Kaposi’s sarcoma following living donor kidney transplantation: review of 7,939 recipients

Einollahi, Behzad; Lessan‐Pezeshki, Mahboob; Nourbala, Mohammad Hossein; Simforoosh, N.; Pourfarziani, Vahid; Nemati, Eghlim; Nafar, Mohsen; Basiri, Abbas; Pour-Reza-Gholi, Fatemeh; Firoozan, Ahmad; Ghadiani, Mohammad Hassan; Makhdoomi, Khadijeh; Ghafari, A.; Pedram, Ahmadpour; Oliaei, Farshid; Ardalan, Mohammadreza; Makhlogh, A; Samimagham, Hamid Reza; Azmandian, Jalal

doi:10.1007/s11255-008-9483-z

Cited by 23 publications

(28 citation statements)

References 17 publications

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“…Kaposi’s sarcoma–associated herpesvirus (KSHV) is one of the most common etiologic agents for cancers, including primary effusion lymphoma (PEL) and Kaposi’s sarcoma (KS), arising preferentially in the setting of HIV infection [1], [2] or organ transplantation [3], [4]. Despite the reduced incidence of KS during antiretroviral therapy (ART), KS remains the most common AIDS-associated tumor worldwide [5] and continues to incur significant morbidity and mortality for these patients [1], [2].…”

Section: Introductionmentioning

confidence: 99%

Sphingosine Kinase-2 Maintains Viral Latency and Survival for KSHV-Infected Endothelial Cells

et al. 2014

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Phosphorylation of sphingosine by sphingosine kinases (SphK1 and SphK2) generates sphingosine-1-phosphate (S1P), a bioactive sphingolipid which promotes cancer cell survival and tumor progression in vivo. We have recently reported that targeting SphK2 induces apoptosis for human primary effusion lymphoma (PEL) cell lines infected by the Kaposi’s sarcoma-associated herpesvirus (KSHV), and this occurs in part through inhibition of canonical NF-κB activation. In contrast, pharmacologic inhibition of SphK2 has minimal impact for uninfected B-cell lines or circulating human B cells from healthy donors. Therefore, we designed additional studies employing primary human endothelial cells to explore mechanisms responsible for the selective death observed for KSHV-infected cells during SphK2 targeting. Using RNA interference and a clinically relevant pharmacologic approach, we have found that targeting SphK2 induces apoptosis selectively for KSHV-infected endothelial cells through induction of viral lytic gene expression. Moreover, this effect occurs through repression of KSHV-microRNAs regulating viral latency and signal transduction, including miR-K12-1 which targets IκBα to facilitate activation of NF-κB, and ectopic expression of miR-K12-1 restores NF-κB activation and viability for KSHV-infected endothelial cells during SphK2 inhibition. These data illuminate a novel survival mechanism and potential therapeutic target for KSHV-infected endothelial cells: SphK2-associated maintenance of viral latency.

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Section: Introductionmentioning

confidence: 99%

Sphingosine Kinase-2 Maintains Viral Latency and Survival for KSHV-Infected Endothelial Cells

et al. 2014

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“…8 In a different study, excessive reduction or withdrawal of immunosuppression after the development of Kaposi sarcoma yielded to a statistically significantly increased risk of graft loss. 9 Similarly, in an observational study, 2 of 11 patients with nonmetastatic cancer lost their grafts due to chronic rejection after conversion to sirolimus. 10 On the other hand, escalation of immunosuppressive drug dose after rejection enhances the relapse of the primary tumor.…”

Section: Discussionmentioning

confidence: 99%

Untitled

Okut

Alp²,

Tatar³

et al. 2017

Exp Clin Transplant

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Objectives: We evaluated patients with nonmelanoma skin cancer after kidney transplant and the effects of immunosuppression reduction and switching to a mammalian target of rapamycin inhibitor drugs. Materials and Methods: Kidney transplant recipients were evaluated retrospectively from patient medical records (between January 2000 and December 2014). A 30% increase in serum creatinine was accepted as indicating renal failure progression. Results: Of 18 patients included (mean follow-up 98 ± 66 mo), 7 (38.8%) had squamous cell carcinoma, 7 (38.8%) had Kaposi sarcoma, and 4 (22.2%) had basal cell carcinoma. At cancer diagnosis, average serum creatinine was 1.6 ± 0.7 mg/dL and proteinuria was 410 ± 766 mg/d. Immunosuppression regimen was changed in 15 patients (83.3%), with new regimen being a single-drug (only prednisolone) in 4 patients, double-drug in 6 patients, and triple-drug protocol in 8 patients. Eight patients were switched to a mammalian target of rapamycin inhibitor-based double (4 patients) or triple (4 patients) regimen. During follow-up after starting new treatment (average 46 ± 50 mo), 6 patients (33.3%) had progressive kidney failure (0 were receiving triple regimen). Those that progressed were using mammalian target of rapamycin inhibitor-based drugs relatively less (33% vs 50%), although often receiving a single-drug immunosuppression treatment (50% vs 8.3%). Three patients (33.3%) had acute rejection (2 receiving double and 1 receiving single immunosuppression treatment). Five patients (27.7%) had local recurrence of the primary tumor. Mammalian target of rapamycin inhibitor use was relatively less common in patients with tumor relapse (20% vs 46%). One patient died (heart failure), and 1 with chronic rejection returned to dialysis. Conclusions: Mammalian target of rapamycin inhibitorbased drugs could reduce local recurrence rate in kidney transplant recipients with nonmelanoma skin cancers. Aggressive reduction and/or cessation of immunosuppressive drugs after skin cancer can lead to graft rejection.

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“…If the tumor size does not diminish, the dosage should be further reduced or withdrawn. 10 Unfortunately, about half of all kidney transplant patients experience irreversible rejection and allograft function loss owing to this adjustment. Renal transplant recipients could return to dialysis if their allografts' functioning fails; however, graft loss is deadly for liver transplant recipients, and agent modulation should be considered cautiously.…”

Section: Discussionmentioning

confidence: 99%

Kaposi Sarcoma of the Ureter After Liver Transplant: Case Report and Literature Review

Chen

Zhao

Qiu³

et al. 2012

Exp Clin Transplant

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Kaposi sarcoma after an organ transplant is rare and infrequently involves internal organs. There are 2 reported cases in the English literature of Kaposi sarcoma originating from the transplant ureter after kidney transplant. We report a case of Kaposi sarcoma that occurred in the native ureter of the liver transplant recipient. Initially, the patient refused any further investigation and management and 2 years subsequent, had to undergo a left radical nephroureterectomy owing to the loss of renal function and distending pain. He recovered very well and no recurrence was detected at 47 months' follow-up. To our knowledge, it is the first report in English. We review the literature on this topic and explore the therapeutic principles and histologic features of this sarcoma.

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Kaposi’s sarcoma following living donor kidney transplantation: review of 7,939 recipients

Abstract: The high incidence of KS in this large population studied, as compared to that reported in other transplant patient groups, suggests that genetic predisposition may play a pathogenetic role.

Cited by 23 publications

References 17 publications

Sphingosine Kinase-2 Maintains Viral Latency and Survival for KSHV-Infected Endothelial Cells

Sphingosine Kinase-2 Maintains Viral Latency and Survival for KSHV-Infected Endothelial Cells

Untitled

Kaposi Sarcoma of the Ureter After Liver Transplant: Case Report and Literature Review

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