Valentina Gambacorta

ORCID: 0000-0003-2302-4083
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About
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Research Areas
  • Acute Myeloid Leukemia Research
  • Hematopoietic Stem Cell Transplantation
  • Immune Cell Function and Interaction
  • Epigenetics and DNA Methylation
  • Immune cells in cancer
  • T-cell and B-cell Immunology
  • CAR-T cell therapy research
  • Histone Deacetylase Inhibitors Research
  • Telomeres, Telomerase, and Senescence
  • Cancer Genomics and Diagnostics
  • Polyomavirus and related diseases
  • RNA modifications and cancer
  • Cytomegalovirus and herpesvirus research
  • Acute Lymphoblastic Leukemia research
  • Hematological disorders and diagnostics
  • Chronic Lymphocytic Leukemia Research
  • Immunotherapy and Immune Responses
  • Retinoids in leukemia and cellular processes
  • Protein Degradation and Inhibitors
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms

Istituto di Ricovero e Cura a Carattere Scientifico San Raffaele
2016-2023

Vita-Salute San Raffaele University
2016-2023

Istituti di Ricovero e Cura a Carattere Scientifico
2016-2023

The San Raffaele Telethon Institute for Gene Therapy
2019-2022

University of Milano-Bicocca
2019-2022

Institute for Stem Cell Biology and Regenerative Medicine
2019

Medical Center Hospital
2016

Leiden University Medical Center
2016

Massachusetts General Hospital
2016

Abstract The major cause of death after allogeneic Hematopoietic Stem Cell Transplantation (HSCT) for acute myeloid leukemia (AML) is disease relapse. We investigated the expression Inhibitory Receptors (IR; PD-1/CTLA-4/TIM-3/LAG-3/2B4/KLRG1/GITR) on T cells infiltrating bone marrow (BM) 32 AML patients relapsing (median 251 days) or maintaining complete remission (CR; median 1 year) HSCT. A higher proportion early-differentiated Memory (T SCM ) and Central BM-T express multiple IR in than...

10.1038/s41467-019-08871-1 article EN cc-by Nature Communications 2019-03-25

Immune escape represents a major driver of acute myeloid leukemia (AML) reemergence after allogeneic hematopoietic cell transplantation (allo-HCT), with up to 40% relapses prompted by nongenomic loss HLA class II expression in cells. By integrative analysis gene expression, DNA methylation, and chromatin accessibility paired diagnosis/relapse primary samples the respective patient-derived xenografts (PDX), we identify polycomb repressive complex 2 (PRC2) as key epigenetic this immune...

10.1158/2159-8290.cd-21-0980 article EN cc-by-nc-nd Cancer Discovery 2022-03-07

ABSTRACT Acute myeloid leukemia (AML) is an aggressive hematological malignancy often curable only by using intensive chemotherapy. Nonetheless, resistance/early relapses are frequent, underscoring the need to investigate molecular events occurring shortly after Therapy-induced senescence (TIS) a fail-safe tumor suppressive mechanism that may elicit immune-mediated responses contributing senescent cell clearance. Yet, TIS functional role in AML eradication and immune surveillance early...

10.1101/2022.11.17.515658 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-11-17

Preferred Presentation Method: Oral PresentationIntroduction: Most patients with relapsing-remitting multiple sclerosis (RRMS) do not achieve a sustained remission after disease-modifying therapy.Material (or patients) and methods: A phase II clinical trial of high-dose immunosuppressive therapy (HDIT; BCNU, etoposide, ara-C, melphalan antithymocyte globulin) autologous hematopoietic cell transplantation (HCT) was conducted in highly active RRMS who had failed conventional to assess the rate...

10.1038/bmt.2016.46 article EN other-oa Bone Marrow Transplantation 2016-03-01

<div>Abstract<p>Immune escape represents a major driver of acute myeloid leukemia (AML) reemergence after allogeneic hematopoietic cell transplantation (allo-HCT), with up to 40% relapses prompted by nongenomic loss HLA class II expression in cells. By integrative analysis gene expression, DNA methylation, and chromatin accessibility paired diagnosis/relapse primary samples the respective patient-derived xenografts (PDX), we identify polycomb repressive complex 2 (PRC2) as key...

10.1158/2159-8290.c.6549653.v1 preprint EN 2023-04-04

<div>Abstract<p>Immune escape represents a major driver of acute myeloid leukemia (AML) reemergence after allogeneic hematopoietic cell transplantation (allo-HCT), with up to 40% relapses prompted by nongenomic loss HLA class II expression in cells. By integrative analysis gene expression, DNA methylation, and chromatin accessibility paired diagnosis/relapse primary samples the respective patient-derived xenografts (PDX), we identify polycomb repressive complex 2 (PRC2) as key...

10.1158/2159-8290.c.6549653 preprint EN 2023-04-04

Background: Acute myeloid leukemia (AML) is an aggressive hematological malignancy currently treated with high-dose chemotherapy. Therapy-induced senescence (TIS) a cell-intrinsic fail-safe mechanism controlling tumor initiation and progression but, if persistent, may even contribute to cancer relapse. Yet, the contribution of TIS early response therapy in AML remains ill-defined. Aims: Our work aims delve into crosstalk between blast adaptive immune cells final long-term goal unveiling...

10.1097/01.hs9.0000968624.55051.32 article EN cc-by-nc-nd HemaSphere 2023-08-01

Abstract Background: Evasion from immune control represents one of the main drivers acute myeloid leukemia (AML) relapse after allogeneic hematopoietic cell transplantation (allo-HCT). In particular, up to 40% AML relapses display complete loss surface expression HLA class II molecules without any genetic lesion explaining this phenotype (Christopher et al, N Engl J Med, 2018; Toffalori Nat 2019). This led us investigate links between epigenetic changes, evasion and post-transplantation...

10.1158/1538-7445.am2022-lb563 article EN Cancer Research 2022-06-15
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