HIV Infection, Immunodeficiency, Viral Replication, and the Risk of Cancer

Background: Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for cancer risk factors. Methods: We followed 20,775 HIV-infected and 215,158 HIV-uninfected individuals enrolled in Kaiser Permanente...

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Published inCancer epidemiology, biomarkers & prevention Vol. 20; no. 12; pp. 2551 - 2559
Main Authors Silverberg, Michael J., Chao, Chun, Leyden, Wendy A., Xu, Lanfang, Horberg, Michael A., Klein, Daniel, Towner, William J., Dubrow, Robert, Quesenberry, Charles P., Neugebauer, Romain S., Abrams, Donald I.
Format Journal Article
LanguageEnglish
Published Philadelphia, PA American Association for Cancer Research 01.12.2011
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Abstract Background: Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for cancer risk factors. Methods: We followed 20,775 HIV-infected and 215,158 HIV-uninfected individuals enrolled in Kaiser Permanente (KP) California for incident cancer from 1996 to 2008. Rate ratios (RR) were obtained from Poisson models comparing HIV-infected (overall and stratified by recent CD4 count and HIV RNA) with HIV-uninfected individuals, adjusted for age, sex, race/ethnicity, calendar period, KP region, smoking, alcohol/drug abuse, and overweight/obesity. Results: We observed elevated RRs for Kaposi sarcoma (KS; RR = 199; P < 0.001), non-Hodgkin lymphoma (NHL; RR = 15; P < 0.001), anal cancer (RR = 55; P < 0.001), Hodgkin lymphoma (HL; RR = 19; P < 0.001), melanoma (RR = 1.8; P = 0.001), and liver cancer (RR = 1.8; P = 0.013), a reduced RR for prostate cancer (RR = 0.8; P = 0.012), and no increased risk for oral cavity/pharynx (RR = 1.4; P = 0.14), lung (RR = 1.2; P = 0.15), or colorectal (RR = 0.9; P = 0.34) cancers. Lung and oral cavity/pharynx cancers were elevated for HIV-infected subjects in models adjusted only for demographics. KS, NHL, anal cancer, HL, and colorectal cancer had significant (P < 0.05) trends for increasing RRs with decreasing recent CD4. The RRs for lung and oral cavity/pharynx cancer were significantly elevated with CD4 < 200 cells/μL and for melanoma and liver cancer with CD4 < 500 cells/μL. Only KS and NHL were associated with HIV RNA. Conclusion: Immunodeficiency was positively associated with all cancers examined except prostate cancer among HIV-infected compared with HIV-uninfected individuals, after adjustment for several cancer risk factors. Impact: Earlier antiretroviral therapy initiation to maintain high CD4 levels might reduce the burden of cancer in this population. Cancer Epidemiol Biomarkers Prev; 20(12); 2551–9. ©2011 AACR.
AbstractList Background: Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for cancer risk factors. Methods: We followed 20,775 HIV-infected and 215,158 HIV-uninfected individuals enrolled in Kaiser Permanente (KP) California for incident cancer from 1996 to 2008. Rate ratios (RR) were obtained from Poisson models comparing HIV-infected (overall and stratified by recent CD4 count and HIV RNA) with HIV-uninfected individuals, adjusted for age, sex, race/ethnicity, calendar period, KP region, smoking, alcohol/drug abuse, and overweight/obesity. Results: We observed elevated RRs for Kaposi sarcoma (KS; RR = 199; P < 0.001), non-Hodgkin lymphoma (NHL; RR = 15; P < 0.001), anal cancer (RR = 55; P < 0.001), Hodgkin lymphoma (HL; RR = 19; P < 0.001), melanoma (RR = 1.8; P = 0.001), and liver cancer (RR = 1.8; P = 0.013), a reduced RR for prostate cancer (RR = 0.8; P = 0.012), and no increased risk for oral cavity/pharynx (RR = 1.4; P = 0.14), lung (RR = 1.2; P = 0.15), or colorectal (RR = 0.9; P = 0.34) cancers. Lung and oral cavity/pharynx cancers were elevated for HIV-infected subjects in models adjusted only for demographics. KS, NHL, anal cancer, HL, and colorectal cancer had significant (P < 0.05) trends for increasing RRs with decreasing recent CD4. The RRs for lung and oral cavity/pharynx cancer were significantly elevated with CD4 < 200 cells/μL and for melanoma and liver cancer with CD4 < 500 cells/μL. Only KS and NHL were associated with HIV RNA. Conclusion: Immunodeficiency was positively associated with all cancers examined except prostate cancer among HIV-infected compared with HIV-uninfected individuals, after adjustment for several cancer risk factors. Impact: Earlier antiretroviral therapy initiation to maintain high CD4 levels might reduce the burden of cancer in this population. Cancer Epidemiol Biomarkers Prev; 20(12); 2551–9. ©2011 AACR.
BACKGROUND: Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for cancer risk factors. METHODS: We followed 20,775 HIV-infected and 215,158 HIV-uninfected individuals enrolled in Kaiser Permanente (KP) California for incident cancer from 1996 to 2008. Rate ratios (RR) were obtained from Poisson models comparing HIV-infected (overall and stratified by recent CD4 count and HIV RNA) with HIV-uninfected individuals, adjusted for age, sex, race/ethnicity, calendar period, KP region, smoking, alcohol/drug abuse, and overweight/obesity. RESULTS: We observed elevated RRs for Kaposi sarcoma (KS; RR = 199; P < 0.001), non-Hodgkin lymphoma (NHL; RR = 15; P < 0.001), anal cancer (RR = 55; P < 0.001), Hodgkin lymphoma (HL; RR = 19; P < 0.001), melanoma (RR = 1.8; P = 0.001), and liver cancer (RR = 1.8; P = 0.013), a reduced RR for prostate cancer (RR = 0.8; P = 0.012), and no increased risk for oral cavity/pharynx (RR = 1.4; P = 0.14), lung (RR = 1.2; P = 0.15), or colorectal (RR = 0.9; P = 0.34) cancers. Lung and oral cavity/pharynx cancers were elevated for HIV-infected subjects in models adjusted only for demographics. KS, NHL, anal cancer, HL, and colorectal cancer had significant (P < 0.05) trends for increasing RRs with decreasing recent CD4. The RRs for lung and oral cavity/pharynx cancer were significantly elevated with CD4 < 200 cells/ mu L and for melanoma and liver cancer with CD4 < 500 cells/ mu L. Only KS and NHL were associated with HIV RNA. CONCLUSION: Immunodeficiency was positively associated with all cancers examined except prostate cancer among HIV-infected compared with HIV-uninfected individuals, after adjustment for several cancer risk factors. IMPACT: Earlier antiretroviral therapy initiation to maintain high CD4 levels might reduce the burden of cancer in this population. Cancer Epidemiol Biomarkers Prev; 20(12); 2551-9. [copy ]2011 AACR.
Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for cancer risk factors.BACKGROUNDFew studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for cancer risk factors.We followed 20,775 HIV-infected and 215,158 HIV-uninfected individuals enrolled in Kaiser Permanente (KP) California for incident cancer from 1996 to 2008. Rate ratios (RR) were obtained from Poisson models comparing HIV-infected (overall and stratified by recent CD4 count and HIV RNA) with HIV-uninfected individuals, adjusted for age, sex, race/ethnicity, calendar period, KP region, smoking, alcohol/drug abuse, and overweight/obesity.METHODSWe followed 20,775 HIV-infected and 215,158 HIV-uninfected individuals enrolled in Kaiser Permanente (KP) California for incident cancer from 1996 to 2008. Rate ratios (RR) were obtained from Poisson models comparing HIV-infected (overall and stratified by recent CD4 count and HIV RNA) with HIV-uninfected individuals, adjusted for age, sex, race/ethnicity, calendar period, KP region, smoking, alcohol/drug abuse, and overweight/obesity.We observed elevated RRs for Kaposi sarcoma (KS; RR = 199; P < 0.001), non-Hodgkin lymphoma (NHL; RR = 15; P < 0.001), anal cancer (RR = 55; P < 0.001), Hodgkin lymphoma (HL; RR = 19; P < 0.001), melanoma (RR = 1.8; P = 0.001), and liver cancer (RR = 1.8; P = 0.013), a reduced RR for prostate cancer (RR = 0.8; P = 0.012), and no increased risk for oral cavity/pharynx (RR = 1.4; P = 0.14), lung (RR = 1.2; P = 0.15), or colorectal (RR = 0.9; P = 0.34) cancers. Lung and oral cavity/pharynx cancers were elevated for HIV-infected subjects in models adjusted only for demographics. KS, NHL, anal cancer, HL, and colorectal cancer had significant (P < 0.05) trends for increasing RRs with decreasing recent CD4. The RRs for lung and oral cavity/pharynx cancer were significantly elevated with CD4 < 200 cells/μL and for melanoma and liver cancer with CD4 < 500 cells/μL. Only KS and NHL were associated with HIV RNA.RESULTSWe observed elevated RRs for Kaposi sarcoma (KS; RR = 199; P < 0.001), non-Hodgkin lymphoma (NHL; RR = 15; P < 0.001), anal cancer (RR = 55; P < 0.001), Hodgkin lymphoma (HL; RR = 19; P < 0.001), melanoma (RR = 1.8; P = 0.001), and liver cancer (RR = 1.8; P = 0.013), a reduced RR for prostate cancer (RR = 0.8; P = 0.012), and no increased risk for oral cavity/pharynx (RR = 1.4; P = 0.14), lung (RR = 1.2; P = 0.15), or colorectal (RR = 0.9; P = 0.34) cancers. Lung and oral cavity/pharynx cancers were elevated for HIV-infected subjects in models adjusted only for demographics. KS, NHL, anal cancer, HL, and colorectal cancer had significant (P < 0.05) trends for increasing RRs with decreasing recent CD4. The RRs for lung and oral cavity/pharynx cancer were significantly elevated with CD4 < 200 cells/μL and for melanoma and liver cancer with CD4 < 500 cells/μL. Only KS and NHL were associated with HIV RNA.Immunodeficiency was positively associated with all cancers examined except prostate cancer among HIV-infected compared with HIV-uninfected individuals, after adjustment for several cancer risk factors.CONCLUSIONImmunodeficiency was positively associated with all cancers examined except prostate cancer among HIV-infected compared with HIV-uninfected individuals, after adjustment for several cancer risk factors.Earlier antiretroviral therapy initiation to maintain high CD4 levels might reduce the burden of cancer in this population.IMPACTEarlier antiretroviral therapy initiation to maintain high CD4 levels might reduce the burden of cancer in this population.
Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for cancer risk factors. We followed 20,775 HIV-infected and 215,158 HIV-uninfected individuals enrolled in Kaiser Permanente (KP) California for incident cancer from 1996 to 2008. Rate ratios (RR) were obtained from Poisson models comparing HIV-infected (overall and stratified by recent CD4 count and HIV RNA) with HIV-uninfected individuals, adjusted for age, sex, race/ethnicity, calendar period, KP region, smoking, alcohol/drug abuse, and overweight/obesity. We observed elevated RRs for Kaposi sarcoma (KS; RR = 199; P < 0.001), non-Hodgkin lymphoma (NHL; RR = 15; P < 0.001), anal cancer (RR = 55; P < 0.001), Hodgkin lymphoma (HL; RR = 19; P < 0.001), melanoma (RR = 1.8; P = 0.001), and liver cancer (RR = 1.8; P = 0.013), a reduced RR for prostate cancer (RR = 0.8; P = 0.012), and no increased risk for oral cavity/pharynx (RR = 1.4; P = 0.14), lung (RR = 1.2; P = 0.15), or colorectal (RR = 0.9; P = 0.34) cancers. Lung and oral cavity/pharynx cancers were elevated for HIV-infected subjects in models adjusted only for demographics. KS, NHL, anal cancer, HL, and colorectal cancer had significant (P < 0.05) trends for increasing RRs with decreasing recent CD4. The RRs for lung and oral cavity/pharynx cancer were significantly elevated with CD4 < 200 cells/μL and for melanoma and liver cancer with CD4 < 500 cells/μL. Only KS and NHL were associated with HIV RNA. Immunodeficiency was positively associated with all cancers examined except prostate cancer among HIV-infected compared with HIV-uninfected individuals, after adjustment for several cancer risk factors. Earlier antiretroviral therapy initiation to maintain high CD4 levels might reduce the burden of cancer in this population.
Author Dubrow, Robert
Horberg, Michael A.
Quesenberry, Charles P.
Towner, William J.
Chao, Chun
Xu, Lanfang
Klein, Daniel
Leyden, Wendy A.
Neugebauer, Romain S.
Abrams, Donald I.
Silverberg, Michael J.
AuthorAffiliation 2 Kaiser Permanente Southern California, Pasadena, CA, USA
1 Kaiser Permanente Northern California, Oakland, CA, USA
3 Mid-Atlantic Permanente Research Institute, Rockville, MD, USA
8 University of California San Francisco, San Francisco, CA, USA
5 Kaiser Permanente Southern California, Los Angeles, CA, USA
6 Yale School of Public Health and School of Medicine, New Haven, CT, USA
7 San Francisco General Hospital, San Francisco, CA, USA
4 Kaiser Permanente Northern California, Hayward, CA, USA
AuthorAffiliation_xml – name: 4 Kaiser Permanente Northern California, Hayward, CA, USA
– name: 3 Mid-Atlantic Permanente Research Institute, Rockville, MD, USA
– name: 1 Kaiser Permanente Northern California, Oakland, CA, USA
– name: 7 San Francisco General Hospital, San Francisco, CA, USA
– name: 2 Kaiser Permanente Southern California, Pasadena, CA, USA
– name: 5 Kaiser Permanente Southern California, Los Angeles, CA, USA
– name: 6 Yale School of Public Health and School of Medicine, New Haven, CT, USA
– name: 8 University of California San Francisco, San Francisco, CA, USA
Author_xml – sequence: 1
  givenname: Michael J.
  surname: Silverberg
  fullname: Silverberg, Michael J.
– sequence: 2
  givenname: Chun
  surname: Chao
  fullname: Chao, Chun
– sequence: 3
  givenname: Wendy A.
  surname: Leyden
  fullname: Leyden, Wendy A.
– sequence: 4
  givenname: Lanfang
  surname: Xu
  fullname: Xu, Lanfang
– sequence: 5
  givenname: Michael A.
  surname: Horberg
  fullname: Horberg, Michael A.
– sequence: 6
  givenname: Daniel
  surname: Klein
  fullname: Klein, Daniel
– sequence: 7
  givenname: William J.
  surname: Towner
  fullname: Towner, William J.
– sequence: 8
  givenname: Robert
  surname: Dubrow
  fullname: Dubrow, Robert
– sequence: 9
  givenname: Charles P.
  surname: Quesenberry
  fullname: Quesenberry, Charles P.
– sequence: 10
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  surname: Neugebauer
  fullname: Neugebauer, Romain S.
– sequence: 11
  givenname: Donald I.
  surname: Abrams
  fullname: Abrams, Donald I.
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25304703$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/22109347$$D View this record in MEDLINE/PubMed
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Issue 12
Keywords Infection
Immunopathology
Cancerology
Viral disease
Risk factor
Risk
Replication
AIDS
Malignant tumor
Immune deficiency
Cancer
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  start-page: 209
  year: 2003
  ident: 2022060919553625800_bib44
  article-title: Correlates of immune activation marker changes in human immunodeficiency virus (HIV)-seropositive and high-risk HIV-seronegative women who use illicit drugs
  publication-title: J Infect Dis
  doi: 10.1086/376509
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Snippet Background: Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group,...
Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group, adjusting for...
BACKGROUND: Few studies have compared cancer risk between HIV-infected individuals and a demographically similar HIV-uninfected internal comparison group,...
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SubjectTerms Adult
Anti-HIV Agents - administration & dosage
Biological and medical sciences
Cohort Studies
Female
HIV Infections - drug therapy
HIV Infections - immunology
HIV Infections - virology
Human viral diseases
Humans
Infectious diseases
Male
Medical sciences
Neoplasms - immunology
Neoplasms - virology
Risk Factors
Tumors
Viral diseases
Viral diseases of the lymphoid tissue and the blood. Aids
Viral Load
Virus Replication
Title HIV Infection, Immunodeficiency, Viral Replication, and the Risk of Cancer
URI https://www.ncbi.nlm.nih.gov/pubmed/22109347
https://www.proquest.com/docview/911931969
https://www.proquest.com/docview/918050428
https://pubmed.ncbi.nlm.nih.gov/PMC3237725
Volume 20
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