Cancer risk in people infected with human immunodeficiency virus in the United States

Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20852, USA.
International Journal of Cancer (Impact Factor: 5.09). 07/2008; 123(1):187-94. DOI: 10.1002/ijc.23487
Source: PubMed

ABSTRACT Data are limited regarding cancer risk in human immunodeficiency virus (HIV)-infected persons with modest immunosuppression, before the onset of acquired immunodeficiency syndrome (AIDS). For some cancers, risk may be affected by highly active antiretroviral therapy (HAART) widely available since 1996. We linked HIV/AIDS and cancer registries in Colorado, Florida and New Jersey. Standardized incidence ratios (SIRs) compared cancer risk in HIV-infected persons (initially AIDS-free) during the 5-year period after registration with the general population. Poisson regression was used to compare incidence across subgroups, adjusting for demographic factors. Among 57,350 HIV-infected persons registered during 1991-2002 (median CD4 count 491 cells/mm(3)), 871 cancers occurred during follow-up. Risk was elevated for Kaposi sarcoma (KS, SIR 1,300 [n = 173 cases]), non-Hodgkin lymphoma (NHL, 7.3 [n = 203]), cervical cancer (2.9 [n = 28]) and several non-AIDS-defining malignancies, including Hodgkin lymphoma (5.6 [n = 36]) and cancers of the lung (2.6 [n = 109]) and liver (2.7 [n = 14]). KS and NHL incidence declined over time but nonetheless remained elevated in 1996-2002. Incidence increased in 1996-2002 compared to 1991-1995 for Hodgkin lymphoma (relative risk 2.7, 95%CI 1.0-7.1) and liver cancer (relative risk infinite, one-sided 95%CI 1.1-infinity). Non-AIDS-defining cancers comprised 31.4% of cancers in 1991-1995, versus 58.0% in 1996-2002. For KS and NHL, risk was inversely related to CD4 count, but these associations attenuated after 1996. We conclude that KS and NHL incidence declined markedly in recent years, likely reflecting HAART-related improvements in immunity, while incidence of some non-AIDS-defining cancers increased. These trends have led to a shift in the spectrum of cancer among HIV-infected persons.

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    • "Od czasu wprowadzenia do leczenia ART zmieniło się podejście do leczenia chłoniaków, ale również zmienił się ich rodzaj i przebieg kliniczny. Wprowadzenie ART spowodowało istotne obniżenie częstości zachorowania na mięsaka Kaposiego i NHL [45] [46], jednak nie udowodniono wpływu ART na częstość występowania HL [47]. Obserwuje się, że u chorych poddawanych ART lokalizacje pozawęzłowe oraz obciążające czynniki prognostyczne oceniane według Międzynarodowego Indeksu Prognostycznego (IPI; International Prognostic Index) występują rzadziej w porównaniu z erą sprzed leczenia ART. "
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    ABSTRACT: Patients with non-Hodgkin's lymphoma (NHL) and coexisting infection with HBV, HCV or HIV constitute a major problem for clinicians concerning interdependence of the viral infection, lymphoma and antineoplatistic treatment. In patients with NHL and HCV infections complex virology diagnostics should be performed before lymphoma treatment is administered. If there are no indications to initiate antiviral therapy, the lymphoma treatment should be administered like in a subject without HCV infection. The risk of life-threatening complications of HCV reactivation is minimal and should not be taken into consideration when decisions related to lymphoma treatment are to be made. In the case of indolent NHL as the efficacy of HCV eradication is associated with remission achievement, it is effective to start therapy with antiviral schedules of inteferon with ribavirin. On the contrary, previous or chronic HBV infection is a risk factor for HBV reactivation and for reactivation-related mortality. Antiviral prophylaxis with lamivudine is to be considered routinely with its duration of 7 days before antineoplastic therapy initiation and ending 6 months after therapy completion. In patients not previously exposed to HBV active immunization is recommended, unless the subject was earlier vaccinated. Finally, patients with HIV infection and NHL should be treated with concomitant ART administration and adequate chemotherapy schedules (including rituximab). Schedules with reduced intensity should be restricted to patients with CD4+ cells count less than 100 cells/mm3. Special attention should be paid to intrathecal therapy and supportive treatment during chemotherapy.
    Acta haematologica Polonica 03/2015; 46(2). DOI:10.1016/j.achaem.2015.02.013
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    • "Table 1 Cohort study design features of cancer risk in HIV/AIDS patients. Study, year (reference) Country Study type Period of follow-up Number of patients Total number of person- years Number of cancers Dorrucci et al., 2001 [27] Italy Cohort 1981—1998 483 3364 6 Bower et al., 2003 [29] UK RL a 1986—2001 8400 22,694 11 Bower et al., 2004 [30] UK Cohort 1984—2003 8640 40,126 26 Hessol et al., 2004 [31] USA RL a 1994—2001 1554 7909 41 Biggar et al., 2006 [15] USA RL a 1980—2002 317,428 477,368 173 D'Souza et al., 2008 [32] USA Cohort 1984—2006 6972 100,000 69 Franceschi et al., 2008 [33] Switzerland Cohort 1984—2006 12,959 73,412 597 Polesel et al., 2008 [34] Switzerland Cohort 1984—2006 12,959 75,222 429 Engels et al., 2008 [35] USA Cohort 1991—2002 57,350 186,157 871 Crum-Cianflone et al., 2009 [4] USA Cohort 1984—2006 4498 33,486 446 Clifford et al., 2009 [36] Switzerland Cohort 1984—2007 14,606 84,611 47 Dal Maso et al., 2009 [43] Italy RL a 1986—2004 21,951 101,668 1995 Leewen et al., 2009 [20] Australia Cohort 1982—2004 37,407 311,496 2283 Powles et al., 2009 [41] UK Cohort 1983—2007 11,112 71,687 156 Buchacz et al., 2010 [37] USA Cohort 1994—2007 8070 3000 16 Crum-Cianflone, 2010 [39] USA Cohort 1985—2008 4506 37,806 66 Franceschi et al., 2010 [42] Switzerland RL a 1985—2006 9429 53,715 1460 Seaberg et al., 2010 [40] USA Cohort 1984—2007 6972 77,320 933 Besson et al., 2011 [38] France RL a 1993—1998 80,000 230,173 900 Kirk et al., 2001 [24] Europe Cohort 1994—2000 8471 26,764 222 Franzetti et al., 2012 [10] "
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    ABSTRACT: After highly active antiretroviral therapy (HAART) became widespread, several studies demonstrated changes in the incidence of defining and non-defining AIDS cancers among HIV/AIDS patients. We conducted a systematic review of observational studies evaluating the incidence of malignancies before and after the introduction of HAART in people with HIV/AIDS. Eligible studies were searched up to December 2012 in the following databases: Pubmed, Embase, Scielo, Cancerlit and Google Scholar. In this study, we determined the cancer risk ratio by comparing the pre- and post-HAART eras. Twenty-one relevant articles were found, involving more than 600,000 people with HIV/AIDS and 10,891 new cases of cancers. The risk for the development of an AIDS-defining cancer decreased after the introduction of HAART: Kaposi's sarcoma (RR = 0.30, 95% CI: 0.28–0.33) and non-Hodgkin's lymphoma (RR = 0.52, 95% CI: 0.48–0.56), in contrast to invasive cervical cancer (RR = 1.46, 95% CI: 1.09–1.94). Among the non-AIDS-defining cancers, the overall risk increased after the introduction of HAART (RR = 2.00, 95% CI: 1.79–2.23). The incidence of AIDS-defining cancers decreased and the incidence of non-AIDS-defining cancers increased after the early use of HAART, probably due to better control of viral replication, increased immunity and increased survival provided by new drugs.
    Journal of Infection and Public Health 10/2014; 8(1). DOI:10.1016/j.jiph.2014.08.003
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    • "Thus, the increased risk of overall malignancy after liver transplantation is partly related to these otherwise less frequent tumours, leading to a specific ‘cancer pattern’ related to immunosuppression. It is not surprising that this ‘cancer pattern’ is reproduced in AIDS wherein effective antiretroviral therapies have prolonged survival [21], and establish a chronic immunosuppressive status [22,23]. New therapies that enhance the immune system are becoming a reality in the management of several types of cancer. "
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    ABSTRACT: Long-term survival of liver transplant recipients is threatened by increased rates of de-novo malignancy and recurrence of hepatocellular carcinoma (HCC), both events tightly related to immunosuppression. There is accumulating evidence linking increased exposure to immunosuppressants and carcinogenesis, particularly concerning calcineurin inhibitors (CNIs), azathioprine and antilymphocyte agents. A recent study including 219 HCC transplanted patients showed that HCC recurrence rates were halved if a minimization of CNIs was applied within the first month after liver transplant. With mammalian target of rapamycin (mTOR) inhibitors as approved immunosuppressants for liver transplant patients, pooled data from several retrospective studies have suggested their possible benefit for reducing HCC recurrence. Randomized controlled trials with sufficiently long follow-up are needed to evaluate the influence of different immunosuppression protocols in preventing malignancy after LT. Currently, early minimization of CNIs with or without mTOR inhibitors or mycophenolate seems a rational strategy for patients with risk factors for de-novo malignancy or recurrence of HCC after liver transplant. A deeper understanding of the immunological pathways of rejection and cancer would allow for designing more specific and safer drugs, and thus to prevent cancer after liver transplant.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivitives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially.
    Current opinion in organ transplantation 03/2014; 19(3). DOI:10.1097/MOT.0000000000000069 · 2.88 Impact Factor
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