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DISEASE of the MONTH J Am Soc Nephrol 15: 1582–1588, 2004 EBERHARD RITZ, FEATURE EDITOR

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DISEASE of the MONTH J Am Soc Nephrol 15: 1582–1588, 2004 EBERHARD RITZ, FEATURE EDITOR DISEASE OF THE MONTH J Am Soc Nephrol 15: 1582–1588, 2004 EBERHARD RITZ, FEATURE EDITOR Malignancy in Renal Transplantation CHRISTIAN MORATH,* MARTINA MUELLER,† HARTMUT GOLDSCHMIDT,‡ VEDAT SCHWENGER,* GERHARD OPELZ,§ and MARTIN ZEIER* Departments of *Nephrology, †Gastroenterology, ‡Hematology/Oncology, and §Transplant Immunology, University of Heidelberg, Heidelberg, Germany. An increased incidence of malignant tumors in transplant (10). Among other factors, duration and intensity of immuno- recipients was recognized as early as in the 1970s, and this suppression emerged as a particularly powerful risk factor (10). effect was ascribed to the administration of immunosuppres- Incidence and type of cancer after renal transplantation vary sive medication (1,2). In the early days of transplantation between centers, countries, and time periods (11). Some of this medicine, however, the clinician faced fulminant acute rejec- variation is accounted for by the impact of competing causes of tion episodes and severe infections; malignancy after trans- death. For instance, according to a report from the Glasgow plantation represented only a minor problem. With longer graft transplant program, during the first 14 yr of the program (1969 survival and older donors (as well as recipients) and with the to 1982), 40% of patient deaths were attributed to infection, introduction of more potent immunosuppressive medication, 23% to cardiovascular disease, and 10% to malignancies. Dur- malignancy represents a major burden in transplantation med- ing the subsequent 14 yr, deaths resulting from infection de- icine. The overall incidence of malignancy after renal trans- creased substantially, and the relative and absolute frequency plantation has been reported as being 3 to 5 times higher of death from cardiovascular disease and malignancy increased compared with the general population (3,4). However, an in- concomitantly (9,11). creased frequency is not found for all types of cancer (Figure In single-center reports from Glasgow and Leiden, death due 1). According to the Cincinnati Transplant Tumor Registry and to malignancy was found in 15% and 14% of kidney graft other reports, the most frequent types of tumors are posttrans- recipients, respectively (9,12). In contrast, only 2.6% of renal plant lymphoproliferative disorder (PTLD) and squamous cell allograft recipients in Japan were reported to have developed a carcinoma (lip, cervix, vulva, skin) (5,6). malignancy between 1970 and 1995 (13). Epidemiology Pathogenesis Many retrospective analyses do not adequately reflect the Malignancy after transplantation can develop in three different magnitude of the problem (3,5). The cumulative prevalence of ways: malignancy increases with the duration of follow-up. After 10 • yr, the risk of cancer in transplant patients was recently re- De novo occurrence in the recipient • ported as being 13.8-fold higher in transplant recipients than in Recurrent malignancy in the recipient • the background population (7). When patients on hemodialysis Transmission of malignancy from the donor were compared with transplanted patients, the risk of develop- ing cancer was 10 times higher in the latter group (8,9). The De Novo Occurrence of Malignancy in the progressive increase with time of observation is impressively Recipient illustrated by the Australian experience. In this high-risk set- Immunosuppression and Malignant Transformation ting of fair-skinned individuals with intense exposure to sun- In renal transplant recipients, the frequency of two types of light, the cumulative incidence of skin cancer, calculated by malignancies stands out: skin cancer and lymphoproliferative life-table analysis, increases progressively from 7% after 1 yr, disease. The spectrum for the latter ranges from benign PTLD to 45% after 11 yr, and 70% after 20 yr of immunosuppression to non-Hodgkin lymphoma (NHL). Evaluation of the literature on PTLD is complicated by the fact that reports commonly include cases with polyclonal proliferation as well as mono- clonal lymphoproliferative disorders. According to the litera- Correspondence to Dr. Christian Morath, Department of Nephrology, Univer- ture, malignancies of the lymphoproliferative system occur sity of Heidelberg, Bergheimerstr. 56 a, 69 115 Heidelberg, Germany. Phone: 49-6221-9112-0; Fax: 49-6221-9112-79; E-mail: christian_morath@med. mostly within the first three yr after renal transplantation. The uni-heidelberg.de high overall risk of malignancy in heavily immunosuppressed 1046-6673/1506-1582 patients is primarily due to the development of NHL. It has Journal of the American Society of Nephrology been claimed that the introduction of new and more potent Copyright © 2004 by the American Society of Nephrology immunosuppressive regimens is associated with an increased DOI: 10.1097/01.ASN.0000126194.77004.9B incidence of cancer after renal transplantation (14), but this J Am Soc Nephrol 15: 1582–1588, 2004 Malignancy and Immunosuppression — A Historical Perspective 1583 dimers, leading to inactivation of the tumor suppressor gene p53. Malignant proliferation is thought to be a result of the failure to repair such mutations. The relationship between tumorigenesis and immunosup- pression is not fully understood. The following points are of interest with respect to the pathogenesis of posttransplant ma- lignancies. Natural killer cells play an important role in the host’s defense against malignancy (27). Depletion of natural killer cells (NK-1.1) in mice increased the implantation and growth of B16 melanoma cells or CT 38 colon carcinoma cells (28). After injecting colonic carcinoma cells into the superior Figure 1. Ratio observed/expected malignancies in graft recipients (76). mesenteric vein of syngenic mice, injection of natural killer cells together with interferon-␥ reduced the tumor cell burden in the liver (29). The administration of anti-T cell antibodies, statement is not supported by solid epidemiologic evidence. e.g., anti-Thy 1.2 or anti-asialo GM-1, was associated with There are conflicting reports on whether the introduction of increased tumor colonization (30). However, this was not true cyclosporine was followed by a higher frequency of malignant for all immunomodulatory antibodies. For instance, anti-CD4 tumors (15,16). It has also been reported that malignancies are monoclonal antibody (keliximab) did not interfere with the more frequent in patients on triple drug regimens that include immune response against malignant cells in mice (30). The cyclosporine, azathioprine, and corticosteroids (17). There is recently introduced immunosuppressive agent rapamycine little dispute that the development of lymphomas is particularly (Sirolimus) is believed to combine immunosuppressive action increased in patients receiving polyclonal or monoclonal anti- with antitumor effects (31). bodies for induction or rescue therapy. This is true for recipi- These clinical and experimental observations are compatible ents of both renal and cardiac allografts (18). In an analysis of with the notion that the increased frequency of malignancies in the United Network of Organ Sharing (UNOS), the risk of allograft recipients results mainly from immunosuppression. malignancy was particularly high in patients who received a But this simple concept does not explain that the excess tumor combination of monoclonal antibodies, tacrolimus, and myco- incidence in kidney recipients is restricted to certain malignan- phenolate mofetil. In patients receiving this immunosuppres- cies, such as skin tumors and lymphoma. It would therefore sive regimen the overall risk of any type of cancer compared appear that immunosuppression alone is not sufficient for with the matched background population was increased by a tumor development: additional risk factors, such as the pa- factor of 5.11, and the risk of PTLD (with the above reserva- tient’s genetic background, viral co-infection, or sun exposure tions) was higher by a factor of 27.2 (19). apparently play also a role (Table 1). The hypothesis that the action of immunosuppressive drugs is responsible for the increased incidence of tumors in trans- Conventional Risk Factors plant recipients is supported by the observation that patients Commonly known risk factors such as advanced age, ciga- also develop tumors if they receive immunosuppressive ther- rette smoking (32), and analgesic abuse (33) are risk factors for apy for conditions other than transplantation, e.g., rheumatoid posttransplant malignancies as well. For instance, in patients arthritis, systemic lupus erythematodes (SLE), or dermatomy- with a history of phenacetin abuse, the risk of developing ositis. An increased frequency of lymphoproliferative disease uroepithelial carcinoma is strikingly increased (34). This ob- in these patients has been attributed to the administration of servation even led to the postulate that nephroureterectomy immunosuppressive agents, such as methotrexate, cyclospor- should be performed before transplantation. ine, or azathioprine (20–22). A relationship between the intensity of immunosuppression Genetic Factors and an increased incidence of tumors has been shown most Genetic factors are known to predispose to the development convincingly for skin cancer. The established risk factors for of malignancies, and this appears to apply also to transplanted basal cell and squamous cell cancer, such as exposure to patients. According to one study, patients who had an invasive sunlight, are also operative in transplanted individuals
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