Mannose binding lectin and ficolin‐2 polymorphisms are associated with increased risk for bacterial infections in children with B acute lymphoblastic leukemia

Pana, Zoe Dorothea; Samarah, Fekri; Papi, Rigini; Antachopoulos, Charalampos; Papageorgiou, Theodotis; Farmaki, Evangelia; Hatzipantelis, Emmanuel; Tragiannidis, Athanasios; Vavatsi-Christaki, Norma; Kyriakidis, Dimitrios A.; Athanassiadou-Piperopoulou, Fani; Roilides, Emmanuel

doi:10.1002/pbc.24951

Cited by 17 publications

(17 citation statements)

References 44 publications

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“…Among these are mannose-binding lectin (MBL2), ficolin, TLR-4 (135,145) and NOD2 (220). Much research has been done for MBL but the evidence for effects of MBL deficiency remains conflicting (7,46,55,62,101,105,116,139,142). Similar conflicting results has been obtained for ficolin deficiency as a risk factor (142,161) (101).…”

Section: Cim Diagnosis and Biomarkers Supported By Animal Modelsmentioning

confidence: 99%

“…Much research has been done for MBL but the evidence for effects of MBL deficiency remains conflicting (7,46,55,62,101,105,116,139,142). Similar conflicting results has been obtained for ficolin deficiency as a risk factor (142,161) (101). It is perhaps unlikely that any single biomarker can effectively identify patients at increased risk and animal models may help validate and guide the selection of relevant soluble factors and gene polymorphisms but also study effects of interacting factors such as age, underlying diagnosis and treatment regimen.…”

Section: Cim Diagnosis and Biomarkers Supported By Animal Modelsmentioning

confidence: 99%

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Animal models of chemotherapy-induced mucositis: translational relevance and challenges

Sangild

Shen

Pontoppidan

et al. 2018

American Journal of Physiology-Gastrointestinal and Liver Physi

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Chemotherapy for cancer patients induces damaging tissue reactions along the epithelium of the gastrointestinal tract (GIT). This chemotherapy-induced mucositis (CIM) is a serious side effect of cytotoxic drugs, and several animal models of CIM have been developed, mainly in rodents and piglets, to help understand the progression of CIM and how to prevent it. Animal models allow highly controlled experimental conditions, detailed organ (e.g., GIT) insights, standardized, clinically relevant treatment regimens, and discovery of new biomarkers. Still, surprisingly few results from animal models have been translated into clinical CIM management and treatments. The results obtained from specific animal models can be difficult to translate to the diverse range of CIM manifestations in patients, which vary according to the antineoplastic drugs, dose, underlying (cancer) disease, and patient characteristics (e.g., age, genetics, and body constitution). Another factor that hinders the direct use of results from animals is inadequate collaboration between basic science and clinical science in relation to CIM. Here, we briefly describe CIM pathophysiology, particularly the basic knowledge that has been obtained from CIM animal models. These model studies have indicated potential new preventive and ameliorating interventions, including supplementation with natural bioactive diets (e.g., milk fractions, colostrum, and plant extracts), nutrients (e.g., polyunsaturated fatty acids, short-chain fatty acids, and glutamine), and growth factor peptides (e.g., transforming growth factor and glucagon-like peptide-2), as well as manipulations of the gut microbiota (e.g., prebiotics, probiotics, and antibiotics). Rodent CIM models allow well-controlled, in-depth studies of animals with or without tumors while pig models more easily make clinically relevant treatment regimens possible. In synergy, animal models of CIM provide the basic physiological understanding and the new ideas for treatment that are required to make competent decisions in clinical practice.

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Section: Cim Diagnosis and Biomarkers Supported By Animal Modelsmentioning

confidence: 99%

Section: Cim Diagnosis and Biomarkers Supported By Animal Modelsmentioning

confidence: 99%

Animal models of chemotherapy-induced mucositis: translational relevance and challenges

Sangild

Shen

Pontoppidan

et al. 2018

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Despite improvements in anticancer therapy resulting in increased survival rates, infections remain the most important cause of treatment-related deaths in pediatric oncology (Alexander et al, 2012) and the second most common reason for unplanned hospital admission (Basu et al, 2005). Several studies have correlated MBL-deficiency to an increased risk for febrile neutropenia (FN) (Hartel et al, 2007;Pana et al, 2014;Schlapbach et al, 2007;Viscoli and Castagnola, 2002), while subsequent studies could not reproduce these findings (Frakking et al, 2006(Frakking et al, , 2011. Both duration and severity of FN were increased in MBL-deficient children and adults (Mullighan et al, 2002;Neth et al, 2001;Peterslund et al, 2001).…”

Section: Pediatric Oncology Patientsmentioning

confidence: 97%

Restoration of MBL-deficiency: Redefining the safety, efficacy and viability of MBL-substitution therapy

Keizer

Wouters

Schlapbach

et al. 2014

Molecular Immunology

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“…In addition, adhesives, coating, and floor covering, which are used in decoration, release toxic substances, such as formaldehyde, lead, and benzene, which severely damage the hemopoietic system of the human body. This is an important cause leading to a high incidence of childhood leukemia over the past few years Pana et al, 2014;Petersen et al, 2014). The VDLD therapeutic regime that has been used clinically is the first-line approach for treatment of A-BLL.…”

Section: Discussionmentioning

confidence: 99%

Effect of Bcl-2-siRNA on proliferation and apoptosis of pediatric acute B lymphoblastic leukemia (A-BLL) cells

2015

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ABSTRACT. This study analyzed the effect of small interfering RNA specific for the Bcl-2 gene (siRNA Bcl-2) on the proliferation and chemotherapeutic sensitivity of pediatric A-BLL cells. Marrow samples were obtained from sixty newly-diagnosed A-BLL pediatric patients. The Bcl-2 mRNA expression in these samples was quantified by real time polymerase chain reaction. The Bcl-2 mRNA re-expression was analyzed by RNA interference using Bcl-2-siRNA. Cellular proliferation was detected using the MTT (Thiazolyl Blue Tetrazolium Bromide) assay. The cell apoptosis was quantified by flow cytometry. The Bcl-2 mRNA expression was significantly higher in the drug-resistance group than in the chemotherapy sensitivity group prior to chemotherapy (P < 0.05). In addition, the Bcl-2 mRNA expression in the chemotherapy sensitivity group was significantly higher before chemotherapy than that after chemotherapy (P < 0.05). The Bcl-2 mRNA expression significantly decreased in the leukemic cells of the Bcl-2-siRNA

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Mannose binding lectin and ficolin‐2 polymorphisms are associated with increased risk for bacterial infections in children with B acute lymphoblastic leukemia

Abstract: MBL2 and FCN2 single or combined deficiencies are associated with increased duration of FN episodes as well as increased number of bacterial infections in children with B-ALL suggesting a prognostic role of these genes.

Cited by 17 publications

References 44 publications

Animal models of chemotherapy-induced mucositis: translational relevance and challenges

Animal models of chemotherapy-induced mucositis: translational relevance and challenges

Restoration of MBL-deficiency: Redefining the safety, efficacy and viability of MBL-substitution therapy

Effect of Bcl-2-siRNA on proliferation and apoptosis of pediatric acute B lymphoblastic leukemia (A-BLL) cells

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