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- W2077779629 abstract "Cancer occurring after transplantation, either recurrent or de novo malignancy, is a serious complication of liver transplantation and of great concern to transplant physicians and patients. Liver transplant (LT) recipients are at risk of developing cancer after transplantation from a variety of mechanisms. Prior to transplantation, long-term exposure to known carcinogens such as alcohol and tobacco or infection with oncogenic viruses such as HBV and HCV place many patients with advanced liver disease at increased risk. After transplantation, immunosuppressive medications result in decreased immune surveillance against malignant cells and increases the risk of malignancies mediated by viruses such as human papilloma virus, Epstein–Barr virus and human herpes virus-6. With the rising incidence of hepatocellular carcinoma (HCC), an increasing number of liver transplantations are being performed for the treatment of hepatic malignancies, which may recur after LT (OPTN Data 2004). Finally, given the demographic shift toward an older population, the majority of patients undergoing LT in the USA are now over the age of 50 (OPTN Data 2004). Given these facts, the question is raised: “Will all liver transplant patients eventually die from cancer?”Recipients of LT can develop cancer either as the recurrence of a pre-transplantation malignancy (e.g. post-transplantation recurrence of HCC), or a de novo malignancy developing after LT. De novo malignancies include sporadic cancers, malignancies associated with the immunocompromised state (e.g. post-transplantation lymphoproliferative disorder) as well as those cancers associated with the patient's pre-transplantation disease state (e.g. colorectal carcinoma complicating inflammatory bowel disease in patients with primary sclerosing cholangitis). While the transmission of tumors of donor origin to organ transplant recipients can occur, the incidence is very low. Among a cohort of over 100,000 cadaveric organ transplant recipients from the Organ Procurement and Transplantation Network/United Network for Organ Sharing, the donor-related tumor rate was 0.017% [[1]Myron Kauffman H. McBride M.A. Cherikh W.S. Spain P.C. Marks W.H. Roza A.M. Transplant tumor registry: donor related malignancies.Transplantation. 2002; 74: 358-362Crossref PubMed Scopus (190) Google Scholar].In order to ascertain whether LT recipients are more likely to die from cancer we need to understand whether LT recipients are at a higher risk of developing cancer and whether they have increased cancer-related mortality than non-LT patients with cancer.1. Cancer incidence after liver transplantationSolid organ transplantation and subsequent chronic immunosuppression has been long associated with an increased risk for the development of cancer. Patients are at increased risk for hematologic malignancies as well as solid cancers. Concerning solid malignancies, several studies have demonstrated a higher incidence of both cutaneous and non-cutaneous solid malignancies in LT recipients compared with the general population. The reported rates in various studies range from 3 to 17%. The reported neoplasia rates are likely to be elevated due to the presence of screening bias among this population of patients where close medical surveillance is routine. These studies are also limited due to heterogeneity in terms of many important variables such as cohort size, patient population, indication for LT, era of transplantation, immunosuppressive regimen and length of follow-up. Many of these studies are further limited by inadequate control groups [2Benlloch S. Berenguer M. Prieto M. Moreno R. San Juan F. Rayon M. et al.De novo internal neoplasms after liver transplantation: increased risk and aggressive behavior in recent years?.Am J Transplant. 2004; 4: 596-604Crossref PubMed Scopus (114) Google Scholar, 3Catena F. Nardo B. Liviano d'Arcangelo G. Stefoni S. Arpesella G. Faenza A. et al.De novo malignancies after organ transplantation.Transplant Proc. 2001; 33: 1858-1859Abstract Full Text Full Text PDF PubMed Scopus (30) Google Scholar, 4Duvoux C. Delacroix I. Richardet J.P. Roudot-Thoraval F. Metreau J.M. Fagniez P.L. et al.Increased incidence of oropharyngeal squamous cell carcinomas after liver transplantation for alcoholic cirrhosis.Transplantation. 1999; 67: 418-421Crossref PubMed Scopus (127) Google Scholar, 5Frezza E.E. Fung J.J. van Thiel D.H. Non-lymphoid cancer after liver transplantation.Hepatogastroenterology. 1997; 44: 1172-1181PubMed Google Scholar, 6Fung J.J. Jain A. Kwak E.J. Kusne S. Dvorchik I. Eghtesad B. De novo malignancies after liver transplantation: a major cause of late death.Liver Transpl. 2001; 7: S109-S118Crossref PubMed Scopus (168) Google Scholar, 7Galve M.L. Cuervas-Mons V. Figueras J. Herrero I. Mata M. Clemente G. et al.Incidence and outcome of de novo malignancies after liver transplantation.Transplant Proc. 1999; 31: 1275-1277Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar, 8Haagsma E.B. Hagens V.E. Schaapveld M. van den Berg A.P. de Vries E.G. Klompmaker I.J. et al.Increased cancer risk after liver transplantation: a population-based study.J Hepatol. 2001; 34: 84-91Abstract Full Text Full Text PDF PubMed Scopus (279) Google Scholar, 9Herrero J.I. Lorenzo M. Quiroga J. Sangro B. Pardo F. Rotellar F. et al.De Novo neoplasia after liver transplantation: an analysis of risk factors and influence on survival.Liver Transpl. 2005; 11: 89-97Crossref PubMed Scopus (131) Google Scholar, 10Jain A.B. Yee L.D. Nalesnik M.A. Youk A. Marsh G. Reyes J. et al.Comparative incidence of de novo nonlymphoid malignancies after liver transplantation under tacrolimus using surveillance epidemiologic end result data.Transplantation. 1998; 66: 1193-1200Crossref PubMed Scopus (186) Google Scholar, 11Jimenez C. Rodriguez D. Marques E. Loinaz C. Alonso O. Hernandez-Vallejo G. et al.De novo tumors after orthotopic liver transplantation.Transplant Proc. 2002; 34: 297-298Abstract Full Text Full Text PDF PubMed Scopus (37) Google Scholar, 12Jonas S. Rayes N. Neumann U. Neuhaus R. Bechstein W.O. Guckelberger O. et al.De novo malignancies after liver transplantation using tacrolimus-based protocols or cyclosporine-based quadruple immunosuppression with an interleukin-2 receptor antibody or antithymocyte globulin.Cancer. 1997; 80: 1141-1150Crossref PubMed Scopus (165) Google Scholar, 13Penn I. Posttransplantation de novo tumors in liver allograft recipients.Liver Transpl Surg. 1996; 2: 52-59Crossref PubMed Scopus (127) Google Scholar, 14Peyregne V. Ducerf C. Adham M. de la Roche E. Berthoux N. Bancel B. et al.De novo cancer after orthotopic liver transplantation.Transplant Proc. 1998; 30: 1484-1485Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar, 15Saigal S. Norris S. Muiesan P. Rela M. Heaton N. O'Grady J. Evidence of differential risk for posttransplantation malignancy based on pretransplantation cause in patients undergoing liver transplantation.Liver Transpl. 2002; 8: 482-487Crossref PubMed Scopus (132) Google Scholar, 16Sanchez E.Q. Marubashi S. Jung G. Levy M.F. Goldstein R.M. Molmenti E.P. et al.De novo tumors after liver transplantation: a single-institution experience.Liver Transpl. 2002; 8: 285-291Crossref PubMed Scopus (113) Google Scholar, 17Sheiner P.A. Magliocca J.F. Bodian C.A. Kim-Schluger L. Altaca G. Guarrera J.V. et al.Long-term medical complications in patients surviving > or =5 years after liver transplant.Transplantation. 2000; 69: 781-789Crossref PubMed Scopus (239) Google Scholar, 18Xiol X. Guardiola J. Menendez S. Lama C. Figueras J. Marcoval J. et al.Risk factors for development of de novo neoplasia after liver transplantation.Liver Transpl. 2001; 7: 971-975Crossref PubMed Scopus (79) Google Scholar].Among the larger published series, Galve et al. reported the cancer prevalence in 1827 Spanish LT recipients. Seventy patients (3.8%) were diagnosed with de novo malignancies after transplantation, including 17 skin cancers, 17 hematologic malignancies and 29 solid tumors including eight upper aerodigestive tract tumors (head, neck and esophageal cancers). Cancer occurred in patients at an average age of 53.5 years. Cancer tended to occur early after transplantation with the mean time to occurrence of 30.7 months. Fifty percent of cancers developed within 2 years of LT [[7]Galve M.L. Cuervas-Mons V. Figueras J. Herrero I. Mata M. Clemente G. et al.Incidence and outcome of de novo malignancies after liver transplantation.Transplant Proc. 1999; 31: 1275-1277Abstract Full Text Full Text PDF PubMed Scopus (39) Google Scholar]. In a series of 1421 US LT recipients, 125 (8.8%) developed de novo malignancies including 41 skin cancers and 35 lymphomas. Fifty-nine patients with de novo malignancies died from tumor related deaths resulting in a 60% mortality for patients with non-cutaneous neoplasms (16).2. Recurrent malignanciesLiver transplantation is considered to be the treatment of choice for patients with hepatocellular carcinoma (HCC) and decompensated cirrhosis [[19]Hassoun Z. Gores G.J. Treatment of hepatocellular carcinoma.Clin Gastroenterol Hepatol. 2003; 1: 10-18Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar]. Despite the use of established criteria for selecting LT candidates with the lowest risk of HCC recurrence, HCC has been reported to recur after LT in approximately 10% of patients [20Mazzaferro V. Regalia E. Doci R. Andreola S. Pulvirenti A. Bozzetti F. et al.Liver transplantation for the treatment of small hepatocellular carcinomas in patients with cirrhosis.N Engl J Med. 1996; 334: 693-699Crossref PubMed Scopus (5576) Google Scholar, 21Roayaie S. Schwartz J.D. Sung M.W. Emre S.H. Miller C.M. Gondolesi G.E. et al.Recurrence of hepatocellular carcinoma after liver transplant: patterns and prognosis.Liver Transpl. 2004; 10: 534-540Crossref PubMed Scopus (364) Google Scholar, 22Yao F.Y. Ferrell L. Bass N.M. Watson J.J. Bacchetti P. Venook A. et al.Liver transplantation for hepatocellular carcinoma: expansion of the tumor size limits does not adversely impact survival.Hepatology. 2001; 33: 1394-1403Crossref PubMed Scopus (1730) Google Scholar]. After the adoption of the model for end-stage liver disease (MELD) score for organ allocation among LT candidates in the USA, the number of patients undergoing LT for HCC tripled during the first year. Subsequently, a number of patients were identified whose diagnosis of HCC could not be rigorously verified and thus a reduction in assigned MELD score was performed. Nonetheless, the proportion of patients undergoing LT who have HCC continues to rise, the number of patients with recurrent HCC is expected to increase (OPTN Data 2004) [[21]Roayaie S. Schwartz J.D. Sung M.W. Emre S.H. Miller C.M. Gondolesi G.E. et al.Recurrence of hepatocellular carcinoma after liver transplant: patterns and prognosis.Liver Transpl. 2004; 10: 534-540Crossref PubMed Scopus (364) Google Scholar].The natural history of recurrent HCC is not well established, although given concomitant immunosuppression, recurrent cancer may run a more aggressive course. In a series of 132 LT recipients from three Italian transplant centers, Regalia et al. reported a 15.9% HCC recurrence rate. Ninety percent of patients developed recurrence within 2 years of transplantation. The authors identified tumors greater than 3 cm in diameter, the presence of a peri-tumoral capsule and tumors, which exceeded the Milan criteria for LT as independent risk factors for post-transplantation recurrence. TNM (American Joint Committee on Cancer Tumor, Nodal Involvement and Metastatis classification system) stage, vascular invasion, pre-transplantation chemoembolization and serum alpha-fetoprotein level did not independently predict HCC recurrence in this study [[23]Regalia E. Fassati L.R. Valente U. Pulvirenti A. Damilano I. Dardano G. et al.Pattern and management of recurrent hepatocellular carcinoma after liver transplantation.J Hepatobiliary Pancreat Surg. 1998; 5: 29-34Crossref PubMed Scopus (137) Google Scholar]. More recently, among a cohort of 67 patients with undergoing LT for HCC complicating HCV-related liver disease at a single US center, 11 patients (16.4%) developed cancer recurrence. Subsequently, eight deaths occurred from recurrent HCC. The majority of patients (81%) had cancer recurrence within 1 year of transplantation. Both patients who had late (>3 years after LT) recurrence presented with lung metastases. TNM staging, vascular invasion and pre-operative tumor diagnosis (as opposed to incidentally discovered tumors) predicted post-operative recurrence of HCC. Survival after transplantation was predicted by lower TMN staging and pre-LT chemoembolization [[24]Shimoda M. Ghobrial R.M. Carmody I.C. Anselmo D.M. Farmer D.G. Yersiz H. et al.Predictors of survival after liver transplantation for hepatocellular carcinoma associated with Hepatitis C.Liver Transpl. 2004; 10: 1478-1486Crossref PubMed Scopus (82) Google Scholar]. Roayaie and colleagues reported the outcomes of 311 patients who had HCC at time of LT from a single US center. Recurrent HCC occurred in 57 patients (18.3%) at a median time of 12.3 months after LT. The prognosis of recurrent HCC was poor, with a median survival of only 8.7 months after recurrence. Multivariate analysis identified larger tumor size (greater than 5 cm in diameter), poorly differentiated histology and bony metastases (irrespective of other metastases) as predictors of decreased survival from time of LT. Early recurrence (less than one year after LT) and bony metastases predicted shortened survival from the time of recurrence, while surgical management of recurrent tumors was shown to increase survival from time of recurrence [[21]Roayaie S. Schwartz J.D. Sung M.W. Emre S.H. Miller C.M. Gondolesi G.E. et al.Recurrence of hepatocellular carcinoma after liver transplant: patterns and prognosis.Liver Transpl. 2004; 10: 534-540Crossref PubMed Scopus (364) Google Scholar]. Together, these studies suggest that the recurrence rate of HCC after LT may be higher than previously reported.While the majority of patients with cancer recurrences have presented early after LT, a minority patients present with cancer recurrence several years after transplantation. Two of the 11 patients in the Shimoda series developed recurrence of HCC more 3 years after transplantation and approximately 10% of patients in the Roayaie series developed recurrence 4 or more years after LT [21Roayaie S. Schwartz J.D. Sung M.W. Emre S.H. Miller C.M. Gondolesi G.E. et al.Recurrence of hepatocellular carcinoma after liver transplant: patterns and prognosis.Liver Transpl. 2004; 10: 534-540Crossref PubMed Scopus (364) Google Scholar, 24Shimoda M. Ghobrial R.M. Carmody I.C. Anselmo D.M. Farmer D.G. Yersiz H. et al.Predictors of survival after liver transplantation for hepatocellular carcinoma associated with Hepatitis C.Liver Transpl. 2004; 10: 1478-1486Crossref PubMed Scopus (82) Google Scholar]. Patients with recurrent liver disease after LT, such as HCV infection, continue to have an oncogenic stimulus which may, in part, account for late recurrence. While patients who developed a HCC early after LT should be considered to have true recurrence, one could speculate that the development of HCC late after LT represents tumors with a different biology or possibly a de novo primary tumor.3. De novo malignancies3.1 Skin cancerCutaneous malignancies are the most commonly occurring cancers after LT. The prevalence of cutaneous malignancies is increased in transplant recipients and varies with the degree of immunosuppression. The majority of cutaneous malignancies are non-melanoma skin cancers such as squamous cell carcinoma and basal cell carcinoma. While basal cell carcinomas are the most common cutaneous malignancy in the general population, squamous cell skin cancer is more common among transplant recipients. The rate of developing squamous cell skin cancer is estimated to be increased over 60-fold in LT recipients compared to the general population. Fortunately, mortality rates from skin cancer in LT recipients are low with melanoma as the major cause of death [9Herrero J.I. Lorenzo M. Quiroga J. Sangro B. Pardo F. Rotellar F. et al.De Novo neoplasia after liver transplantation: an analysis of risk factors and influence on survival.Liver Transpl. 2005; 11: 89-97Crossref PubMed Scopus (131) Google Scholar, 25Mithoefer A.B. Supran S. Freeman R.B. Risk factors associated with the development of skin cancer after liver transplantation.Liver Transpl. 2002; 8: 939-944Crossref PubMed Scopus (80) Google Scholar]. While the transmission of donor-related tumors is rare, malignant melanoma is the most commonly transmitted tumor. Transplant recipient mortality due to the transmission of donor melanoma to a LT recipient has been reported [[26]Morris-Stiff G. Steel A. Savage P. Devlin J. Griffiths D. Portman B. et al.Transmission of donor melanoma to multiple organ transplant recipients.Am J Transplant. 2004; 4: 444-446Crossref PubMed Scopus (59) Google Scholar]. LT recipients, particularly those in sunny climates, should be counseled on photoprotection and require cancer surveillance with regular dermatologic examinations.3.2 Post-transplant lymphoproliferative disorderPost-transplant lymphoproliferative disorders (PTLD) comprises a spectrum of abnormal lymphoid tissue proliferation among in organ transplant recipients. PTLD is associated with chronically immunosuppression and is frequently associated with Ebstein–Barr virus (EBV) infected B-lymphocytes. PTLD has been reported to occur with a prevalence of 1.7–4% of LT recipients. While many cases of PTLD respond to a reduction in the level of immunosuppression, PTLD can present as an aggressive B-cell lymphoma [27Ben-Ari Z. Amlot P. Lachmanan S.R. Tur-Kaspa R. Rolles K. Burroughs A.K. Posttransplantation lymphoproliferative disorder in liver recipients: characteristics, management, and outcome.Liver Transpl Surg. 1999; 5: 184-191Crossref PubMed Scopus (37) Google Scholar, 28Hezode C. Duvoux C. Germanidis G. Roudot-Thoraval F. Vincens A.L. Gaulard P. et al.Role of hepatitis C virus in lymphoproliferative disorders after liver transplantation.Hepatology. 1999; 30: 775-778Crossref PubMed Scopus (69) Google Scholar, 29Andreone P. Gramenzi A. Lorenzini S. Biselli M. Cursaro C. Pileri S. et al.Posttransplantation lymphoproliferative disorders.Arch Intern Med. 2003; 163: 1997-2004Crossref PubMed Scopus (79) Google Scholar]. PTLD frequently involves the liver allograft with allograft PTLD (accounting for approximately 44%) and carries a mortality rate of approximately 50% despite therapy [13Penn I. Posttransplantation de novo tumors in liver allograft recipients.Liver Transpl Surg. 1996; 2: 52-59Crossref PubMed Scopus (127) Google Scholar, 28Hezode C. Duvoux C. Germanidis G. Roudot-Thoraval F. Vincens A.L. Gaulard P. et al.Role of hepatitis C virus in lymphoproliferative disorders after liver transplantation.Hepatology. 1999; 30: 775-778Crossref PubMed Scopus (69) Google Scholar].Among recipients of LT, infection with the hepatitis C virus may represent an additional risk for the development of PTLD. This is of concern given the universal recurrence of HCV after LT. The hepatitis C virus may induce B-cell proliferation either independently or through a synergistic effect with the EBV virus. In one study of 480 consecutive French LT recipients, multivariate analysis identified age (older than 50 years), the use antilymphocyte antibody therapy, and LT for either hepatitis C related cirrhosis or alcoholic cirrhosis as risk factors for the subsequent development of PTLD. The relative risk of developing PTLD among HCV-infected LT recipients was 8.7 (95% CI 1–78.3, P=0.015) compared to patients transplanted for non-HCV, non-alcoholic liver diseases [[30]Duvoux C. Pageaux G.P. Vanlemmens C. Roudot-Thoraval F. Vincens-Rolland A.L. Hezode C. et al.Risk factors for lymphoproliferative disorders after liver transplantation in adults: an analysis of 480 patients.Transplantation. 2002; 74: 1103-1109Crossref PubMed Scopus (106) Google Scholar]. A case–control study of 57 HCV-infected LT recipients, the odds ratio of developing PTLD was 9.5 (P=0.02) among HCV-infected patients compared to non-HCV infected LT recipients [[31]McLaughlin K. Wajstaub S. Marotta P. Adams P. Grant D.R. Wall W.J. et al.Increased risk for posttransplant lymphoproliferative disease in recipients of liver transplants with hepatitis C.Liver Transpl. 2000; 6: 570-574Crossref PubMed Scopus (63) Google Scholar]. In another study of 157 LT recipients, PTLD was more common in HCV-infected patients than in non-infected patients (10.5% vs 1.7%; P=0.03). Patients undergoing LT for HCV-related ESLD were more likely to have received antithymocyte globulins. However, among patients who received antithymocyte globulins, PTLD seemed to occur more frequently among those HCV-related disease (27.1% vs 6.4%, P=0.08) [[28]Hezode C. Duvoux C. Germanidis G. Roudot-Thoraval F. Vincens A.L. Gaulard P. et al.Role of hepatitis C virus in lymphoproliferative disorders after liver transplantation.Hepatology. 1999; 30: 775-778Crossref PubMed Scopus (69) Google Scholar].In contrast, PTLD is a relatively uncommon disease, and the studies which find an increased risk among HCV-infected LT recipients are limited by small numbers of patients. In a prospective study of 394 patients with lymphoproliferative disorders (including 164 patients with non-Hodgkin's lymphoma), Hausfater and colleagues found a low prevalence rate of HCV infection (2.79 and 1.83%, respectively). While patients with lymphoproliferative disorders did have a higher prevalence of HCV compared to controls (2.79% vs 0.43%), the authors concluded that the low rate of HCV infection suggests that HCV does not play an important role in the pathogenesis of lymphoproliferative disorders [[32]Hausfater P. Cacoub P. Sterkers Y. Thibault V. Amoura Z. Nguyen L. et al.Hepatitis C virus infection and lymphoproliferative diseases: prospective study on 1,576 patients in France.Am J Hematol. 2001; 67: 168-171Crossref PubMed Scopus (80) Google Scholar]. Among 660 patients undergoing LT at Mayo Clinic, Zein et al. found no link between HCV infection and the development of PTLD [[33]Zein N.N. Perez R.G. Wiesner R.H. Hepatitis C virus infection and lymphoproliferative disorders after liver transplantation.Hepatology. 2000; 31: 808-809Crossref PubMed Scopus (13) Google Scholar]. Given the small numbers of patients who developed PTLD and the differences in immunosuppressive regimens used at different institutions, the link between HCV infection and PTLD remains unclear [28Hezode C. Duvoux C. Germanidis G. Roudot-Thoraval F. Vincens A.L. Gaulard P. et al.Role of hepatitis C virus in lymphoproliferative disorders after liver transplantation.Hepatology. 1999; 30: 775-778Crossref PubMed Scopus (69) Google Scholar, 33Zein N.N. Perez R.G. Wiesner R.H. Hepatitis C virus infection and lymphoproliferative disorders after liver transplantation.Hepatology. 2000; 31: 808-809Crossref PubMed Scopus (13) Google Scholar].3.3 Solid organ malignanciesMultiple studies have reported an increased risk for developing solid organ malignancy after LT. Data from the International Transplant Tumor Registry (formerly the Cincinnati Transplant Tumor Registry) demonstrates a significantly increased risk of cancers such as skin cancer, Kaposi's sarcoma, cervical, vulvar and anal squamous cell carcinomas among organ transplant recipients compared to the general population. Among liver transplant recipients, 324 patients developed 329 cancers after LT. When compared to a cohort of 7200 renal transplant recipients with cancer, LT recipients had a higher rate of lymphoma (57% vs 12% of cancers). In LT recipients both solid tumors (27 vs 72 months) and lymphomas (15 vs 46 months) occurred earlier in the post-transplant course compared to renal transplant recipients. The higher proportion of pediatric LT recipients and the longer follow-up of renal transplant recipients may explain the observed differences [[13]Penn I. Posttransplantation de novo tumors in liver allograft recipients.Liver Transpl Surg. 1996; 2: 52-59Crossref PubMed Scopus (127) Google Scholar].A population-based study of 174 transplant recipients from the Netherlands who survived more than 1 year from LT revealed an increased relative risk of developing solid organ malignancy compared to expected rates in the Dutch population. The relative risk of developing any non-cutaneous, solid organ malignancy was 2.7, with the relative risk being highest for colon and renal cell carcinomas (12.5 and 30.0, respectively). Of note, renal cell carcinoma was noted incidentally in two of three cases and none of the three patients who developed colorectal neoplasia had underlying PSC or IBD. Age greater than 40 years was identified as an important risk factor for post-transplant cancer [[8]Haagsma E.B. Hagens V.E. Schaapveld M. van den Berg A.P. de Vries E.G. Klompmaker I.J. et al.Increased cancer risk after liver transplantation: a population-based study.J Hepatol. 2001; 34: 84-91Abstract Full Text Full Text PDF PubMed Scopus (279) Google Scholar].Based on center-specific practices, a number of LT recipients may be evaluated longitudinally to ensure stable allograft function and for the prevention of immunosuppression-related medical complications. However, the use of cancer surveillance methods in this setting does not appear to guarantee the prospect of early detection time based on annual visits or problem-specific issues. Herrero and colleagues reported a retrospective review of 187 Spanish LT recipients who survived beyond 3 months after transplantation. Despite an aggressive pre- and post-LT cancer screening protocol (including upper and lower GI endoscopy, thoracic and abdominal computed tomography, magnetic resonance neuroimaging and otorhinolaryngology evaluation for smokers), 27 patients developed 28 non-cutaneous malignancies (including nine PTLD and one Kaposi's sarcoma). The majority of solid organ malignancies were diagnosed at advanced stages (50% of upper aerodigestive tract tumors diagnosed at stage IV, 66% of non-small cell lung cancers and 71% of abdominal and genitourinary tract tumors diagnosed at stages III–IV). Multivariate analysis identified only age, and a history of smoking or history of alcohol abuse as risk factors for post-LT non-cutaneous malignancy [[9]Herrero J.I. Lorenzo M. Quiroga J. Sangro B. Pardo F. Rotellar F. et al.De Novo neoplasia after liver transplantation: an analysis of risk factors and influence on survival.Liver Transpl. 2005; 11: 89-97Crossref PubMed Scopus (131) Google Scholar].3.4 Colorectal neoplasiaPrimary sclerosing cholangitis (PSC) is associated with inflammatory bowel disease (IBD) with 60–80% of patients with PSC having concurrent IBD. Patients with IBD are at risk for developing colorectal carcinoma (CRC) and coexisting PSC may be an additional cancer risk, although this association remains controversial [[34]Loftus Jr, E.V. Harewood G.C. Loftus C.G. Tremaine W.J. Harmsen W.S. Zinsmeister A.R. et al.PSC-IBD: a unique form of inflammatory bowel disease associated with primary sclerosing cholangitis.Gut. 2005; 54: 91-96Crossref PubMed Scopus (543) Google Scholar].Studies have also examined the continued risk for CRC in patients undergoing LT for PSC in the setting of inflammatory bowel disease. Vera et al. reviewed 100 patients with PSC and IBD who underwent transplantation at a single center in the UK. Among 83 patients with intact colons after LT, five patients subsequently developed dysplasia requiring colectomy and an additional eight patients developed CRC. Among patients developing CRC, three were diagnosed with stage I disease, one with stage II disease, three with stage III disease and two patients had metastatic (stage IV) disease at diagnosis. Patients with CRC had a decreased 5-year survival compared to other LT recipients with PSC and IBD (53% vs 73%); four patients with CRC died during the study period [[35]Vera A. Gunson B.K. Ussatoff V. Nightingale P. Candinas D. Radley S. et al.Colorectal cancer in patients with inflammatory bowel disease after liver transplantation for primary sclerosing cholangitis.Transplantation. 2003; 75: 1983-1988Crossref PubMed Scopus (156) Google Scholar].In contrast, data from the Mayo Clinic found no survival difference among patients who developed CRC complicating LT for PSC. Among 108 patients undergoing LT for PSC with coexisting IBD in 81 patients, the cumulative risk for CRC was 4% at 5 years. While there was a higher incidence of colorectal neoplasia (dysplasia and carcinoma) among LT recipients compared to historical controls, there was no excess mortality attributed to CRC in this study [[36]Loftus Jr, E.V. Aguilar H.I. Sandborn W.J. Tremaine W.J. Krom R.A. Zinsmeister A.R. et al.Risk of colorectal neoplasia in patients with primary sclerosing cholangitis and ulcerative colitis following orthotopic liver transplantation.Hepatology. 1998; 27: 685-690Crossref PubMed Scopus (171) Google Scholar]. Routine surveillance for neoplasia and subsequent colectomy for dysplasia may account for the low mortality from CRC in LT patients with IBD [[8]Haagsma E.B. Hagens V.E. Schaapveld M. van den Berg A.P. de Vries E.G. Klompmaker I.J. et al.Increased cancer risk after liver transplantation: a population-based study.J Hepatol. 2001; 34: 84-91Abstract Full Text Full Text PDF PubMed Scopus (279) Google Scholar].3.5 Upper aerodigestive tract malignanciesUpper aerodigestive tract malignancies, such as oral, laryngeal and esophageal carcinoma, have been reported to be more common in patients after LT. In an analysis of 1000 consecutive LT patients treated with a tacrolimus-based immunosuppressive regimen, the incidence of oropharyngeal cancer was dramatic" @default.
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- W2077779629 title "“Will all liver transplantation patients eventually die from cancer?”" @default.
- W2077779629 cites W1556511066 @default.
- W2077779629 cites W1969333586 @default.
- W2077779629 cites W1976082980 @default.
- W2077779629 cites W1981521465 @default.
- W2077779629 cites W1989312090 @default.
- W2077779629 cites W1992284814 @default.
- W2077779629 cites W1992431640 @default.
- W2077779629 cites W1993763408 @default.
- W2077779629 cites W1996883206 @default.
- W2077779629 cites W2005498062 @default.
- W2077779629 cites W2007885575 @default.
- W2077779629 cites W2017912874 @default.
- W2077779629 cites W2020329640 @default.
- W2077779629 cites W2021299297 @default.
- W2077779629 cites W2022112812 @default.
- W2077779629 cites W2027286769 @default.
- W2077779629 cites W2029079150 @default.
- W2077779629 cites W2030097249 @default.
- W2077779629 cites W2031576581 @default.
- W2077779629 cites W2038583170 @default.
- W2077779629 cites W2049612107 @default.
- W2077779629 cites W2050485376 @default.
- W2077779629 cites W2052868106 @default.
- W2077779629 cites W2054630419 @default.
- W2077779629 cites W2061062185 @default.
- W2077779629 cites W2062615357 @default.
- W2077779629 cites W2065754270 @default.
- W2077779629 cites W2076145256 @default.
- W2077779629 cites W2076738785 @default.
- W2077779629 cites W2087637645 @default.
- W2077779629 cites W2102007986 @default.
- W2077779629 cites W2109810752 @default.
- W2077779629 cites W2116437061 @default.
- W2077779629 cites W2133676969 @default.
- W2077779629 cites W2147882685 @default.
- W2077779629 cites W2157836255 @default.
- W2077779629 cites W2315027248 @default.
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