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        <title>Infectious Agents and Cancer - Most accessed articles</title>
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        <description>The most accessed research articles published by Infectious Agents and Cancer</description>
        <dc:date>2012-04-19T00:00:00Z</dc:date>
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        <title>Chlamydia psittaci in Ocular Adnexa MALT Lymphoma: a possible role in lymphomagenesis and a different geographical distribution</title>
        <description>Ocular adnexa MALT-lymphomas represent approximatively 5-15% of all extranodal lymphomas. Almost 75% of OAMLs are localized in orbital fat, while 25% of cases involves conjunctive. MALT-lymphomas often recognize specific environmental factors responsible of lymphoma development and progression. In particular as Helicobacter pylori in gastric MALT lymphomas, other bacterial infections have been recognized related to MALT lymphomas in specific site. Recently Chlamydia psittaci has been identified in Ocular Adnexa MALT lymphomas, with variable frequence dependently from geographic areas. Thus bacterial infection is responsible of clonal selection on induced MALT with subsequent lymphoma development. Moreover Chlamydia psittaci could promote chromosomal aberration either through genetic instability as a consequence of induced proliferation and probably through DNA oxidative damage. The most common translocation described in MALT lymphomas affects NF-kB pathway with a substantial antiapoptotic effect. Several therapeutic approaches are now available, but the use of antibiotic-therapy in specific cases, although with conflicting results, could improve the treatment of ocular adnexa MALT lymphomas. In this review we analyse the most relevant features of Ocular adnexa MALT lymphomas, underlining specific biological characteristics mainly related to the potential role of Chlamydia psittaci in lymphomagenesis.</description>
        <link>http://www.infectagentscancer.com/content/7/1/8</link>
                <dc:creator>Francesca Collina</dc:creator>
                <dc:creator>Anna De Chiara</dc:creator>
                <dc:creator>Amalia De Renzo</dc:creator>
                <dc:creator>Gaetano De Rosa</dc:creator>
                <dc:creator>Gerardo Botti</dc:creator>
                <dc:creator>Renato Franco</dc:creator>
                <dc:source>Infectious Agents and Cancer 2012, null:8</dc:source>
        <dc:date>2012-04-02T00:00:00Z</dc:date>
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        <title>Ultraviolet radiation exposure and HIV-associated non-Hodgkin lymphoma risk</title>
        <description>No description available</description>
        <link>http://www.infectagentscancer.com/content/7/S1/P25</link>
                <dc:source>Infectious Agents and Cancer 2012, null:P25</dc:source>
        <dc:date>2012-04-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-7-S1-P25</dc:identifier>
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        <title>The prevalence of HIV-1 DNA in AIDS-related lymphoma and Kaposi Sarcoma throughout the AIDS epidemic</title>
        <description>No description available</description>
        <link>http://www.infectagentscancer.com/content/7/S1/P43</link>
                <dc:source>Infectious Agents and Cancer 2012, null:P43</dc:source>
        <dc:date>2012-04-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-7-S1-P43</dc:identifier>
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        <title>R-CHOP versus CHOP in HIV-associated lymphoma: a meta-analysis of prospective studies</title>
        <description>No description available</description>
        <link>http://www.infectagentscancer.com/content/7/S1/P22</link>
                <dc:source>Infectious Agents and Cancer 2012, null:P22</dc:source>
        <dc:date>2012-04-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-7-S1-P22</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/7/1/4">
        <title>Evaluation of a combined triple method to detect causative HPV in oral and oropharyngeal squamous cell carcinomas: p16 Immunohistochemistry, Consensus PCR HPV-DNA, and In Situ Hybridization</title>
        <description>Background:
Recent emerging evidences identify Human Papillomavirus (HPV) related Head and Neck squamous cell carcinomas (HN-SCCs) as a separate subgroup among Head and Neck Cancers with different epidemiology, histopathological characteristics, therapeutic response to chemo-radiation treatment and clinical outcome. However, there is not a worldwide consensus on the methods to be used in clinical practice. The endpoint of this study was to demonstrate the reliability of a triple method which combines evaluation of: 1. p16 protein expression by immunohistochemistry (p16-IHC); 2. HPV-DNA genotyping by consensus HPV-DNA PCR methods (Consensus PCR); and 3 viral integration into the host by in situ hybridization method (ISH). This triple method has been applied to HN-SCC originated from oral cavity (OSCC) and oropharynx (OPSCC), the two anatomical sites in which high risk (HR) HPVs have been clearly implicated as etiologic factors. Methylation-Specific PCR (MSP) was performed to study inactivation of p16-CDKN2a locus by epigenetic events. Reliability of multiple methods was measured by Kappa statistics.
Results:
All the HN-SCCs confirmed HPV positive by PCR and/or ISH were also p16 positive by IHC, with the latter showing a very high level of sensitivity as single test (100% in both OSCC and OPSCC) but lower specificity level (74% in OSCC and 93% in OPSCC).Concordance analysis between ISH and Consensus PCR showed a faint agreement in OPSCC (&#954; = 0.38) and a moderate agreement in OSCC (&#954; = 0.44). Furthermore, the addition of double positive score (ISHpositive and Consensus PCR positive) increased significantly the specificity of HR-HPV detection on formalin-fixed paraffin embedded (FFPE) samples (100% in OSCC and 78.5% in OPSCC), but reduced the sensitivity (33% in OSCC and 60% in OPSCC). The significant reduction of sensitivity by the double method was compensated by a very high sensitivity of p16-IHC detection in the triple approach.
Conclusions:
Although HR-HPVs detection is of utmost importance in clinical settings for the Head and Neck Cancer patients, there is no consensus on which to consider the &apos;golden standard&apos; among the numerous detection methods available either as single test or combinations. Until recently, quantitative E6 RNA PCR has been considered the &apos;golden standard&apos; since it was demonstrated to have very high accuracy level and very high statistical significance associated with prognostic parameters. In contrast, quantitative E6 DNA PCR has proven to have very high level of accuracy but lesser prognostic association with clinical outcome than the HPV E6 oncoprotein RNA PCR. However, although it is theoretically possible to perform quantitative PCR detection methods also on FFPE samples, they reach the maximum of accuracy on fresh frozen tissue. Furthermore, worldwide diagnostic laboratories have not all the same ability to analyze simultaneously both FFPE and fresh tissues with these quantitative molecular detection methods. Therefore, in the current clinical practice a p16-IHC test is considered as sufficient for HPV diagnostic in accordance with the recently published Head and Neck Cancer international guidelines. Although p16-IHC may serve as a good prognostic indicator, our study clearly demonstrated that it is not satisfactory when used exclusively as the only HPV detecting method. Adding ISH, although known as less sensitive than PCR-based detection methods, has the advantage to preserve the morphological context of HPV-DNA signals in FFPE samples and, thus increase the overall specificity of p16/Consensus PCR combination tests.</description>
        <link>http://www.infectagentscancer.com/content/7/1/4</link>
                <dc:creator>Giuseppe Pannone</dc:creator>
                <dc:creator>Vito Rodolico</dc:creator>
                <dc:creator>Angela Santoro</dc:creator>
                <dc:creator>Lorenzo Lo Muzio</dc:creator>
                <dc:creator>Renato Franco</dc:creator>
                <dc:creator>Gerardo Botti</dc:creator>
                <dc:creator>Gabriella Aquino</dc:creator>
                <dc:creator>Maria Carmela Pedicillo</dc:creator>
                <dc:creator>Simona Cagiano</dc:creator>
                <dc:creator>Giuseppina Campisi</dc:creator>
                <dc:creator>Corrado Rubini</dc:creator>
                <dc:creator>Silvana Papagerakis</dc:creator>
                <dc:creator>Gaetano De Rosa</dc:creator>
                <dc:creator>Maria Lina Tornesello</dc:creator>
                <dc:creator>Franco Buonaguro</dc:creator>
                <dc:creator>Stefania Staibano</dc:creator>
                <dc:creator>Pantaleo Bufo</dc:creator>
                <dc:source>Infectious Agents and Cancer 2012, null:4</dc:source>
        <dc:date>2012-02-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-7-4</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/7/1/7">
        <title>Innate immunity and hepatitis C virus infection: a microarray&apos;s view</title>
        <description>Hepatitis C virus (HCV) induces a chronic infection in more than two-thirds of HCV infected subjects. The inefficient innate and adaptive immune responses have been shown to play a major pathogenetic role in the development and persistence of HCV chronic infection.Several aspects of the interactions between the virus and the host immune system have been clarified and, in particular, mechanisms have been identified which underlie the ability of HCV to seize and subvert innate as well as adaptive immune responses.The present review summarizes recent findings on the interaction between HCV infection and innate immune response whose final effect is the downstream inefficient development of antigen-specific adaptive immunity, thereby contributing to virus persistence.</description>
        <link>http://www.infectagentscancer.com/content/7/1/7</link>
                <dc:creator>Luigi Buonaguro</dc:creator>
                <dc:creator>Annacarmen Petrizzo</dc:creator>
                <dc:creator>Maria Lina Tornesello</dc:creator>
                <dc:creator>Franco Buonaguro</dc:creator>
                <dc:source>Infectious Agents and Cancer 2012, null:7</dc:source>
        <dc:date>2012-03-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-7-7</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/2/1/11">
        <title>Routine human papillomavirus genotyping by DNA sequencing in community hospital laboratories</title>
        <description>Background:
Human papillomavirus (HPV) genotyping is important for following up patients with persistent HPV infection and for evaluation of prevention strategy for the individual patients to be immunized with type-specific HPV vaccines. The aim of this study was to optimize a robust &quot;low-temperature&quot; (LoTemp&#8482;) PCR system to streamline the research protocols for HPV DNA nested PCR-amplification followed by genotyping with direct DNA sequencing. The protocol optimization facilitates transferring this molecular technology into clinical laboratory practice. In particular, lowering the temperature by 10&#176;C at each step of thermocycling during in vitro DNA amplification yields more homogeneous PCR products. With this protocol, template purification before enzymatic cycle primer extensions is no longer necessary.
Results:
The HPV genomic DNA extracted from liquid-based alcohol-preserved cervicovaginal cells was first amplified by the consensus MY09/MY11 primer pair followed by nested PCR with GP5+/GP6+ primers. The 150 bp nested PCR products were subjected to direct DNA sequencing. The hypervariable 34&#8211;50 bp DNA sequence downstream of the GP5+ primer site was compared to the known HPV DNA sequences stored in the GenBank using on-line BLAST for genotyping. The LoTemp&#8482; ready-to-use PCR polymerase reagents proved to be stable at room temperature for at least 6 weeks. Nested PCR detected 107 isolates of HPV in 513 cervicovaginal clinical samples, all validated by DNA sequencing. HPV-16 was the most prevalent genotype constituting 29 of 107 positive cases (27.2%), followed by HPV-56 (8.5%). For comparison, Digene HC2 test detected 62.6% of the 107 HPV isolates and returned 11 (37.9%) of the 29 HPV-16 positive cases as &quot;positive for high-risk HPV&quot;.
Conclusion:
The LoTemp&#8482; ready-to-use PCR polymerase system which allows thermocycling at 85&#176;C for denaturing, 40&#176;C for annealing and 65&#176;C for primer extension can be adapted for target HPV DNA amplification by nested PCR and for preparation of clinical materials for genotyping by direct DNA sequencing. HPV genotyping is performed by on-line BLAST algorithm of a hypervariable L1 region. The DNA sequence is included in each report to the physician for comparison in following up patients with persistent HPV infection, a recognized tumor promoter in cancer induction.</description>
        <link>http://www.infectagentscancer.com/content/2/1/11</link>
                <dc:creator>Sin Hang Lee</dc:creator>
                <dc:creator>Veronica Vigliotti</dc:creator>
                <dc:creator>Jessica Vigliotti</dc:creator>
                <dc:creator>Suri Pappu</dc:creator>
                <dc:source>Infectious Agents and Cancer 2007, null:11</dc:source>
        <dc:date>2007-06-05T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-2-11</dc:identifier>
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        <prism:startingPage>11</prism:startingPage>
        <prism:publicationDate>2007-06-05T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.infectagentscancer.com/content/7/1/10">
        <title>Detection of helicobacter pylori in benign laryngeal lesions by polymerase chain reaction: a cross sectional study</title>
        <description>Background:
Although Helicobacter Pylori (HP) was detected in some cases of chronic laryngitis, the results were not confirmed by polymerase chain reaction (PCR). By this time, it has not been found in laryngeal lesions by in house PCR, the most sensitive method for detecting the genome tracks. Regarding the previous results and also few numbers of studies about the presence of HP in benign laryngeal lesions, specifically by PCR, we aimed to investigate the presence of HP in benign laryngeal lesions by in-house PCR.
Methods:
The samples were taken from 55 patients with benign laryngeal lesions and frozen in 20degreesC. One milliliter (ml) of lysis buffer was added to 100 mg (mg) of each sample and the tube was placed in 56degreesC overnight. Then DNA extraction was carried out.
Results:
To find HP DNA, in-house PCR was performed that revealed 5 positive results among 55 patients with benign laryngeal lesions. Of them, 3 were polyp, 1 was nodule and 1 was papilloma.
Conclusion:
Although the number of positive results was not a lot in this study, it was in contrast with previous studies which could not find any HP tracks in benign laryngeal lesions by other methods. More studies about the prevalence of HP in benign laryngeal lesions improve judging about the effect of this infection on benign laryngeal lesions.</description>
        <link>http://www.infectagentscancer.com/content/7/1/10</link>
                <dc:creator>Farzad Izadi</dc:creator>
                <dc:creator>Aslan Ahmadi</dc:creator>
                <dc:creator>Shadi Ghourchian</dc:creator>
                <dc:creator>Ahmad Daneshi</dc:creator>
                <dc:creator>Faramarz Memari</dc:creator>
                <dc:creator>Ehsan Khadivi</dc:creator>
                <dc:creator>Shabahang Mohammadi</dc:creator>
                <dc:source>Infectious Agents and Cancer 2012, null:10</dc:source>
        <dc:date>2012-04-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-7-10</dc:identifier>
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        <prism:startingPage>10</prism:startingPage>
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        <item rdf:about="http://www.infectagentscancer.com/content/7/1/9">
        <title>Activating KIR/HLA complexes in classic Kaposi&apos;s Sarcoma</title>
        <description>Background:
Classic Kaposi&apos;s Sarcoma (cKS) is a rare vascular tumor associated with Human Herpesvirus 8 (KSHV) infection, nevertheless not all KSHV-infected individuals have cKS.ObjectiveWe investigated whether particular KIR/HLA receptor/ligand genotypes would be preferentially present in KSHV-infected and uninfected individuals who have or have not developed cKS.
Methods:
KIR/HLA genotypes were analyzed by molecular genotyping in 50 KSHV-infected individuals who did or did not have cKS and in 33 age-and sex-matched KSHV seronegative individuals.
Results:
There was no association of individual KIR, HLA or receptor ligand combinations with KSHV infection. However, activating KIR and KIR/HLA genotypes were significantly more frequent in cKS cases, specifically KIR3DS1, KIR2DS1, and KIR2DS1 with its HLA-C2 ligand.
Conclusion:
A nonspecific inflammatory response triggered by activation of NK cells upon KIR-HLA interaction could be associated with the pathogenesis of KS.</description>
        <link>http://www.infectagentscancer.com/content/7/1/9</link>
                <dc:creator>Franca Guerini</dc:creator>
                <dc:creator>Roberta Mancuso</dc:creator>
                <dc:creator>Simone Agostini</dc:creator>
                <dc:creator>Cristina Aglairdi</dc:creator>
                <dc:creator>Milena Zanzottera</dc:creator>
                <dc:creator>Ambra Hernis</dc:creator>
                <dc:creator>Athanasia Tourlaki</dc:creator>
                <dc:creator>Maria Calvo</dc:creator>
                <dc:creator>Monica Bellinvia</dc:creator>
                <dc:creator>Lucia Brambilla</dc:creator>
                <dc:creator>Mario Clerici</dc:creator>
                <dc:source>Infectious Agents and Cancer 2012, null:9</dc:source>
        <dc:date>2012-04-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-7-9</dc:identifier>
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        <prism:startingPage>9</prism:startingPage>
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        <item rdf:about="http://www.infectagentscancer.com/content/4/1/7">
        <title>The evolving definition of carcinogenic human papillomavirus</title>
        <description>Thirteen human papillomavirus (HPV) genotypes have been judged to be carcinogenic or probably carcinogenic, and the cause of virtually all cervical cancer worldwide. Other HPV genotypes could possibly be involved. Although the inclusion of possibly carcinogenic HPV genotypes may hurt test specificity, it may indirectly increase the reassurance following a negative HPV test (i.e. the negative predictive value of an HPV test for cervical precancer and cancer). The future of cervical cancer screening in low-resource setting, however, may include once-in-a-lifetime, low-cost and rapid HPV testing. However, the tradeoff of more false positives for greater reassurance may not be acceptable if the local infrastructure cannot manage the screen positives. Now is the time for the community of scientists, doctors, and public health advocates to use the data presented at the 100th International Agency for Research on Cancer monograph meeting to rationally decide the target HPV genotypes for the next generation of HPV tests for use in high-resource and low-resource settings. The implications of including possibly HPV genotypes on HPV test performance, also for guidance on the use of these tests for cervical cancer prevention programs, are discussed.</description>
        <link>http://www.infectagentscancer.com/content/4/1/7</link>
                <dc:creator>Philip Castle</dc:creator>
                <dc:source>Infectious Agents and Cancer 2009, null:7</dc:source>
        <dc:date>2009-05-11T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-4-7</dc:identifier>
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