What we know and mostly do not know about bronchiolitis obliterans syndrome

Martin, Paul J.; Chien, Jason W.

doi:10.1038/bmt.2011.38

Cited by 13 publications

(8 citation statements)

References 17 publications

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“…Relative risk was defined as Relative risk=(proportion of plants with tumors in antagonist treatment)/(proportion of plants with tumors in water treatment). Meta-analyses were performed using EZR (10), which is a graphical user interface for R (The R Foundation for Statistical Computing, version 2.14.0). The tumor formation ratio was defined as Tumor formation ratio=100×(total number of tumors in antagonist treatment)/(total number of tumors in water treatment).…”

Section: Methodsmentioning

confidence: 99%

Biological Control of Crown Gall on Grapevine and Root Colonization by Nonpathogenic <i>Rhizobium vitis</i> Strain ARK-1

Kawaguchi¹

2013

Microb. Environ.

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A nonpathogenic strain of Rhizobium vitis ARK-1 was tested as a biological control agent for grapevine crown gall. When grapevine roots were soaked in a cell suspension of strain ARK-1 before planting in the field, the number of plants with tumors was reduced. The results from seven field trials from 2009 to 2012 were combined in a meta-analysis. The integrated relative risk after treatment with ARK-1 was 0.15 (95% confidence interval: 0.07–0.29, P<0.001), indicating that the disease incidence was significantly reduced by ARK-1. In addition, the results from four field trials from 2007 to 2009 using R. vitis VAR03-1, a previously reported biological control agent for grapevine crown gall, were combined in a meta-analysis. The integrated relative risk after treatment with VAR03-1 was 0.24 (95% confidence interval: 0.11–0.53, P<0.001), indicating the superiority of ARK-1 in inhibiting grapevine crown gall over VAR03-1 under field conditions. ARK-1 did not cause necrosis on grapevine shoot explants. ARK-1 established populations on roots of grapevine tree rootstock and persisted inside roots for two years.

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Section: Methodsmentioning

confidence: 99%

Biological Control of Crown Gall on Grapevine and Root Colonization by Nonpathogenic <i>Rhizobium vitis</i> Strain ARK-1

Kawaguchi¹

2013

Microb. Environ.

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“…In each scenario, collagen deposition and the development of fibrosis either in the peri-bronchiolar (OLD) or interstitial (RLD) space contribute to the resultant patterns of lung dysfunction (283). The complex pathophysiology that characterizes lung fibrosis after HCT is poorly understood and represents the most significant gap in current knowledge for this spectrum of chronic GVHD (20, 289, 290). This limitation stems from the lack of correlative data obtained from afflicted HCT recipients, and the paucity of suitable HCT animal models for either the restrictive or the obstructive form of chronic lung injury.…”

Section: A Three Phase Model For Chronic Gvhd Biologymentioning

confidence: 99%

The Biology of Chronic Graft-versus-Host Disease: A Task Force Report from the National Institutes of Health Consensus Development Project on Criteria for Clinical Trials in Chronic Graft-versus-Host Disease

Cooke

Luznik

Sarantopoulos

et al. 2017

Biology of Blood and Marrow Transplantation

364

322

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Summary Chronic graft-versus-host disease (GVHD) is the leading cause of late, non-relapse, mortality and disability in allogeneic hematopoietic cell transplantation (HCT) patients and a major obstacle to improving outcomes. Chronic GVHD biology remains enigmatic, but understanding the underpinnings of the immunologic mechanisms responsible for the initiation and progression of disease is fundamental to developing effective prevention and treatment strategies. The goals of this task force review are as follows: Summarize the current “state-of-the-science” regarding pathogenic mechanisms of chronic GVHD and critical knowledge gaps.Develop working hypotheses/overriding concepts for chronic GVHD development.Define the usefulness of current preclinical models to test working hypotheses and ultimately discover and develop new therapeutic strategies.Identify shortcomings of preclinical models, and define criteria for the creation of additional models to address these limitations. This document is intended as a review of our understanding of chronic GVHD biology and therapies resulting from preclinical studies, and as a platform for developing innovative clinical strategies to prevent and treat chronic GVHD.

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“…4,5 Although alternative treatments such as azithromycin, montelukast, imatinib and extracorporeal photopheresis may in some cases reverse or halt the progressive decline in lung function in cGVHD/BOS, the response to pharmacological therapy is uncertain and often disappointing and results have not improved over the past 20 years. [6][7][8][9] Lung transplantation (LTx) could be a therapeutic option for selected patients developing severe lung dysfunction in the course of cGVHD/BOS, and several case reports have been published. [10][11][12][13] According to the registry of the International Society of Heart and Lung Transplantation (ISHLT), in the period from 1995 to 2010, 1% of all LTx were performed due to obliterative bronchiolitis (retransplants excluded), 14 but the proportion of these that have previously had a hematopoietic SCT is not registered (Edwards L, ISHLT, personal communication).…”

Section: Introductionmentioning

confidence: 99%