Incidence and Long-Term Prognosis of Cancer After Kidney Transplantation

Mier, V. Pendón-Ruiz de; Cabello, M.D. Navarro; Vaquera, S. Martínez; Lopez-Andreu, M.; Morales, María Luisa Agüera; Rodríguez‐Benot, Alberto; García, Pedro Aljama

doi:10.1016/j.transproceed.2015.08.043

Cited by 22 publications

(12 citation statements)

References 16 publications

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“…The effect of calcineurin in colorectal cancer remains controversial, and calcineurin may act as both a tumor suppressor while also inducing oncogenic activity in colorectal cancer (26,38,39). Previous epidemiologic studies have reported the increased risk in the incidence of colorectal cancer among patients receiving calcineurin inhibitors as immunosuppressants, probably due to an impaired calcineurin-dependent tumor immunosurveillance (40,41). Moreover, a previous report suggested that FK506 promotes colorectal cancer cell line growth, although cyclosporin A inhibits the tumor growth independent of the calcineurin pathway (38).…”

Section: Discussionmentioning

confidence: 99%

The Tissue-Reconstructing Ability of Colon CSCs Is Enhanced by FK506 and Suppressed by GSK3 Inhibition

Ishida

Koyanagi-Aoi

Oshima

et al. 2017

Molecular Cancer Research

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Cancer stem cells (CSC) are capable of reconstructing cancer tissues, are involved in both recurrence and metastasis, and contribute to therapeutic resistance. Therefore, elucidating the molecular mechanism in CSCs is important to successfully treat unresectable cancers. Previously, we observed that colon cancer stem-like cells can be induced from human colon cancer cell lines by retrovirally introducing OCT3/4, SOX2, and KLF4, and we have designated such cells as induced cancer stem cells (iCSC). In the current study, we used iCSCs to evaluate the molecular mechanism of colon CSCs and developed new methods to control them. The spheres that were derived in vitro from the iCSCs, but not those from parental cells, mimicked human colon cancer tissues in terms of their immunohistologic patterns; therefore, sphere-forming ability was assessed as a measure of the tissuereconstructing ability of iCSCs. Interestingly, the calcineurin inhibitor FK506 enhanced the sphere-forming ability of iCSCs, whereas GSK3 inhibition by RNAi, CHIR99021, and valproic acid (VPA) impeded the sphere-forming ability and expansion of iCSCs. FK506 and GSK3 inhibition showed the opposite effect regarding the NFATc3 localization of iCSCs. These data reveal the crucial role that NFAT localization, as regulated by calcineurin and GSK3, plays in the tissue-reconstructing ability of colon cancer stem cells and the potential of GSK3 inhibitors, such as VPA, in colon cancer stem cell-targeting therapy.

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Section: Discussionmentioning

confidence: 99%

The Tissue-Reconstructing Ability of Colon CSCs Is Enhanced by FK506 and Suppressed by GSK3 Inhibition

Ishida

Koyanagi-Aoi

Oshima

et al. 2017

Molecular Cancer Research

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“…NMSC is also a significant challenge in posttransplant management, estimated to affect between 6% and 7.5% of kidney transplant patients within 10 years [6, 10]. More than 90% of NMSC lesions are basal cell carcinomas (BCC) or squamous cell carcinomas (SCC) [61], with kidney transplant patients experiencing a 10-fold and 100-fold increase in risk for BCC and SCC, respectively, compared to the general population [62].…”

Section: Kidney Transplantationmentioning

confidence: 99%

“…CNI therapy has been shown to increase the risk of malignancy after kidney [8–10], liver [11], and heart [12–14] transplantation in a dose-dependent manner. It is unclear how much of this effect is due to high intensity of immunosuppression under CNI therapy or to specific CNI-related effects which promote oncogenesis, such as stimulation of transforming growth factor beta (TGF- β ) [8] and increased production of proangiogenic vascular endothelial growth factor (VEGF) [15].…”

Section: Introductionmentioning

confidence: 99%

Everolimus and Malignancy after Solid Organ Transplantation: A Clinical Update

Holdaas

Simone

Zuckermann

2016

Journal of Transplantation

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Malignancy after solid organ transplantation remains a major cause of posttransplant mortality. The mammalian target of rapamycin (mTOR) inhibitor class of immunosuppressants exerts various antioncogenic effects, and the mTOR inhibitor everolimus is licensed for the treatment of several solid cancers. In kidney transplantation, evidence from registry studies indicates a lower rate of de novo malignancy under mTOR inhibition, with some potentially supportive data from randomized trials of everolimus. Case reports and small single-center series have suggested that switch to everolimus may be beneficial following diagnosis of posttransplant malignancy, particularly for Kaposi's sarcoma and nonmelanoma skin cancer, but prospective studies are lacking. A systematic review has shown mTOR inhibition to be associated with a significantly lower rate of hepatocellular carcinoma (HCC) recurrence versus standard calcineurin inhibitor therapy. One meta-analysis has concluded that patients with nontransplant HCC experience a low but significant survival benefit under everolimus monotherapy, so far unconfirmed in a transplant population. Data are limited in heart transplantation, although observational data and case reports have indicated that introduction of everolimus is helpful in reducing the recurrence of skin cancers. Overall, it can be concluded that, in certain settings, everolimus appears a promising option to lessen the toll of posttransplant malignancy.

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“…Most of them are de novo malignancies rather than those recurrent of pre-transplant malignancy, or donor-derived tumors. Th e incidence of cancer is increased by the duration of immunosuppressive therapy and use of steroids [5][6][7][8][9][10][11][12][13][14]. Despite the developing malignancy does not aff ect graft survival, the reduction of malignancy risk among transplant patients is very important since they experience worse outcomes with increased cancer-related mortality.…”

Section: Resultsmentioning

confidence: 99%

“…Despite the developing malignancy does not aff ect graft survival, the reduction of malignancy risk among transplant patients is very important since they experience worse outcomes with increased cancer-related mortality. Th is may be achieved by using immunosuppressive drugs with antitumor eff ects or adopting low-level immunosuppression as well as regular cancer screening of the transplanted patients [1,9,15]. Specifi c cancer prevention, screening and treatment programs for people with solid organ transplantation are highly recommended [4,13].…”

Section: Resultsmentioning

confidence: 99%

Synchronous skin squamous cell carcinoma and papillary thyroid carcinoma after renal transplantation: a case report

Hamdy¹,

Raafat²,

Abouzid³

et al. 2018

CTT

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Secondary malignancies following renal transplantation are not an uncommon event. In this report we considered one of the causes of posttransplant mortality. We report a renal transplant case and immune suppression treatment followed 11 years later by synchronous skin squamous cell carcinoma and papillary thyroid carcinoma that was diagnosed, presented and managed at the Oncology Center at Mansoura University.

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Incidence and Long-Term Prognosis of Cancer After Kidney Transplantation

Cited by 22 publications

References 16 publications

The Tissue-Reconstructing Ability of Colon CSCs Is Enhanced by FK506 and Suppressed by GSK3 Inhibition

The Tissue-Reconstructing Ability of Colon CSCs Is Enhanced by FK506 and Suppressed by GSK3 Inhibition

Everolimus and Malignancy after Solid Organ Transplantation: A Clinical Update

Synchronous skin squamous cell carcinoma and papillary thyroid carcinoma after renal transplantation: a case report

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