Variant morphology and random chromosomal integration of BK polyomavirus in posttransplant urothelial carcinomas

Bertz, Simone; Ensser, Armin; Stoehr, Robert; Eckstein, Markus; Apel, Hendrik; Mayr, Doris; Buettner-Herold, Maike; Gaisa, Nadine T.; Compérat, Éva; Wullich, Bernd; Hartmann, Arndt; Knöll, Antje

doi:10.1038/s41379-020-0489-0

Cited by 13 publications

(14 citation statements)

References 56 publications

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“…Many recent studies detected BKPyV gene integration in urinary tract epithelial cell tumors, providing further evidence for the correlation between BKPyV and urinary tract tumors [8,[12][13][14][15][16][17]. Interestingly, almost all of these integrations occurred in post-transplant tumors, but not in non-transplant tumors [17].…”

Section: Introductionmentioning

confidence: 79%

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Zeng

Sun²,

Bao

et al. 2020

Preprint

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Background: Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. Methods: We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results: Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. Conclusions: We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

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Section: Introductionmentioning

confidence: 79%

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Zeng

Sun²,

Bao

et al. 2020

Preprint

View full text Add to dashboard Cite

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“…All of these were samples of high-grade tumors from transplant recipients (four KTR and one heart transplant recipient) and two were micropapillary subtype tumors in KTR. 28 Despite the growing evidence of BKV large T antigen inclusion within tumor tissue detected by SV40 staining; the exact mechanism of oncogenesis remains uncertain. The BKV genome has three functional regions, the early region, the non-coding region, and the late region.…”

Section: Discussionmentioning

confidence: 99%

High grade urothelial carcinoma in kidney transplant patients with a history of BK viremia – Just a coincidence?

Cannon,

Ntala,

Joss

et al. 2023

Clinical Transplantation

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IntroductionKidney transplant recipients (KTR) have a three‐to‐four‐fold increased risk of developing urothelial carcinoma (UC) compared to the general population. BK polyoma virus (BKV) infection is known to affect approximately 15% of KTR. In vitro models support a potential pathogenic role for BKV in the development of UC. We describe a series of UC in kidney transplant recipients.MethodsElectronic patient records were searched to identify KTR with UC who had undergone kidney only or simultaneous kidney and pancreas transplantation in a single UK center between 2009 and 2015. Where available, stored pathological samples were retrieved, re‐examined and stained for SV40 as a marker of BKV using standard staining protocols for kidney biopsy samples.ResultsFourteen KTR had developed UC post‐transplant. Of these, 10 KTR had a history of BKV infection post‐transplant. Six of these 10 KTR developed a rare micropapillary tumor subtype of UC which is typically only found in <1% of UC cases. All six micropapillary tumor samples stained positive for SV40, including samples from metastases. Three tumor samples were available from the four KTR with no history of BKV infection and were not micropapillary subtype and were negative for SV40. Three micropapillary tumors from immunocompetent patients were examined as controls and were negative for SV40.ConclusionsThese findings would support a pathogenic role for BK virus in the development of rare micropapillary subtype urothelial tumors in the kidney transplant population.

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“…Many recent studies detected BKPyV gene integration in urinary tract epithelial cell tumors, providing further evidence for the correlation between BKPyV and urinary tract tumors [ 8 , 12 – 17 ]. Interestingly, almost all of these integrations occurred in post-transplant tumors, but not in non-transplant tumors [ 17 ]. Therefore, BKPyV reactivation in immunosuppressed environments may be considered as a transforming factor leading to urothelial carcinomas.…”

Section: Introductionmentioning

confidence: 90%

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Zeng

Sun

Bao

et al. 2020

Virol J

View full text Add to dashboard Cite

Background Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. Methods We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. Conclusions We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

show abstract

Variant morphology and random chromosomal integration of BK polyomavirus in posttransplant urothelial carcinomas

Cited by 13 publications

References 56 publications

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

High grade urothelial carcinoma in kidney transplant patients with a history of BK viremia – Just a coincidence?

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

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