Nowotwory po przeszczepie nerki

Watorek, Ewa; Boratyńska, Maria; Smolska, Danuta; Patrzałek, D.; Klinger, Marian

doi:10.12659/aot.881859

Cited by 39 publications

(5 citation statements)

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“…Two months post-transplant her serum tested positive for anti-Fy a antibodies and a repeat biopsy at 3 months showed acute and C4d+ antibody-mediated rejection in the absence of HLA donor-specific antibodies (DSA). The authors concluded that the unfavorable outcome of her transplant is a result of the presence of antibodies to Fy a [21]. At the time of writing this paper, this is the only case report found linking the cause of kidney rejection to anti-Fy antibodies.…”

Section: Discussionmentioning

confidence: 86%

The Role of the Duffy Blood Group Antigens in Renal Transplantation and Rejection. A Mini Review

Hariri,

Bordas,

Elkins

et al. 2023

Transpl Int

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Finding a compatible donor for kidney transplant candidates requires overcoming immunological barriers such as human leukocyte antigens (HLA) compatibility and ABO compatibility. Emerging data suggest a role for red blood cell antigens (RCA) in renal transplant outcomes. The incidence of RCA alloimmunization is high in chronically transfused individuals, such as end stage renal disease patients, but whether antibodies to RCA can mediate renal graft rejection remains debatable. The Duffy blood group antigens (Fy) has been shown to be expressed in the kidney, among other tissues. There are some data to suggest that donor-recipient Fy mismatches may increase the risk for chronic allograft damage and that anti-Fy antibodies may be involved in renal graft rejection, however, while it is routine to screen renal transplant candidates for ABO antigens, detailed RCA phenotyping of the donor kidney is not routinely tested. In this paper, we review the current data on the role of Fy in renal transplantation and discuss the potential mechanisms of its biological function.

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Section: Discussionmentioning

confidence: 86%

The Role of the Duffy Blood Group Antigens in Renal Transplantation and Rejection. A Mini Review

Hariri,

Bordas,

Elkins

et al. 2023

Transpl Int

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“…Our results provide basic evidence that MMF use may prevent PTLD after transplants. In fact, previous studies have found that the use of MMF in transplant patients reduces the risk and incidence of PTLD ( 48 – 55 ) or, at least, does not increase the risk for PTLD ( 56 – 59 ). However, MMF increases the incidence of PTLD involving the central nerve system (CNS) ( 60 , 61 ).…”

Section: Discussionmentioning

confidence: 99%

Growth Transformation of B Cells by Epstein-Barr Virus Requires IMPDH2 Induction and Nucleolar Hypertrophy

et al. 2023

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EBV infections cause nucleolar enlargement via the induction of IMPDH2, which are essential for B cell growth transformation by EBV. Although the significance of IMPDH2 induction and nuclear hypertrophy in the tumorigenesis of glioblastoma has been reported, EBV infection brings about the change quickly by using its transcriptional cofactor, EBNA2, and MYC. Moreover, we present here, for the novel, basic evidence that an IMPDH2 inhibitor, namely, MPA or MMF, can be used for EBV-positive posttransplant lymphoproliferative disorder (PTLD).

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“…23,24 Indeed, while possibly showing a minor reduction of overall cancer incidence compared to other immunosuppressive regimens, Watorek et al have reported early occurrence of neoplastic disease, specifically urinary tract tumors and non-Hodgkin lymphoma, upon combination of MMF with tacrolimus and prednisone after renal transplantation. 25 This is of particular importance as the combination of MMF with tacrolimus is predicted to be synergistic by the explicit synlet network discussed later.…”

Section: Synthetic Lethal Interactions Between Pathways: Disease Asso...mentioning

confidence: 96%

Synthetic lethality for linking the mycophenolate mofetil mode of action with molecular disease and drug profiles

et al. 2012

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Systematic study of the effect of mycophenolate mofetil (MMF) on the molecular level in the context of other drugs and molecular disease profiles became possible due to the availability of large scale molecular profiles on both disease characterization and drug mode of action. Such analysis is of particular value in elucidating alternative drug use for addressing clinically unmet needs, and the concept of synthetic lethality provides an alternative tool for such repositioning strategies. Resting on consolidation of transcriptomics data and literature mining, a MMF molecular footprint became available including a set of 170 genes specifically affected by the drug. Analysis of this profile on a molecular pathway level reveals a set of 14 pathways as affected. Next to assignment of molecular pathways and associated diseases synergistic drug combinations are proposed by utilizing the synthetic lethal interaction network. Of particular interest is the combination of MMF with adenosine deaminase inhibitors, sulfasalazine, and other selected drugs interfering with calcium-based regulatory pathways and metabolism. Indeed analysis of drugs in clinical trials positively identifies combinations with MMF in the context of synthetic lethality and affected pathways, particularly in diseases such as multiple sclerosis, vasculitis, GVHD and lupus nephritis. Importantly, the synthetic lethal interaction of the drug mode of action is an interesting basis for rational repositioning strategies by suggesting combinations which exhibit a synergistic rather than a mere additive effect, as for example is evident for the combination of tacrolimus and MMF. Inherent is also the assessment of possible adverse effects of drug combinations.

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Nowotwory po przeszczepie nerki

Cited by 39 publications

References 0 publications

The Role of the Duffy Blood Group Antigens in Renal Transplantation and Rejection. A Mini Review

The Role of the Duffy Blood Group Antigens in Renal Transplantation and Rejection. A Mini Review

Growth Transformation of B Cells by Epstein-Barr Virus Requires IMPDH2 Induction and Nucleolar Hypertrophy

Synthetic lethality for linking the mycophenolate mofetil mode of action with molecular disease and drug profiles

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