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Preview: pubmed: Blood[Jour]

pubmed: Blood[Jour]



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Mechanisms of platelet clearance and translation to improve platelet storage.

Mechanisms of platelet clearance and translation to improve platelet storage.

Blood. 2018 Feb 23;:

Authors: Quach ME, Chen W, Li R

Abstract
Hundreds of billions of platelets are cleared daily from circulation via efficient and highly regulated mechanisms. These mechanisms may be stimulated by exogenous reagents or environmental changes to accelerate platelet clearance, leading to thrombocytopenia. The interplay between anti-apoptotic Bcl-xL and pro-apoptotic molecules Bax and Bak sets an internal clock for the platelet lifespan, and BH3-only proteins, mitochondrial permeabilization, and phosphatidylserine (PS) exposure may also contribute to apoptosis-induced platelet clearance. Binding of plasma VWF or antibodies to the ligand-binding domain of glycoprotein (GP)Ibα on platelets can activate GPIb-IX in a shear-dependent manner by inducing unfolding of the mechanosensory domain therein, and trigger downstream signaling in the platelet including desialylation and PS exposure. Deglycosylated platelets are recognized by the Ashwell-Morell receptor and potentially other scavenger receptors, and are rapidly cleared by hepatocytes and/or macrophages. Inhibitors of platelet clearance pathways, including inhibitors of GPIbα shedding, neuraminidases, and platelet signaling, are efficacious at preserving the viability of platelets during storage and improving their recovery and survival in vivo. Overall, common mechanisms of platelet clearance have begun to emerge, suggesting potential strategies to extend the shelf-life of platelets stored at room temperature or to enable refrigerated storage.

PMID: 29475962 [PubMed - as supplied by publisher]




Alterations in the Rho pathway contribute to Epstein-Barr virus-induced lymphomagenesis in immunosuppressed environments.

Alterations in the Rho pathway contribute to Epstein-Barr virus-induced lymphomagenesis in immunosuppressed environments.

Blood. 2018 Feb 23;:

Authors: Cho SY, Sung CO, Chae J, Lee J, Na D, Kang W, Kang J, Min S, Lee A, Kwak E, Kim J, Choi B, Kim H, Chuang JH, Pak HK, Park CS, Park S, Ko YH, Lee D, Roh J, Cho MS, Park S, Ju YS, Suh YS, Kong SH, Lee HJ, Keck J, Banchereau J, Liu ET, Kim WH, Park H, Yang HK, Kim JI, Lee C

Abstract
Epstein-Barr virus (EBV)-positive diffuse large B cell lymphomas (EBV+-DLBLs) tend to occur in immunocompromised patients, such as the elderly or those undergoing solid organ transplantation. The pathogenesis and genomic characteristics of EBV+-DLBLs are largely unknown because of the limited availability of human samples and lack of experimental animal models. We observed the development of 25 human EBV+-DLBLs during the engraftment of gastric adenocarcinomas into immunodeficient mice. An integrated genomic analysis of the human-derived EBV+-DLBLs revealed enrichment of mutations in Rho pathway genes, including RHPN2, and Rho pathway transcriptomic activation. Targeting the Rho pathway using a ROCK inhibitor, fasudil, markedly decreased tumor growth in EBV+-DLBL patient-derived xenograft (PDX) models. Thus, alterations in the Rho pathway appear to contribute to EBV-induced lymphomagenesis in immunosuppressed environments.

PMID: 29475961 [PubMed - as supplied by publisher]




The phosphotyrosine phosphatase SHP2 promotes anergy in chronic lymphocytic leukemia.

The phosphotyrosine phosphatase SHP2 promotes anergy in chronic lymphocytic leukemia.

Blood. 2018 Feb 23;:

Authors: Schliffke S, Buhs S, Bolz S, Gerull H, von Wenserski L, Riecken K, Fehse B, Nollau P, Binder M

PMID: 29475960 [PubMed - as supplied by publisher]




High grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements with diffuse large B-cell lymphoma morphology.

High grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements with diffuse large B-cell lymphoma morphology.

Blood. 2018 Feb 23;:

Authors: Scott DW, King RL, Staiger AM, Ben-Neriah S, Jiang A, Horn H, Mottok A, Farinha P, Slack GW, Ennishi D, Schmitz N, Pfreundschuh M, Nowakowski GS, Kahl BS, Connors JM, Gascoyne RD, Ott G, Macon WR, Rosenwald A

Abstract
High grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangements (HGBL-DH/TH) is a newly defined entity in the latest World Health Organization Classification. Accurate diagnosis would appear to mandate fluorescence in situ hybridization (FISH) for all tumors with diffuse large B-cell lymphoma (DLBCL) morphology. We present the results of FISH, cell-of-origin and immunohistochemistry (IHC) testing from 1228 DLBCL biopsies from three clinical trials and a population-based registry. HGBL-DH/TH made up 7.9% of DLBCL, confined primarily to the germinal centre B-cell-like (GCB - 13.3%) compared with activated B-cell-like (ABC - 1.7%) subtype (P<0.001). HGBL-DH/TH with BCL2 rearrangement is a GCB phenomenon with no cases observed in 415 ABC DLBCL. A screening strategy restricting FISH testing to tumors of GCB subtype (by Lymph2Cx or Hans IHC) plus dual protein expression of MYC and BCL2 by IHC could limit testing to 11-14% of tumors, with a positive predictive value of 30-37%; however, this strategy would miss approximately a quarter of tumors with HBGL-DH/TH with BCL2 rearrangement and a third of all HGBL-DH/TH. These results provide accurate estimation of the proportion of HGBL-DH/TH among tumors with DLBCL morphology and allow determination of the impact of various methods available to screen DLBCL tumors for FISH testing.

PMID: 29475959 [PubMed - as supplied by publisher]




B-cell acute lymphoblastic leukemia in JAK2 V617F-positive polycythemia vera.
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B-cell acute lymphoblastic leukemia in JAK2 V617F-positive polycythemia vera.

Blood. 2018 Feb 22;131(8):941

Authors: Jaitly V, Wang W

PMID: 29472375 [PubMed - in process]




Chewing the bone: bone marrow with adult T-cell leukemia/lymphoma.
Related Articles

Chewing the bone: bone marrow with adult T-cell leukemia/lymphoma.

Blood. 2018 Feb 22;131(8):940

Authors: Siref A, Huang Q

PMID: 29472374 [PubMed - in process]




HSCT for PID: not just for children.
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HSCT for PID: not just for children.

Blood. 2018 Feb 22;131(8):843-844

Authors: Dávila Saldaña BJ

PMID: 29472373 [PubMed - in process]




VWF clearance: it's glycomplicated.
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VWF clearance: it's glycomplicated.

Blood. 2018 Feb 22;131(8):842-843

Authors: Denis CV, Lenting PJ

PMID: 29472372 [PubMed - in process]




How does hepcidin hinder ferroportin activity?
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How does hepcidin hinder ferroportin activity?

Blood. 2018 Feb 22;131(8):840-842

Authors: Zhang DL, Rouault TA

PMID: 29472371 [PubMed - in process]




Dual PI3K blockade: PTCL's Achilles heel?
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Dual PI3K blockade: PTCL's Achilles heel?

Blood. 2018 Feb 22;131(8):839-840

Authors: Brammer JE

PMID: 29472370 [PubMed - in process]




No red blood cell damage and no hemolysis in G6PD-deficient subjects after ingestion of low vicine/convicine Vicia faba seeds.
Related Articles

No red blood cell damage and no hemolysis in G6PD-deficient subjects after ingestion of low vicine/convicine Vicia faba seeds.

Blood. 2018 Feb 21;:

Authors: Gallo V, Skorokhod OA, Simula LF, Marrocco T, Tambini E, Schwarzer E, Marget P, Duc G, Arese P

PMID: 29467185 [PubMed - as supplied by publisher]




Low catalase expression confers redox hypersensitivity and identifies an indolent clinical behavior in CLL.
Related Articles

Low catalase expression confers redox hypersensitivity and identifies an indolent clinical behavior in CLL.

Blood. 2018 Feb 21;:

Authors: Cavallini C, Chignola R, Dando I, Perbellini O, Mimiola E, Lovato O, Laudanna C, Pizzolo G, Donadelli M, Scupoli MT

Abstract
B-cell receptor (BCR) signaling is a key determinant of variable clinical behavior and a target for therapeutic interventions in chronic lymphocytic leukemia (CLL). Endogenously produced H2O2 is thought to fine-tune the BCR signaling by reversibly inhibiting phosphatases. However, little is known about how CLL cells sense and respond to such redox cues and what impact they have on CLL. We characterized the response of BCR signaling proteins to exogenous H2O2 in cells from CLL patients using phospho-specific flow cytometry. Exogenous H2O2 in the absence of BCR engagement induced a signaling response of BCR proteins that was higher in CLL with favorable prognostic parameters and an indolent clinical course. We identified low catalase expression as a possible mechanism accounting for redox signaling hypersensitivity. Decreased catalase could cause an escalated accumulation of exogenous H2O2 in leukemic cells with a consequent greater inhibition of phosphatases and an increase of redox signaling sensitivity. Moreover, lower levels of catalase were significantly associated with a slower progression of the disease. In leukemic cells characterized by redox hypersensitivity, we also documented an elevated accumulation of ROS and an increased mitochondrial amount. Taken together, our data identified redox sensitivity and metabolic profiles that are linked to differential clinical behavior in CLL. This study advances our understanding of the redox and signaling heterogeneity of CLL and provides the rationale for the development of therapies targeting redox pathways in CLL.

PMID: 29467184 [PubMed - as supplied by publisher]




The search for new antithrombotic mechanisms and therapies that may spare hemostasis.
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The search for new antithrombotic mechanisms and therapies that may spare hemostasis.

Blood. 2018 Feb 21;:

Authors: Plow EF, Wang Y, Simon DI

Abstract
Current antithrombotic drugs, including widely used antiplatelet agents and anticoagulants, are associated with significant bleeding risk, which increases morbidity and mortality. Nevertheless, there is emerging experimental evidence that suggests that the molecular and cellular mechanisms of hemostasis and thrombosis can be separated, thereby raising the possibility of new antithrombotic therapeutic targets with reduced bleeding risk. We summarize some recently emerging examples of agents with antithrombotic activities that seem to spare hemostasis. Specific activities within each of the two major pathways leading to thrombus formation, from within the platelet and the coagulation system, give credence to the notion that physiologic hemostasis and pathologic thrombosis are mechanistically distinct and can be selectively inhibited. Targeting these differences may be the forerunning of a new generation of antithrombotic therapy. Among the less widely appreciated targets, we highlight the interaction between integrin αMβ2 (Mac-1, CD11b/CD18) on leukocytes and GPIbα on platelets that appears to distinguish thrombosis from hemostasis. This specific receptor: counter-receptor pairing not only emphasizes the role of leukocytes in thrombosis, but also identifies a novel interaction that could be targeted and might ultimately lead to a safer antithrombotic strategy.

PMID: 29467183 [PubMed - as supplied by publisher]




Somatic IL4R Mutations in Primary Mediastinal Large B-cell lymphoma lead to constitutive JAK-STAT signaling activation.
Related Articles

Somatic IL4R Mutations in Primary Mediastinal Large B-cell lymphoma lead to constitutive JAK-STAT signaling activation.

Blood. 2018 Feb 21;:

Authors: Viganò E, Gunawardana J, Mottok A, Van Tol T, Mak K, Chan FC, Chong L, Chavez E, Woolcock B, Takata K, Twa D, Shulha HP, Telenius A, Kutovaya O, Hung SS, Healy S, Ben-Neriah S, Leroy K, Gaulard P, Diepstra A, Kridel R, Savage KJ, Rimsza L, Gascoyne R, Steidl C

Abstract
Primary mediastinal large B cell lymphoma (PMBCL) is a distinct subtype of diffuse large B cell lymphoma thought to arise from thymic medullary B cells. Gene mutations underlying the molecular pathogenesis of the disease are incompletely characterized. Here, we describe novel somatic IL4R mutations in 15 out of 62 primary cases of PMBCL (24.2%) and in all PMBCL-derived cell lines tested. The majority of mutations (11/21; 52%) were hotspot single nucleotide variants in exon 8 leading to an I242N amino acid change in the transmembrane domain. Functional analyses establish this mutation as gain-of-function leading to constitutive activation of the JAK-STAT pathway and upregulation of downstream cytokine expression profiles and B cell specific antigens. Moreover, expression of I242N mutant IL4R in a mouse xenotransplantation model conferred growth advantage in vivo The pattern of concurrent mutations within the JAK-STAT signaling pathway suggests additive/synergistic effects of these gene mutations contributing to lymphomagenesis. Our data establish IL4R mutations as novel driver alterations and provide a strong preclinical rationale for therapeutic targeting of JAK-STAT signaling in PMBCL.

PMID: 29467182 [PubMed - as supplied by publisher]




In vivo thrombin generation and subsequent APC formation are increased in factor V Leiden carriers.
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In vivo thrombin generation and subsequent APC formation are increased in factor V Leiden carriers.

Blood. 2018 Feb 21;:

Authors: Rühl H, Winterhagen FI, Berens C, Müller J, Oldenburg J, Pötzsch B

PMID: 29467181 [PubMed - as supplied by publisher]