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  • HBX 41108 br Infection Main Main factor s for Carcinogenic m


    Infection Main Main factor(s) for Carcinogenic mechanism(s)b Gold standard for Cancers with sufficient Cancers with limited
    transmission transmission From Bouvard 2009 detection evidencec evidencec
    Hepatitis B HBX 41108 (HBV), Sera and other Reusing needles, Inflammation HBsAg Hepatocellular carcinoma Cholangiocarcino-
    chronic infection body fluids sexual intercourse Liver cirrhosis
    ma, non-Hodgkin
    Hepatitis C virus (HCV), Sera Reusing needles Chronic hepatitis HCV RNA Hepatocellular carcinoma, lymphoma
    Inflammation Cholangiocarcino-
    chronic infection
    Liver cirrhosis
    non-Hodgkin lymphoma ma
    Helicobacter pylori Oral/fecal Crowding, Liver fibrosis Immunoblot Non-cardia gastric None
    contaminated water Oxidative stress
    carcinoma, low-grade B-cell
    Altered cellular turn-over and
    MALT gastric lymphoma
    gene expression
    Epstein-Barr virusd Oral/saliva Pre-chewing food for Mutation EBER ISH Burkitt lymphoma, Hodgkin Gastric carcinoma,
    Cell proliferation
    babies, sharing Inhibition of apoptosis LMP1 IHC for lymphoma, extranodal lymphoepithe-
    utensils, kissing Genomic instability Hodgkin natural killer T-cell lioma-like
    Cell migration lymphoma lymphoma - nasal type, carcinoma
    (Gulley and Tang, nasopharyngeal carcinoma,
    2008) immune suppression-related
    Human papillomavirus Skin-to-skin/ Sexual contact Immortalisation PCR alone or non-Hodgkin lymphoma Laryngeal
    Cancers of the cervix, anus,
    (HPV), type 16 mucosal including oral sex Genomic instability with p16 for penis, vagina, vulva, carcinoma
    and open mouth Inhibition of DNA damage anogenital oropharynx, tonsil, and oral
    kissing response cancers cavity
    Anti-apoptotic activity E6 and/or E7
    mRNA for head
    Human herpesvirus, Oral/saliva Sexual contact Cell proliferation and neck cancers Kaposi sarcoma, primary Multicentric
    type 8e
    including oral sex Inhibition of apoptosis
    effusion lymphoma Castleman's disease
    and open mouth Genomic instability
    Human T-cell Sera and other kissing Cell migration PCR Adult T-cell leukemia/ None
    Breast-feeding, sexual Immortalisation and
    lymphotropic virus, body fluids, intercourse, and transformation of T cells
    type 1 (HTLV-1) including breast reusing needles
    milk (Goncalves et al.,
    Abbreviations: HBsAg = Hepatitis B surface antigen, RNA = ribonucleic acid, mRNA = messenger ribonucleic acid, EBER ISH = Epstein-Barr virus encoding region in situ hybridization, LMP1 = latent member protein 1, IHC = immunohistochemistry, PCR = polymerase chain reaction, IFA = immunofluorescent assays, MALT = mucosa-associated lymphoid tissue. a Included infections have been categorized by IARC as Group 1 carcinogens. b Carcinogenic mechanisms were taken from Bouvard 2009 (Bouvard et al., 2009). c Cancer sites were categorized by IARC as having sufficient or limited evidence. d Epstein-Barr virus is also referred to as human herpesvirus, type 4. e Human herpesvirus, type 8 is also referred to as Kaposi sarcoma virus.
    (HIV) because HIV acts indirectly through immunosuppression, thereby amplifying the carcinogenic effects of co-infections such as Epstein-Barr virus (EBV), HCV, and HPV, infections that are already included in our analysis. Table 1 also enumerates the cancers for which there was ‘sufficient’ evidence for the role of infections in carcinogenesis, as concluded by IARC (International Agency for Research on Cancer, 2012). There was one exception; we estimated the impact of HPV16 on laryngeal cancer incidence because more data have accumulated since the last IARC monograph publication on HPV in support of an etiologic role of HPV in laryngeal cancer (Li et al., 2013; Torrente et al., 2011).
    2.2. Population attributable risk calculations
    To estimate the proportion of cancer incidence that could have been avoided had the infection been eliminated, we calculated population attributable risks (PARs). The three equations below can estimate PARs for binary exposures (infected or not). The first formula requires the infection prevalence in the general population (Pe) and the relative risk
    (RR) or odds ratio (OR) associated with the cancer (Levin, 1953). When Pe is not known, the second formula can estimate PARs using pre-valence in cases (Pc) in place of Pe (Miettinen, 1974). The third formula is used when the attributable risk in the exposed approaches 1.0 (i.e., RRs are very high), such that the prevalence in cases approximates the PAR.