Silvia de Sanjosé

IDIBELL Bellvitge Biomedical Research Institute, Barcino, Catalonia, Spain

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Publications (345)2005.89 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Country-level HPV genotyping data may be sought by decision-makers to gauge the genotype-specific burden of HPV-related diseases in their jurisdiction and assess the potential impact of HPV vaccines. We investigated, by country, the availability of published literature on HPV genotypes in cervical, vaginal and vulvar cancers and intraepithelial neoplasms (CINs, VaINs and VINs) and on prevalence and incidence of genital HPV infections among women without clinically manifest disease. Findings Primary sources of publications were the PubMed/Medline and EMBASE databases. Original studies or meta-analyses published from 2000, covering genotypes 16 and 18 and at least one of genotypes 31/33/45/52/58, were included. Key exclusion criteria were language not English, cervical lesions not histologically confirmed (cytology only), special populations (e.g., immunocompromised) and, for cervical studies, small population (<50). A total of 727 studies reporting HPV genotype-specific data were identified: 366 for cervical cancers and CINs, 43 for vulvar or vaginal cancers and VINs/VaINs, and 395 and 21 for infection prevalence and incidence, respectively, in general female population samples. A large proportion of studies originated from a small set of countries. Cervical cancer/CIN typing data was scarce for several regions with the highest cervical cancer burden, including Eastern, Middle and Western Africa, Central America, South-East Asia, South Asia, and Eastern Europe. Data for vulvar/vaginal disease was limited outside of Europe and North America. Conclusions Although a large body of published HPV genotype-specific data is currently available, data gaps exist for genotype-specific infection incidence and several world regions with the highest cervical cancer burden. Electronic supplementary material The online version of this article (doi:10.1186/s13027-015-0008-y) contains supplementary material, which is available to authorized users.
    Infectious Agents and Cancer 12/2015; 10(1). DOI:10.1186/s13027-015-0008-y · 2.07 Impact Factor
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    ABSTRACT: Excess adiposity has been associated with lymphomagenesis, possibly mediated by increased cytokine production causing a chronic inflammatory state. The relationship between obesity, cytokine polymorphisms and selected mature B-cell neoplasms is reported. Data on 4979 cases and 4752 controls from nine American/European studies from the InterLymph consortium (1988-2008) were pooled. For diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL) and chronic lymphocytic leukaemia/small lymphocytic lymphoma (CLL/SLL), joint associations of body mass index (from self-reported height and weight) and 12 polymorphisms in cytokines IL1A (rs1800587), IL1B (rs16944, rs1143627), IL1RN (rs454078), IL2 (rs2069762), IL6 (rs1800795, rs1800797), IL10 (rs1800890, rs1800896), TNF (rs1800629), LTA (rs909253), and CARD15 (rs2066847) were investigated using unconditional logistic regression. BMI-polymorphism interaction effects were estimated using the relative excess risk due to interaction (RERI). Obesity (BMI≥30kg m-2) was associated with DLBCL risk (OR=1.33, 95%CI 1.02-1.73), as was TNF-308GA+AA (OR=1.24, 95%CI 1.07-1.44). Together, being obese and TNF-308GA+AA increased DLBCL risk almost two-fold relative to those of normal weight and TNF-308GG (OR=1.93 95%CI 1.27-2.94), with a RERI of 0.41 (95%CI -0.05,0.84, P(interaction)=0.13). For FL and CLL/SLL, no associations with obesity or TNF-308GA+AA, either singly or jointly, were observed. No evidence of interactions between obesity and the other polymorphisms were detected. Our results suggest that cytokine polymorphisms do not generally interact with BMI to increase lymphoma risk but obesity and TNF-308GA+AA may interact to increase DLBCL risk. Studies using better measures of adiposity are needed to further investigate the interactions between obesity and TNF-308G>A in the pathogenesis of lymphoma. Copyright © 2015, American Association for Cancer Research.
    Cancer Epidemiology Biomarkers & Prevention 05/2015; DOI:10.1158/1055-9965.EPI-14-1355 · 4.32 Impact Factor
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    ABSTRACT: Merkel cell polyomavirus (MCPyV) has been suspected to cause chronic lymphocytic leukemia (CLL) but previous data are inconsistent. We measured seroreactivities of 9 polyomaviruses (MCPyV, BKPyV, JCPyV, LPyV, KIPyV, WUPyV, HPyV-6, HPyV-7 and TSPyV) in 359 CLL cases and 370 controls using bead-based multiplex serology technology. We additionally tested two herpesviruses (HSV-1 and CMV). Associations between disease and viral seroreactivities were assessed using logistic regression. All human viruses showed high seroprevalences (69-99%) against structural proteins in controls but significant lower viral seroprevalences in cases (58-94%; OR range=0.21-0.70, p-value<0.05), except for MCPyV (OR=0.79, 95%CI=0.54-1.16). Lower seroreactivity levels were observed among CLL subjects, with significant differences already observed at early stages of diseases, unrelated to treatment status. Seroreactivities against polyomaviruses related oncoproteins were almost null. Our data suggest no association for MCPyV polyomavirus with CLL development and an unlikely association for other polyomaviruses tested.
    Journal of General Virology 04/2015; DOI:10.1099/vir.0.000167 · 3.53 Impact Factor
  • Anna R Giuliano, Aimée R Kreimer, Silvia de Sanjose
    CancerSpectrum Knowledge Environment 04/2015; 107(6). DOI:10.1093/jnci/djv128 · 15.16 Impact Factor
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    ABSTRACT: Background:Incidence rates of lymphoma are usually higher in men than in women, and oestrogens may protect against lymphoma.Methods:We evaluated occupational exposure to endocrine disrupting chemicals (EDCs) among 2457 controls and 2178 incident lymphoma cases and subtypes from the European Epilymph study.Results:Over 30 years of exposure to EDCs compared to no exposure was associated with a 24% increased risk of mature B-cell neoplasms (P-trend=0.02). Associations were observed among men, but not women.Conclusions:Prolonged occupational exposure to endocrine disruptors seems to be moderately associated with some lymphoma subtypes.British Journal of Cancer advance online publication, 5 March 2015; doi:10.1038/bjc.2015.83 www.bjcancer.com.
    British Journal of Cancer 03/2015; 112(7). DOI:10.1038/bjc.2015.83 · 4.82 Impact Factor
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    ABSTRACT: Analysis of the cervical cancer screening activity in the National Health System of Catalonia has identified a cytological coverage at 3 years of 40.8%, an interval of 2.4 years between Pap smears and a loss to follow-up of 50% at 3 years in women aged 25-65 years old. The introduction of human papillomavirus testing in the management of women with cytological results of atypical squamous cell of undetermined significance and as an adjunct to cytology in women with a history of inadequate screening has facilitated the management and detection of women at risk of developing cervical intraepithelial neoplasia grade 2 or worse (CIN2 + ).
    Progresos de Obstetricia y Ginecología 02/2015; 58(5). DOI:10.1016/j.pog.2014.10.004
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    ABSTRACT: Recently the International Agency for Research on Cancer (IARC) Programme for the Evaluation of Carcinogenic Risks to Humans has been criticized for several of its evaluations, and also the approach used to perform these evaluations. Some critics have claimed that IARC Working Groups' failures to recognize study weaknesses and biases of Working Group members have led to inappropriate classification of a number of agents as carcinogenic to humans. The authors of this paper are scientists from various disciplines relevant to the identification and hazard evaluation of human carcinogens. We have examined here criticisms of the IARC classification process to determine the validity of these concerns. We review the history of IARC evaluations and describe how the IARC evaluations are performed. We conclude that these recent criticisms are unconvincing. The procedures employed by IARC to assemble Working Groups of scientists from the various discipline and the techniques followed to review the literature and perform hazard assessment of various agents provide a balanced evaluation and an appropriate indication of the weight of the evidence. Some disagreement by individual scientists to some evaluations is not evidence of process failure. The review process has been modified over time and will undoubtedly be altered in the future to improve the process. Any process can in theory be improved, and we would support continued review and improvement of the IARC processes. This does not mean, however, that the current procedures are flawed. The IARC Monographs have made, and continue to make, major contributions to the scientific underpinning for societal actions to improve the public's health.
    Environmental Health Perspectives 02/2015; DOI:10.1289/ehp.1409149 · 7.03 Impact Factor
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    ABSTRACT: Autoimmune conditions and immune system-related genetic variations are associated with risk of non-Hodgkin lymphoma (NHL). In a pooled analysis of 8,692 NHL cases and 9,260 controls from 14 studies (1988-2007) within the International Lymphoma Epidemiology Consortium, we evaluated the interaction between immune system genetic variants and autoimmune conditions in NHL risk. We evaluated the immunity-related single nucleotide polymorphisms rs1800629 (tumor necrosis factor gene (TNF) G308A), rs1800890 (interleukin-10 gene (IL10) T3575A), rs6457327 (human leukocyte antigen gene (HLA) class I), rs10484561 (HLA class II), and rs2647012 (HLA class II)) and categorized autoimmune conditions as primarily mediated by B-cell or T-cell responses. We constructed unconditional logistic regression models to measure associations between autoimmune conditions and NHL with stratification by genotype. Autoimmune conditions mediated by B-cell responses were associated with increased NHL risk, specifically diffuse large B-cell lymphoma (odds ratio (OR) = 3.11, 95% confidence interval (CI): 2.25, 4.30) and marginal zone lymphoma (OR = 5.80, 95% CI: 3.82, 8.80); those mediated by T-cell responses were associated with peripheral T-cell lymphoma (OR = 2.14, 95% CI: 1.35, 3.38). In the presence of the rs1800629 AG/AA genotype, B-cell-mediated autoimmune conditions increased NHL risk (OR = 3.27, 95% CI: 2.07, 5.16; P-interaction = 0.03) in comparison with the GG genotype (OR = 1.82, 95% CI: 1.31, 2.53). This interaction was consistent across major B-cell NHL subtypes, including marginal zone lymphoma (P-interaction = 0.02) and follicular lymphoma (P-interaction = 0.04). © The Author 2015. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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    ABSTRACT: Epstein-Barr virus (EBV)-related malignancies harbour distinct serological responses to EBV antigens. We hypothesized that EBV serological patterns can be useful to identify different stages of chronic lymphocytic leukemia. Information on 150 cases with chronic lymphocytic leukemia and 157 frequency-matched (by age, sex and region) population-based controls from a Spanish multicentre case-control study was obtained. EBV immunoglobulin G serostatus was evaluated through a peptide-based ELISA and further by immunoblot analysis to EBV early antigens (EA), nuclear antigen (EBNA1), VCA-p18, VCA-p40 and Zebra. Two independent individuals categorized the serological patterns of the western blot analysis. Patients with very high response and diversity in EBV-specific polypeptides, in particular with clear responses to EA-associated proteins, were categorized as having an abnormal reactive pattern (ab_EBV). Adjusted odds ratios (OR) and 95% confidence interval (CI) were estimated using logistic regression models. Almost all subjects were EBV-IgG positive (>95% of cases and controls) whereas ab_EBV patterns were detected in 23% of cases (N = 34) and 11% of controls (N = 17; OR: 2.44, 95% CI, 1.29 to 4.62; P = 0.006), particularly in intermediate/high risk patients. Although based on small numbers, the association was modified by smoking with a gradual reduction of ab_EBV-related OR for all Rai stages from never smokers to current smokers. Highly distinct EBV antibody diversity patterns revealed by immunoblot analysis were detected in cases compared to controls, detectable at very early stages of the disease and particularly among non smokers. This study provides further evidence of an abnormal immunological response against EBV in patients with chronic lymphocytic leukemia.
    Infectious Agents and Cancer 02/2015; 10. DOI:10.1186/1750-9378-10-5 · 2.07 Impact Factor
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    ABSTRACT: Anal condylomata are common in HIV-positive individuals and among men who have sex with men (MSM). Generally attributable to infection by low-risk human papillomaviruses (HPVs), condylomata are considered benign low-grade Squamous Intraepithelial Lesions (SILs). However, anal condylomata have occasionally been linked to high-grade SIL and to oncogenic, high-risk HPVs. Here we describe the range of intraepithelial lesions and of the associated HPVs in heterosexual men/women and MSM. Perianal and anal condylomata were collected from 243 patients (56 heterosexual women, 61 heterosexual men and 126 MSM, including 41 HIV-positive MSM). We assessed lesion histology and HPV genotype. Prevalence estimates and Poisson models were used. Irrespective of HIV-infection status, MSM showed higher proportion of condylomata as high-grade SILs compared with heterosexual men/women. High-grade SILs were also more prevalent in anal than in perianal lesions in all patient groups. HIV-positive MSM exhibited increased prevalence ratio [4.6; 95% CI: 2.1-10.0] of perianal low-grade SILs containing only high-risk HPVs compared with HIV-negative MSM. In addition, more than 64% of anal SILs with a high-grade component, regardless of HIV infection, were exclusively associated with low-risk HPVs. In anal condylomata, both high-grade and low-grade SILs can be associated with high-risk and/or low-risk HPVs. Particularly, low-grade perianal SILs associated with high-risk HPVs were common in HIV-positive MSM, while presence of only low-risk HPVs in high-grade SILs were common in both MSM groups. Our findings sound a note of caution for the common clinical practice for the treatment of anal condylomata as benign lesions in MSM and HIV+ patients.
    Clinical Microbiology and Infection 02/2015; in press. DOI:10.1016/j.cmi.2015.02.009 · 5.20 Impact Factor
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    ABSTRACT: Great controversy exists about the association between Human Papillomavirus (HPV) and breast tumors. The aim of this study was to explore the presence of HPV DNA in a large set of breast cancer cases. Techniques used followed the standards for an international retrospective survey of HPV-DNA genotyping, coordinated by our own group and the DDL Laboratories in Rijswijk, the Netherlands. Paraffin-embedded samples were used. SPF-10 broad-spectrum primers were applied, followed by deoxyribonucleic acid enzyme immunoassay and genotyping by reverse-line probe assay. A total of 78 samples were included in the study, 2 of benign conditions and 76 carcinomas, including different histological subtypes. HPV was not present in any of the specimens studied irrespective of histology, hormonal status and stage of disease. Our data do not support the involvement of HPV in breast carcinogenesis as no evidence of its presence was found. Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.
    Anticancer research 02/2015; 35(2):851-6. · 1.87 Impact Factor
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    ABSTRACT: We present the protocol of a large population-based case-control study of 5 common tumors in Spain (MCC-Spain) that evaluates environmental exposures and genetic factors. Between 2008-2013, 10,183 persons aged 20-85 years were enrolled in 23 hospitals and primary care centres in 12 Spanish provinces including 1,115 cases of a new diagnosis of prostate cancer, 1,750 of breast cancer, 2,171 of colorectal cancer, 492 of gastro-oesophageal cancer, 554 cases of chronic lymphocytic leukaemia (CLL) and 4,101 population-based controls matched by frequency to cases by age, sex and region of residence. Participation rates ranged from 57% (stomach cancer) to 87% (CLL cases) and from 30% to 77% in controls. Participants completed a face-to-face computerized interview on sociodemographic factors, environmental exposures, occupation, medication, lifestyle, and personal and family medical history. In addition, participants completed a self-administered food-frequency questionnaire and telephone interviews. Blood samples were collected from 76% of participants while saliva samples were collected in CLL cases and participants refusing blood extractions. Clinical information was recorded for cases and paraffin blocks and/or fresh tumor samples are available in most collaborating hospitals. Genotyping was done through an exome array enriched with genetic markers in specific pathways. Multiple analyses are planned to assess the association of environmental, personal and genetic risk factors for each tumor and to identify pleiotropic effects. This study, conducted within the Spanish Consortium for Biomedical Research in Epidemiology & Public Health (CIBERESP), is a unique initiative to evaluate etiological factors for common cancers and will promote cancer research and prevention in Spain. Copyright © 2014 SESPAS. Published by Elsevier Espana. All rights reserved.
    Gaceta Sanitaria 01/2015; DOI:10.1016/j.gaceta.2014.12.003 · 1.25 Impact Factor
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    ABSTRACT: Epstein-Barr virus (EBV) causes rare malignant lymphomas. The role of EBV in other non-Hodgkin lymphomas (NHL) remains unclear, but mildly reduced immune function could lead to reactivation of EBV and subsequent NHL. We examined the association between prospectively-collected plasma EBV antibodies and NHL risk in the Cancer Prevention Study-II (CPS-II) Nutrition Cohort and conducted a meta-analysis of our and published results. The CPS-II study included 225 NHL cases and 2:1 matched controls. No associations were observed between EBV serostatus or antibody levels and risk of NHL overall. However, when including only the three most common types of NHL (diffuse large B-cell lymphoma, follicular lymphoma, chronic lymphocytic leukemia/small lymphocytic lymphoma), high compared to low early antigen-diffuse (EA-D) and BZLF1-encoded replication activator (ZEBRA) antibodies were associated with approximately 60% higher risk of NHL. Odds ratios (OR) for EBV nuclear antigen-1 and viral capsid antigen (VCA)-p18 were elevated but not statistically significant. In the meta-analysis, both EA (summary OR=1.52, 95% confidence interval (CI): 1.16-2.00) and VCA (summary OR=1.20, 95% CI: 1.00-1.44) were positively associated with NHL risk. These results suggest EBV may be associated with a wider spectrum of NHL subtypes, but further study is needed to confirm and fully understand these associations. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 01/2015; 136(1). DOI:10.1002/ijc.28971 · 5.01 Impact Factor
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    ABSTRACT: Marginal zone lymphoma (MZL) is the third most common subtype of B-cell non-Hodgkin lymphoma. Here we perform a two-stage GWAS of 1,281 MZL cases and 7,127 controls of European ancestry and identify two independent loci near BTNL2 (rs9461741, P=3.95 × 10(-15)) and HLA-B (rs2922994, P=2.43 × 10(-9)) in the HLA region significantly associated with MZL risk. This is the first evidence that genetic variation in the major histocompatibility complex influences MZL susceptibility.
    Nature Communications 01/2015; 6:5751. DOI:10.1038/ncomms6751 · 10.74 Impact Factor
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    ABSTRACT: Background:CLL is a chronic disease that often progresses slowly from a precursor stage, monoclonal B-cell lymphocytosis (MBL), and that can remain undiagnosed for a long time. Methods:Within the European EPIC cohort, we measured pre-diagnostic plasma sCD23 for 179 individuals who eventually were diagnosed with CLL and an equal number of matched control subjects who remained free of cancer. Results: In a very large proportion of CLL patients plasma sCD23 was clearly elevated 7 or more years before diagnosis. Considering sCD23 as a disease predictor, the area under the ROC curve (AUROC) was 0.95 [95% CI (0.90, 1.00)] for CLL diagnosed within 0.1-2.7 years after blood measurement, 0.90 [0.86-0.95] for diagnosis within 2.8-7.3 years, and 0.76 [0.65-0.86] for CLL diagnosed between 7.4 and 12.5 years. Even at a 7.4-year and longer time interval, elevated plasma sCD23 could predict a later clinical diagnosis of CLL with 100% specificity at >45% sensitivity. Conclusions:Our findings provide unique documentation for the very long latency times during which measurable B-cell lympho-proliferative disorder exists prior to the clinical manifestation of CLL. Impact:Our findings have relevance for the interpretation of prospective epidemiologic studies on the causes of CLL in terms of reverse causation bias. The lag-times indicate a time frame within which an early detection of CLL would be theoretically possible. Copyright © 2014, American Association for Cancer Research.
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    ABSTRACT: Background: Past investigations of cigarette smoking and multiple myeloma have been underpowered to detect moderate associations, particularly within subgroups. To clarify this association we conducted a pooled analysis of nine case-control studies in the International Multiple Myeloma Consortium, with individual-level questionnaire data on cigarette smoking history and other covariates. Methods: Using a pooled population of 2,670 cases and 11,913 controls, we computed odds ratios (ORs) and 95% confidence intervals (CIs) relating smoking to multiple myeloma risk using unconditional logistic regression adjusting for gender, age group, race, education, body mass index, alcohol consumption, and study center. Results: Neither ever smokers (OR=0.95, 95% CI 0.87-1.05), current smokers (OR=0.82, 95% CI 0.73-0.93), nor former smokers (OR=1.03, 95% CI 0.92-1.14) had increased risks of multiple myeloma compared to never smokers. Analyses of smoking frequency, pack-years, and duration did not reveal significant or consistent patterns, and there was no significant effect modification by subgroups. Conclusion: Findings from this large pooled analysis do not support the hypothesis of cigarette smoking as a causal factor for multiple myeloma. Impact: Cigarette smoking is one of the most important risk factors for cancer, but the association with multiple myeloma was inconclusive. This study had excellent power to detect modest associations, and had individual-level data to evaluate confounding and effect modification by potentially important factors that were not evaluated in previous studies. Our findings confirm that smoking is not a risk factor for multiple myeloma. Copyright © 2014, American Association for Cancer Research.
  • Laura Costas, Silvia de Sanjosé, Claire Infante-Rivard
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    ABSTRACT: Considerable efforts have been made to elucidate non-Hodgkin lymphoma's (NHL) etiology during the last decades. Some evidence points to an association with reproductive factors, as incidence rates for most NHL subtypes are usually higher in men than in women, and several subtypes express hormonal receptors. Although the evidence is not compelling, some studies show an inverse association with gravidity. Associations with postmenopausal hormone therapy are usually derived from unopposed estrogen use, rather than for the combination of estrogen with progestin, but these findings vary by study design. Inconsistencies in the results are likely due to the complex relationship between reproductive, biological, and sociodemographic factors, as well as to study limitations. Elucidating the role of hormonal factors should provide clues for therapeutic options and public health decisions. We provide an overview of the available evidence on reproductive factors in NHL etiology, underscoring potential sources of discrepancies and bias.
    Critical Reviews in Oncology/Hematology 12/2014; 92(3). DOI:10.1016/j.critrevonc.2014.07.004 · 4.05 Impact Factor
  • Revista Española de Salud Pública 12/2014; 88(6):735-743. DOI:10.4321/S1135-57272014000600006 · 0.71 Impact Factor
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    ABSTRACT: Eight HPV types (HPV26, 53, 66, 67, 68, 70, 73 and 82) that are phylogenetically closely related to 12 WHO-defined high-risk (HR-)HPV have been rarely but consistently identified as single HPV infections in about 3% of cervical cancer (CxCa) tissues. Due to lack of biological data, these types are referred to as probable/possible (p)HR-HPV. To analyze their biological activity in direct comparison to HR-HPV types, we selected 55 formalin-fixed paraffin-embedded (FFPE) CxCa tissues harboring single pHR-HPV infections (2-13 cases per type) and 266 tissues harboring single HR-HPV (7-40 cases per type) from a worldwide, retrospective, cross-sectional study. Single HPV infection was verified by two genotyping methods. Presence of type-specific spliced E6*I mRNA transcripts and expression of cellular proteins indicative of HPV transformation were assessed in all cases. In 55 CxCa tissues with pHR-HPV, E6*I mRNA expression was 100%, high p16INK4a, 98%; low pRb, 96%; low CyD1, 93% and low p53, 84%. Compared to HPV16 tissues as a reference, individual frequencies of these five markers did not differ significantly, either for any of the eight pHR-HPV and the 11 other HR-types individually, or for the groups of pHR- and HR-types without HPV16. We conclude that the eight pHR-HPV types, when present as a single infection in CxCa, are biologically active and affect the same cellular pathways as any of the fully-recognized carcinogenic HR-HPV types. Therefore we have provided molecular evidence of carcinogenicity for types currently classified as probably/possibly carcinogenic. Although this evidence is crucial for HPV type carcinogenicity classification, per se it is not sufficient for inclusion of these HPV types into population-wide primary and secondary prevention programs. Such decisions have to include careful estimation of effectiveness and cost-benefit analyses.
    The Journal of Pathology 12/2014; 234(4). DOI:10.1002/path.4405 · 7.33 Impact Factor

Publication Stats

17k Citations
2,005.89 Total Impact Points

Institutions

  • 2006–2015
    • IDIBELL Bellvitge Biomedical Research Institute
      Barcino, Catalonia, Spain
    • Università degli studi di Cagliari
      Cagliari, Sardinia, Italy
    • VU University Amsterdam
      Amsterdamo, North Holland, Netherlands
  • 2001–2015
    • Catalan Institute of Oncology
      • Infections and Cancer Unit
      Badalona, Catalonia, Spain
  • 2014
    • Mayo Clinic - Rochester
      • Department of Health Science Research
      Рочестер, Minnesota, United States
    • Centro de Investigación Biomedica En Red del Área de Salud Mental
      Madrid, Madrid, Spain
  • 2013–2014
    • National Cancer Institute (USA)
      • • Radiation Epidemiology
      • • Division of Cancer Epidemiology and Genetics
      베서스다, Maryland, United States
  • 2008–2014
    • University of Barcelona
      Barcino, Catalonia, Spain
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
    • IDIBGI Girona Biomedical Research Institute
      Girona, Catalonia, Spain
  • 2006–2014
    • National Institutes of Health
      • • Branch of Radiation Epidemiology
      • • Division of Cancer Epidemiology and Genetics
      베서스다, Maryland, United States
  • 1996–2014
    • Institut Català d'Oncologia
      Barcino, Catalonia, Spain
    • Clinica Girona
      Girona, Catalonia, Spain
  • 2012–2013
    • Madrid Salud
      Madrid, Madrid, Spain
    • Vall d’Hebron Institute of Oncology
      Barcino, Catalonia, Spain
    • Universitätsklinikum Freiburg
      • Center for Chronic Immunodeficiency (CCI)
      Freiburg, Lower Saxony, Germany
  • 2011
    • University of Amsterdam
      Amsterdamo, North Holland, Netherlands
    • DDL Diagnostic Laboratory
      Rijswijk, South Holland, Netherlands
  • 2010
    • University of California, Berkeley
      • School of Public Health
      Berkeley, California, United States
  • 2007
    • Hospital Universitario Ramón y Cajal
      Madrid, Madrid, Spain
    • University of Crete
      Retimo, Crete, Greece
  • 1998–2006
    • Molecular Biology Institute of Barcelona
      Barcino, Catalonia, Spain
  • 2002–2004
    • Hospital Monte Aranco
      Oviedo, Asturias, Spain
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 2003
    • VU University Medical Center
      Amsterdamo, North Holland, Netherlands
  • 1991–2003
    • International Agency for Research on Cancer
      • Section of Cancer Information
      Lyons, Rhône-Alpes, France
  • 2000
    • Johns Hopkins Bloomberg School of Public Health
      Baltimore, Maryland, United States
  • 1995
    • Hospital Universitario Virgen del Rocío
      Hispalis, Andalusia, Spain