal blood progenitors, highlighting its potential as
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Haematopoietic stem cell (HSC) transplantation (HSCT) is the only curative treatment for a broad range of haematological malignancies, but the standard of care relies on untargeted chemotherapies and limited possibilities to treat malignant cells after HSCT without affecting the transplanted healthy cells. Antigen-specific cell-depleting therapies hold the promise of much more targeted elimination of diseased cells, as witnessed in the past decade by the revolution of clinical practice for B cell malignancies. However, target selection is complex and limited to antigens expressed on subsets of haematopoietic cells, resulting in a fragmented therapy landscape with high development costs.

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Survival of patients with acute myeloid leukemia (AML) can be improved by allogeneic hematopoietic stem cell transplantation (allo-HSCT) because of the antileukemic activity of T and natural killer cells from the donor. However, the use of allo-HSCT is limited by donor availability, recipient age, and potential severe side effects. Similarly, the efficacy of immunotherapies directing autologous T cells against tumor cells, including T-cell recruiting antibodies, chimeric antigen receptor T-cell therapy, and immune checkpoint inhibitors are limited in AML because of multiple mechanisms of leukemia immune escape.

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Targeted eradication of transformed or otherwise dysregulated cells using monoclonal antibodies (mAb), antibody-drug conjugates (ADC), T cell engagers (TCE), or chimeric antigen receptor (CAR) cells is very effective for hematologic diseases. Unlike the breakthrough progress achieved for B cell malignancies, there is a pressing need to find suitable antigens for myeloid malignancies. CD123, the interleukin-3 (IL-3) receptor alpha-chain, is highly expressed in various hematological malignancies, including acute myeloid leukemia (AML).

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Glioblastoma (GBM) is a deadly and the most common primary brain tumor in adults. Due to their regulation of a high number of mRNA transcripts, microRNAs (miRNAs) are key molecules in the control of biological processes and are thereby promising therapeutic targets for GBM patients. In this regard, we recently reported miRNAs as strong modulators of GBM aggressiveness.

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Autologous hematopoietic stem cell transplant (ASCT) is the standard curative treatment for patients with high-risk relapsed/refractory Hodgkin lymphoma (R/R HL). The AETHERA study showed survival gain with Brentuximab Vedotin (BV) maintenance after ASCT in BV-naive patients, which was recently confirmed in the retrospective AMAHRELIS cohort, including a majority of BV-exposed patients. However, this approach has not been compared to intensive tandem auto/auto or auto/allo transplant strategies, which were used before BV approval.

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  • The study explores the role of the transcription factor CCAAT-enhancer binding protein α (C/EBPα) in lipid metabolism and cellular homeostasis in acute myeloid leukemia (AML), particularly with mutations in FLT3.
  • Researchers found that C/EBPα and FLT3 activation enhance lipid production and desaturation in AML cells, leading to increased vulnerability to oxidative stress.
  • Inhibiting C/EBPα or FLT3 demonstrates potential for therapeutic strategies targeting lipid metabolism to promote ferroptotic cell death in FLT3-mutant AML, a type of leukemia affecting 30% of patients.
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Primary central nervous system lymphomas (PCNSLs) classically remain confined within the CNS throughout their evolution for unknown reasons. Our objective was to analyse the rare extracerebral relapses of PCNSL in a nationwide population-based study. We retrospectively selected PCNSL patients who experienced extracerebral relapse during their follow-up from the French LOC database.

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  • Mitochondrial metabolism is crucial for acute myeloid leukemia (AML) and is regulated by proteins that manage mitochondrial shape through fusion and fission processes.* -
  • Research indicates that targeting mitochondrial fusion presents a new vulnerability in AML cells, demonstrated through studies using patient-derived xenograft (PDX) models.* -
  • Disruption of mitochondrial fusion through genetic depletion or pharmacological inhibition significantly impairs AML cell growth by affecting respiration and causing cell cycle arrest, suggesting a potential therapeutic strategy.*
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Introduction: Brain surgery is required to ascertain the diagnosis of central nervous system lymphoma. We assessed the diagnostic yield and safety of the surgical procedures, the predictors of postoperative morbidity, and of overall survival.

Methods: Observational single-institution retrospective cohort study (1992-2020) of 101 consecutive adult patients who underwent stereotactic biopsy, open biopsy, or resection for a newly diagnosed central nervous system lymphoma.

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Study Question: What biological processes are linked to the signaling of the energy sensor 5'-AMP-activated protein kinase (AMPK) in mouse and human granulosa cells (GCs)?

Summary Answer: The lack of α1AMPK in GCs impacted cell cycle, adhesion, lipid metabolism and induced a hyperandrogenic response.

What Is Known Already: AMPK is expressed in the ovarian follicle, and its activation by pharmacological medications, such as metformin, inhibits the production of steroids. Polycystic ovary syndrome (PCOS) is responsible for infertility in approximately 5-20% of women of childbearing age and possible treatments include reducing body weight, improving lifestyle and the administration of a combination of drugs to improve insulin resistance, such as metformin.

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  • Recent advances in targeted therapies for acute myeloid leukemia (AML) have not significantly addressed many cases, especially those lacking actionable therapy targets.
  • In a study of 127 AML cases, 40% showed alterations in RAS pathway genes, which correlated with worse outcomes and survival rates for patients.
  • The combination of the MEK inhibitor trametinib and the anti-helminthic drug pyrvinium pamoate showed promising antileukemic effects in both laboratory tests and mouse models, suggesting a potential new treatment strategy for RAS+ AML.
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  • Therapy resistance is a big issue in treating acute myeloid leukemia (AML), and researchers have created a 'MitoScore' to identify patients with high oxidative phosphorylation in their cells.
  • AML cells that resist treatment with cytarabine (AraC) show reliance on certain mitochondrial proteins and respond well to a combination of venetoclax (VEN) and AraC, but not to VEN with azacytidine.
  • Further research found that resistant AML cells adapt by altering their mitochondrial functions, and targeting these adaptations could improve treatment outcomes, suggesting a potential strategy to alternate between VEN therapies based on MitoScore levels to boost effectiveness.
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  • AMPK is a key regulator of energy balance in cells, influencing growth and survival, and activation of AMPK has shown potential anti-cancer effects, particularly in acute myeloid leukemia (AML).
  • The study reveals that the AMPK activator GSK621 triggers the unfolded protein response (UPR) in AML cells, causing changes in energy metabolism that promote cell death.
  • Combining GSK621 with the Bcl-2 inhibitor venetoclax enhances the effectiveness of treatment, suggesting that AMPK activation could be a promising strategy for AML therapy through reshaping mitochondrial processes.
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