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  • 1
    Language: English
    In: Bone marrow transplantation (Basingstoke), 2017-01, Vol.52 (1), p.7-14
    Description: Advances in biological techniques have potentiated great progresses in understanding the interaction between human beings and the ∼10 to 100 trillion microbes living in their gastrointestinal tract: gut microbiota (GM). In this review, we describe recent emerging data on the role of GM in hematopoietic stem cell transplantation, with a focus on immunomodulatory properties in the immune system recovery and the impact in the development of the main complications, as GvHD and infections.
    Subject(s): Immunomodulation ; Infection - immunology ; Humans ; Hematopoietic Stem Cell Transplantation ; Infection - microbiology ; Gastrointestinal Microbiome - immunology ; Graft vs Host Disease - immunology ; Graft vs Host Disease - microbiology ; Transplantation ; Research ; Microbiota (Symbiotic organisms) ; Health aspects ; Hematopoietic stem cells ; Index Medicus
    ISSN: 0268-3369
    E-ISSN: 1476-5365
    Source: Nature Open Access
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Bone marrow transplantation (Basingstoke), 2015-07, Vol.50 (7), p.992-998
    Description: Acute GvHD (aGvHD) is the main complication of hematopoietic SCT (HSCT) during the treatment of hematological disorders. We carried out the first longitudinal study to follow the gut microbiota trajectory, from both the phylogenetic and functional points of view, in pediatric patients undergoing HSCT. Gut microbiota trajectories and short-chain fatty acid production profiles were followed starting from before HSCT and through the 3-4 months after transplant in children developing and not developing aGvHD. According to our findings, HSCT procedures temporarily cause a structural and functional disruption of the gut microbial ecosystem, describing a trajectory of recovery during the following 100 days. The onset of aGvHD is associated with specific gut microbiota signatures both along the course of gut microbiota reconstruction immediately after transplant and, most interestingly, prior to HSCT. Indeed, in pre-HSCT samples, non-aGvHD patients showed higher abundances of propionate-producing Bacteroidetes, highly adaptable microbiome mutualists that showed to persist during the HSCT-induced ecosystem disruption. Our data indicate that structure and temporal dynamics of the gut microbial ecosystem can be a relevant factor for the success of HSCT and opens the perspective to the manipulation of the pre-HSCT gut microbiota configuration to favor mutualistic persisters with immunomodulatory properties in the gut.
    Subject(s): Acute Disease ; Graft vs Host Disease - complications ; Humans ; Hematopoietic Stem Cell Transplantation - adverse effects ; Female ; Gastrointestinal Microbiome - physiology ; Child ; Longitudinal Studies ; Transplantation, Homologous - adverse effects ; Microbiota (Symbiotic organisms) ; Analysis ; Phylogeny ; Index Medicus
    ISSN: 0268-3369
    E-ISSN: 1476-5365
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Bone marrow transplantation (Basingstoke), 2017-03, Vol.52 (3), p.494-497
    Subject(s): Complications and side effects ; Development and progression ; Transplantation ; Liver diseases ; Hematopoietic stem cells ; Index Medicus
    ISSN: 0268-3369
    E-ISSN: 1476-5365
    Source: Nature Open Access
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: Leukemia, 2011-05, Vol.25 (5), p.781-791
    Description: The mammalian Target Of Rapamycin (mTOR) serine/threonine kinase belongs to two multi-protein complexes, referred to as mTORC1 and mTORC2. mTOR-generated signals have critical roles in leukemic cell biology by controlling mRNA translation of genes that promote proliferation and survival. However, allosteric inhibition of mTORC1 by rapamycin has only modest effects in T-cell acute lymphoblastic leukemia (T-ALL). Recently, ATP-competitive inhibitors specific for the mTOR kinase active site have been developed. In this study, we have explored the therapeutic potential of active-site mTOR inhibitors against both T-ALL cell lines and primary samples from T-ALL patients displaying activation of mTORC1 and mTORC2. The inhibitors affected T-ALL cell viability by inducing cell-cycle arrest in G(0)/G(1) phase, apoptosis and autophagy. Western blot analysis demonstrated a Ser 473 Akt dephosphorylation (indicative of mTORC2 inhibition) and a dephosphorylation of mTORC1 downstream targets. Unlike rapamycin, we found a marked inhibition of mRNA translation in T-ALL cell lines treated with active-site mTOR inhibitors. The inhibitors strongly synergized with both vincristine and the Bcl-2 inhibitor, ABT-263. Remarkably, the drugs targeted a putative leukemia-initiating cell sub-population (CD34(+)/CD7(-)/CD4(-)) in patient samples. In conclusion, the inhibitors displayed remarkable anti-leukemic activity, which emphasizes their future development as clinical candidates for therapy in T-ALL.
    Subject(s): Hematologic and hematopoietic diseases ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Biological and medical sciences ; Medical sciences ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology ; Apoptosis - drug effects ; Humans ; Multiprotein Complexes ; Autophagy - drug effects ; Mechanistic Target of Rapamycin Complex 1 ; Flow Cytometry ; Phosphorylation - drug effects ; Immunosuppressive Agents - pharmacology ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy ; Catalytic Domain ; RNA, Messenger - genetics ; Transcription Factors - antagonists & inhibitors ; Reverse Transcriptase Polymerase Chain Reaction ; Sirolimus - pharmacology ; Blotting, Western ; Transcription Factors - metabolism ; Animals ; Proteins - metabolism ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Mice ; Protein Kinase Inhibitors - pharmacology ; TOR Serine-Threonine Kinases ; Cell Cycle - drug effects ; Proteins - antagonists & inhibitors ; Prognosis ; Physiological aspects ; Rapamycin ; Acute lymphocytic leukemia ; Research ; Drug therapy ; T cells ; Health aspects ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 5
    Language: English
    In: Leukemia, 2010-02, Vol.24 (2), p.255-264
    Description: We analyzed the long-term outcome of 4865 patients treated in Studies 82, 87, 88, 91 and 95 for childhood acute lymphoblastic leukemia (ALL) of the Italian Association of Pediatric Hematology and Oncology (AIEOP). Treatment was characterized by progressive intensification of systemic therapy and reduction of cranial radiotherapy. A progressive improvement of results with reduction of isolated central nervous system relapse rate was obtained. Ten-year event-free survival increased from 53% in Study 82 to 72% in Study 95, whereas survival improved from 64 to 82%. Since 1991, all patients were treated according to Berlin-Frankfurt-Muenster (BFM) ALL treatment strategy. In Study 91, reduced treatment intensity (25%) yielded inferior results, but intensification of maintenance with high-dose (HD)-L-asparaginase (randomized) allowed to compensate for this disadvantage; in high-risk patients (HR, 15%), substitution of intensive polychemotherapy blocks for conventional BFM backbone failed to improve results. A marked improvement of results was obtained in HR patients when conventional BFM therapy was intensified with three polychemotherapy blocks and double delayed intensification (Study 95). The introduction of minimal residual disease monitoring and evaluation of common randomized questions by AIEOP and BFM groups in the protocol AIEOP-BFM-ALL 2000 are expected to further ameliorate treatment of children with ALL.
    Subject(s): Hematology - organization & administration ; Prognosis ; Follow-Up Studies ; Humans ; Risk Factors ; Child, Preschool ; Infant ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - mortality ; Survival Rate ; Treatment Outcome ; Cranial Irradiation ; Remission Induction ; Medical Oncology - organization & administration ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy ; Time Factors ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Adolescent ; Female ; Italy ; Child ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - radiotherapy ; Pediatrics ; Care and treatment ; Chemotherapy ; Acute lymphocytic leukemia ; Research ; Radiotherapy ; Health aspects ; Cancer ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: Leukemia, 2014-03-01, Vol.28 (3), p.543-553
    Description: Leukemia (2014) 28, 543-553; doi: 10.1038/leu.2013.349
    Subject(s): Leukemia research ; Physiological aspects ; Development and progression ; Acute lymphocytic leukemia ; Research ; T cells ; Drug therapy ; Protein kinases ; Apoptosis ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 7
    Language: English
    In: British journal of cancer, 2007-04-10, Vol.96 (7), p.1047-1051
    Description: To investigate the role of gefitinib in patients with high-grade gliomas (HGGs), a phase II trial (1839IL/0116) was conducted in patients with disease recurrence following surgery plus radiotherapy and first-line chemotherapy. Adult patients with histologically confirmed recurrent HGGs following surgery, radiotherapy and first-line chemotherapy, were considered eligible. Patients were treated with gefitinib (250 mg day(-1)) continuously until disease progression. The primary end point was progression-free survival at 6 months progression-free survival at 6 months (PFS-6). Tissue biomarkers (epidermal growth factor receptor (EGFR) gene status and expression, phosphorylated Akt (p-Akt) expression) were assessed. Twenty-eight patients (median age, 55 years; median ECOG performance status, 1) were enrolled; all were evaluable for drug activity and safety. Sixteen patients had glioblastoma, three patients had anaplastic oligodendrogliomas and nine patients had anaplastic astrocytoma. Five patients (17.9%, 95% CI 6.1-36.9%) showed disease stabilisation. The overall median time to progression was 8.4 (range 2-104+) weeks and PFS-6 was 14.3% (95% CI 4.0-32.7%). The median overall survival was 24.6 weeks (range 4-104+). No grade 3-4 gefitinib-related toxicity was found. Gefitinib showed limited activity in patients affected by HGGs. Epidermal growth factor receptor expression or gene status, and p-Akt expression do not seem to predict activity of this drug.
    Subject(s): Neurology ; Biological and medical sciences ; Medical sciences ; Tumors of the nervous system. Phacomatoses ; Tumors ; Humans ; Middle Aged ; Oligodendroglioma - secondary ; Neoplasm Recurrence, Local - drug therapy ; Male ; Survival Rate ; Treatment Outcome ; Antineoplastic Agents - therapeutic use ; Brain Neoplasms - drug therapy ; Astrocytoma - secondary ; Neoplasm Recurrence, Local - pathology ; Disease-Free Survival ; Brain Neoplasms - secondary ; Maximum Tolerated Dose ; Quinazolines - therapeutic use ; Glioma - pathology ; Astrocytoma - drug therapy ; Receptor, Epidermal Growth Factor - antagonists & inhibitors ; Adult ; Female ; Aged ; Neoplasm Staging ; Glioma - drug therapy ; Oligodendroglioma - drug therapy ; high-grade gliomas ; gefitinib ; Akt ; Clinical Studies ; EGFR
    ISSN: 0007-0920
    E-ISSN: 1532-1827
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Nature Journals Online
    Source: PubMed Central
    Source: Alma/SFX Local Collection
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  • 8
    Language: English
    In: Leukemia, 2014-06, Vol.28 (6), p.1196-1206
    Description: Constitutively active phosphoinositide 3-kinase (PI3K) signaling is a common feature of T-cell acute lymphoblastic leukemia (T-ALL), where it upregulates cell proliferation, survival and drug resistance. These observations lend compelling weight to the application of PI3K inhibitors in the therapy of T-ALL. Here, we have analyzed the therapeutic potential of the pan-PI3K inhibitor NVP-BKM120 (BKM120), an orally bioavailable 2,6-dimorpholino pyrimidine derivative, which has entered clinical trials for solid tumors, on both T-ALL cell lines and patient samples. BKM120 treatment resulted in G2/M phase cell cycle arrest and apoptosis, being cytotoxic to a panel of T-ALL cell lines and patient T lymphoblasts, and promoting a dose- and time-dependent dephosphorylation of Akt and S6RP. BKM120 maintained its pro-apoptotic activity against Jurkat cells even when cocultured with MS-5 stromal cells, which mimic the bone marrow microenvironment. Remarkably, BKM120 synergized with chemotherapeutic agents currently used for treating T-ALL patients. Moreover, in vivo administration of BKM120 to a subcutaneous xenotransplant model of human T-ALL significantly delayed tumor growth, thus prolonging survival time. Taken together, our findings indicate that BKM120, either alone or in combination with chemotherapeutic drugs, may be an efficient treatment for T-ALLs that have aberrant upregulation of the PI3K signaling pathway.
    Subject(s): Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology ; Apoptosis - drug effects ; Humans ; Morpholines - pharmacology ; Mice, SCID ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Blotting, Western ; Xenograft Model Antitumor Assays ; Animals ; Flow Cytometry ; Aminopyridines - pharmacology ; Mice, Inbred NOD ; Cell Proliferation - drug effects ; Mice ; Tumor Cells, Cultured ; Cell Cycle - drug effects ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism ; Antimitotic agents ; Physiological aspects ; Acute lymphocytic leukemia ; Research ; Drug therapy ; Antineoplastic agents ; Protein kinases ; Health aspects ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: Bone marrow transplantation (Basingstoke), 2015-02, Vol.50 (2), p.181-188
    Description: We analyzed the outcome of 243 children with high-risk (HR) AML in first CR1 enrolled in the AIEOP-2002/01 protocol, who were given either allogeneic (ALLO; n=141) or autologous (AUTO; n=102) hematopoietic SCT (HSCT), depending on the availability of a HLA-compatible sibling. Infants, patients with AML-M7, or complex karyotype or those with FLT3-ITD, were eligible to be transplanted also from alternative donors. All patients received a myeloablative regimen combining busulfan, cyclophosphamide and melphalan; [corrected] AUTO-HSCT patients received BM cells in most cases, while in children given ALLO-HSCT stem cell source was BM in 96, peripheral blood in 19 and cord blood in 26. With a median follow-up of 57 months (range 12-130), the probability of disease-free survival (DFS) was 73% and 63% in patients given either ALLO- or AUTO-HSCT, respectively (P=NS). Although the cumulative incidence (CI) of relapse was lower in ALLO- than in AUTO-HSCT recipients (17% vs 28%, respectively; P=0.043), the CI of TRM was 7% in both groups. Patients transplanted with unrelated donor cord blood had a remarkable 92.3% 8-year DFS probability. Altogether, these data confirm that HSCT is a suitable option for preventing leukemia recurrence in HR children with CR1 AML.
    Subject(s): Autografts ; Follow-Up Studies ; Leukemia, Myeloid, Acute - pathology ; Humans ; Child, Preschool ; Hematopoietic Stem Cell Transplantation ; Infant ; Male ; Survival Rate ; Abnormal Karyotype ; Cord Blood Stem Cell Transplantation ; Leukemia, Myeloid, Acute - mortality ; fms-Like Tyrosine Kinase 3 - genetics ; Disease-Free Survival ; Allografts ; Adolescent ; Myeloablative Agonists - administration & dosage ; Female ; Transplantation Conditioning - methods ; Child ; Leukemia, Myeloid, Acute - therapy ; Leukemia, Myeloid, Acute - genetics ; Transplantation ; Health aspects ; Patient outcomes ; Hematopoietic stem cells ; Index Medicus
    ISSN: 0268-3369
    E-ISSN: 1476-5365
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: Leukemia, 2012, Vol.26 (1), p.91-100
    Description: The mammalian target of rapamycin (mTOR) serine/threonine kinase is the catalytic subunit of two multi-protein complexes, referred to as mTORC1 and mTORC2. Signaling downstream of mTORC1 has a critical role in leukemic cell biology by controlling mRNA translation of genes involved in both cell survival and proliferation. mTORC1 activity can be downmodulated by upregulating the liver kinase B1/AMP-activated protein kinase (LKB1/AMPK) pathway. Here, we have explored the therapeutic potential of the anti-diabetic drug, metformin (an LKB1/AMPK activator), against both T-cell acute lymphoblastic leukemia (T-ALL) cell lines and primary samples from T-ALL patients displaying mTORC1 activation. Metformin affected T-ALL cell viability by inducing autophagy and apoptosis. However, it was much less toxic against proliferating CD4(+) T-lymphocytes from healthy donors. Western blot analysis demonstrated dephosphorylation of mTORC1 downstream targets. Unlike rapamycin, we found a marked inhibition of mRNA translation in T-ALL cells treated with metformin. Remarkably, metformin targeted the side population of T-ALL cell lines as well as a putative leukemia-initiating cell subpopulation (CD34(+)/CD7(-)/CD4(-)) in patient samples. In conclusion, metformin displayed a remarkable anti-leukemic activity, which emphasizes future development of LKB1/AMPK activators as clinical candidates for therapy in T-ALL.
    Subject(s): Hematologic and hematopoietic diseases ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Biological and medical sciences ; Medical sciences ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology ; Phosphorylation ; Signal Transduction ; Humans ; Metformin - pharmacology ; Multiprotein Complexes ; RNA, Messenger - genetics ; DNA Primers ; Mechanistic Target of Rapamycin Complex 1 ; Flow Cytometry ; Proteins - metabolism ; Adenylate Kinase - metabolism ; Base Sequence ; Cell Line, Tumor ; Protein Biosynthesis - drug effects ; TOR Serine-Threonine Kinases ; Real-Time Polymerase Chain Reaction ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism ; Apoptosis ; Physiological aspects ; Acute lymphocytic leukemia ; Research ; Drug therapy ; T cells ; Protein kinases
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
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