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        <title>Infectious Agents and Cancer - Latest Articles</title>
        <link>http://www.infectagentscancer.com</link>
        <description>The latest research articles published by Infectious Agents and Cancer</description>
        <dc:date>2013-05-09T00:00:00Z</dc:date>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/5">
        <title>Infectious Agents &amp; Cancer reviewer acknowledgement 2012</title>
        <description>Contributing reviewersThe editor of Infectious Agents &amp; Cancer would like to thank all our reviewers who have contributed to the journal in Volume 7 (2012).</description>
        <link>http://www.infectagentscancer.com/content/8/1/5</link>
                <dc:creator>Franco Buonaguro</dc:creator>
                <dc:creator>Sam Mbulaiteye</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:5</dc:source>
        <dc:date>2013-05-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-5</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/16">
        <title>Infections and cancer: debate about using vaccines as a cancer control tool</title>
        <description>In 2012, Infectious Agents and Cancer commissioned a thematic series collection of articles on Prevention of HPV related cancer. The articles have attracted wide interest and stimulated debate, including about the utility of vaccines in cancer control. The application of vaccines to cancer control fulfills a promise envisioned at the turn of the 20th century when remarkable experiments showed that some cancers were caused by infections. This suggested the possibility of applying infection-control strategies to cancer control. Vaccines represent the most practical cost-effective technology to prevent wide human suffering and death from many acute infectious diseases, such as small pox or polio. Hitherto applied to control of acute fatal infections, vaccines, if developed, might provide a potent way to control cancer. The articles in the HPV thematic series show success in developing and applying a vaccine against human papilloma virus (HPV). A vaccine is also available against hepatitis B virus (HBV), which causes liver cancer. These vaccines augment the tools available to control the associated cancers. Scientific endeavor continues for six other cancer-associated infections, mostly viruses. Not surprisingly, debate about the safety of vaccines targeting cancer has been triggered in the scientific community. Questions about safety have been raised for those populations where other means to control these cancers may be available. Although it is difficult to quantify risk from vaccines in individuals where other cancer control services exist, it is likely to be low. Vaccines are much safer today than before. Technological advancement in vaccine development and manufacture and improved regulatory review and efficient distribution have minimized substantially the risk for harm from vaccines. Formal and informal debate about the pros and cons of applying vaccines as a cancer control tools is ongoing in scientific journals and on the web. Infectious Agents and Cancer encourages evidence-based discussion to clarify understanding of the role of vaccines in cancer control. In a similar vein, the journal will not consider anecdotal reports and rhetorical arguments because they are unlikely to inform policy, regulation, or the public.</description>
        <link>http://www.infectagentscancer.com/content/8/1/16</link>
                <dc:creator>Sam Mbulaiteye</dc:creator>
                <dc:creator>Franco Buonaguro</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:16</dc:source>
        <dc:date>2013-05-04T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-16</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/15">
        <title>HPV prevalence and genetic predisposition to cervical cancer in Saudi Arabia</title>
        <description>Background:
Cervical cancer incidence is low in Saudi Arabian women, suggesting low prevalence to HPV infection due to environmental, cultural and genetic differences. Therefore, we investigated HPV prevalence and genotype distribution in cervical cancer as well as the association with 9 genetic single nucleotide polymorphisms (SNPs): CDKN1A (p21) C31A, TP53 C72G, ATM G1853A, HDM2 promoter T309G, HDM2 A110G, LIG4 A591G, XRCC1 G399A, XRCC3 C241T and TGFbeta1 T10C, presumed to predispose to cancer.
Methods:
One hundred cervical cancer patients (90 squamous cell carcinoma and 10 adenocarcinoma) and 100 age/sex-matched controls were enrolled. SNPs were genotyped by direct sequencing and HPV was detected and typed in tumors using the HPV Linear Array Test.
Results:
Eighty-two cases (82%) were positive for HPV sequences. Seven HPV genotypes were present as single infections (16, 18, 31, 45, 56, 59, 73) and five double infections (16/18, 16/39, 16/70, 35/52, 45/59) were detected. Most common genotypes were HPV-16 (71%), 31 (7%), and 18, 45, 73 (4% each). Only XRCC1 SNP was significantly associated with cervical cancer (P=0.02, OD=1.69; 95% CI= 1.06--2.66). However, nested analysis revealed a preponderance of HPV-positivity in patients harboring the presumed risk allele TP53 G (P=0.06). Both XRCC1 and TP53 SNPs tended to deviate from Hardy-Weinberg equilibrium (HWE; P=0.03-0.07).
Conclusions:
HPV prevalence (82%) in cervical cancer is at the lower range of the worldwide estimation (85 - 99%). While XRCC1 G399A was significantly associated with cervical cancer, TP53 G72C showed borderline association only in HPV-positive patients. Deviation from HWE in HPV-positive patients indicates co-selection, hence implicating the combination of HPV and SNPs in cancer predisposition. Thus, SNPs could be more relevant biomarkers of susceptibility to cervical cancer when associated with HPV infection.</description>
        <link>http://www.infectagentscancer.com/content/8/1/15</link>
                <dc:creator>Ghazi Alsbeih</dc:creator>
                <dc:creator>Najla Al-Harbi</dc:creator>
                <dc:creator>Medhat El-Sebaie</dc:creator>
                <dc:creator>Ismail Al-Badawi</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:15</dc:source>
        <dc:date>2013-05-04T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-15</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/14">
        <title>The role of human papillomavirus in head and neck cancer in Senegal</title>
        <description>Background:
Exploring the presence and role of human papillomavirus (HPV) in head and neck cancer (HNC) is a necessary step to evaluate the potential impact of HPV prophylactic vaccines.ObjectiveTo assess the prevalence and oncogenic role of HPV in HNC in Senegal.
Methods:
This is a multicenter cross-sectional study. Paraffin-embedded blocks of cases diagnosed with invasive HNC between 2002 and 2010 were collected from 4 pathology laboratories in Senegal. Presence of HPV DNA was determined by PCR and DEIA, and genotyping performed with LiPA25. Tubulin analysis was performed to assess DNA quality. HPV DNA-positive cases were tested for p16INK4a expression.FindingsA total of 117 cases were included in the analysis: 71% were men, mean age was 52&#8201;years old (SD &#177;18.3), and 96% of cases were squamous cell carcinoma. Analysis was performed on 41 oral cavity tumors, 64 laryngeal tumors, 5 oropharyngeal tumors and 7 pharyngeal tumors. Only four cases (3.4%; 95% CI&#8201;=&#8201;0.9%-8.5%) harbored HPV DNA. HPV types detected were HPV16, HPV35 and HPV45. However, among HPV-positive cases, none showed p16INK4a overexpression.
Conclusion:
Our findings indicate that HPV DNA prevalence in HNC in Senegal is very low, suggesting that HPV is not a strong risk factor for these cancers. Additional larger studies are needed to confirm these findings and explore other potential risk factors specific to the region.</description>
        <link>http://www.infectagentscancer.com/content/8/1/14</link>
                <dc:creator>Cathy Ndiaye</dc:creator>
                <dc:creator>Laia Alemany</dc:creator>
                <dc:creator>Yankhoba Diop</dc:creator>
                <dc:creator>Nafissatou Ndiaye</dc:creator>
                <dc:creator>Marie-Joseph Diémé</dc:creator>
                <dc:creator>Sara Tous</dc:creator>
                <dc:creator>Jo Ellen Klaustermeier</dc:creator>
                <dc:creator>Maria Alejo</dc:creator>
                <dc:creator>Xavier Castellsagué</dc:creator>
                <dc:creator>F Bosch</dc:creator>
                <dc:creator>Helen Trottier</dc:creator>
                <dc:creator>Silvia de Sanjosé</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:14</dc:source>
        <dc:date>2013-04-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-14</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/13">
        <title>c-Met inhibitors</title>
        <description>c-Met is a receptor tyrosine kinase that encodes protein such as hepatocyte growth factor receptor (HGFR). Inappropriate activity of c-Met can cause wide variety of carcinomas. c-Met inhibitor are relatively new class of small molecules that inhibit the enzymatic activity of c-Met tyrosine kinase. Met inhibitors divided into two main classes: class I (SU-11274-like) and class II (AM7-like). The use of c-Met inhibitors with other therapeutic agents could be crucial for overcoming potential resistance as well as for improving overall clinical benefit. Met pathway inhibitors might be used in combination with other treatments, including chemo-, radio- or immunotherapy</description>
        <link>http://www.infectagentscancer.com/content/8/1/13</link>
                <dc:creator>Anum Mughal</dc:creator>
                <dc:creator>Hafiz Aslam</dc:creator>
                <dc:creator>Asfandyar Sheikh</dc:creator>
                <dc:creator>Agha Khan</dc:creator>
                <dc:creator>Shafaq Saleem</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:13</dc:source>
        <dc:date>2013-04-08T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-13</dc:identifier>
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        <prism:startingPage>13</prism:startingPage>
        <prism:publicationDate>2013-04-08T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/12">
        <title>Is human cytomegalovirus associated with breast cancer progression?</title>
        <description>Background:
It has been hypothesized that human cytomegalovirus (HCMV) may be associated with breast cancer progression. However, the role of HCMV infection in breast cancer remains controversial. We aimed to assess whether HCMV genes (UL122 and UL83) could be detected in breast carcinomas and reinvestigated their possible association with breast cancer progression. DNA from paraffin-embedded tissues was analyzed by real-time PCR. We investigated 20 fibroadenomas and 27 primary breast carcinomas (stages II, III, and IV).FindingsTwo carcinomas were positive for HCMV, one was positive for two TaqMan viral detection probes, and one was positive for a sole TaqMan viral detection probe (UL83), whereas the remainder of the samples was negative.
Conclusions:
Samples studied showed no association between HCMV infection and breast cancer progression.</description>
        <link>http://www.infectagentscancer.com/content/8/1/12</link>
                <dc:creator>Dolores Utrera-Barillas</dc:creator>
                <dc:creator>Hilda-Alicia Valdez-Salazar</dc:creator>
                <dc:creator>David Gómez-Rangel</dc:creator>
                <dc:creator>Isabel Alvarado-Cabrero</dc:creator>
                <dc:creator>Penélope Aguilera</dc:creator>
                <dc:creator>Alejandro Gómez-Delgado</dc:creator>
                <dc:creator>Martha-Eugenia Ruiz-Tachiquin</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:12</dc:source>
        <dc:date>2013-04-04T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-12</dc:identifier>
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        <prism:startingPage>12</prism:startingPage>
        <prism:publicationDate>2013-04-04T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/11">
        <title>Bacteria and tumours: causative agents or opportunistic inhabitants?</title>
        <description>Associations between different bacteria and various tumours have been reported in patients for decades. Studies involving characterisation of bacteria within tumour tissues have traditionally been in the context of tumourigenesis as a result of bacterial presence within healthy tissues, and in general, dogma holds that such bacteria are causative agents of malignancy (directly or indirectly). While evidence suggests that this may be the case for certain tumour types and bacterial species, it is plausible that in many cases, clinical observations of bacteria within tumours arise from spontaneous infection of established tumours. Indeed, growth of bacteria specifically within tumours following deliberate systemic administration has been demonstrated for numerous bacterial species at preclinical and clinical levels. We present the available data on links between bacteria and tumours, and propose that besides the few instances in which pathogens are playing a pathogenic role in cancer, in many instances, the prevalent relationship between solid tumours and bacteria is opportunistic rather than causative, and discuss opportunities for exploiting tumour-specific bacterial growth for cancer treatment.</description>
        <link>http://www.infectagentscancer.com/content/8/1/11</link>
                <dc:creator>Joanne Cummins</dc:creator>
                <dc:creator>Mark Tangney</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:11</dc:source>
        <dc:date>2013-03-28T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-11</dc:identifier>
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        <prism:startingPage>11</prism:startingPage>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/10">
        <title>Histone de-acetylase inhibitors: a promising future for cancer treatment?</title>
        <description>Histone de-acetylase proteins or lysine de-acetylases, represent a group of enzymes regulating DNA and gene expression by eliminating acetyl groups (de-acetylation) from lysine amino acids on histones and non-histone proteins. Histone de-acetylase functions normally by being involved in a series of cellular pathways like cell growth, cell cycle, signal transduction, notch signaling pathway and especially transcription.However, abnormal acetylation of histone tails becomes tumorigenic with the resulting transcriptional lesions disrupting the apoptotic program of cells leading to neoplasia. Interaction with the catalytic site and blocking substrate access of histone de-acetylases in proliferation of tumor cells, anti-neoplastic agents called histone de-acetylase inhibitors (HDIs) shift the balance by inducing cell-cycle arrest in G1, activation of differentiation programs and activation of death-receptor and intrinsic apoptotic pathways in neoplastic cells. HDIs anti-proliferative effect in down regulation of BMI1 and c-MYC protein levels has shown promising results in treatment of the incurable AML as well as silencing estrogen receptor alpha in prevention of breast cancer.</description>
        <link>http://www.infectagentscancer.com/content/8/1/10</link>
                <dc:creator>Raja Samir Khan</dc:creator>
                <dc:creator>Harris Hameed</dc:creator>
                <dc:creator>Ramsha Ali Bhutta</dc:creator>
                <dc:creator>Abdul Nafey Kazi</dc:creator>
                <dc:creator>Haris Riaz</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:10</dc:source>
        <dc:date>2013-03-11T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-10</dc:identifier>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/9">
        <title>Immunohistochemical expression of COX2 and iNOS in bladder cancer and its association with urinary schistosomiasis among Sudanese patients</title>
        <description>AimsThe purpose of this study was to determine if any relationship exists between expression of COX2 and iNOS markers and urinary schistosomiasis in bladder cancers.MethodologyImmunohistochemical expression of COX2 and iNOS was assessed in formalin fixed paraffin wax processed tissues obtained from 155 patients with bladder cancers (87 SCC and 68 TCC) and 39 patients with benign bladder cystitis.
Results:
The overall immune-expressions of COX2 and iNOS were 71.6% and 57.2% respectively, of the 194 bladder lesions. A significant Positive association between COX2 or iNOS expression with bladder lesions (SCC, TCC and cystitis) was found (p.value&#8201;=&#8201;0.000). COX2 and iNOS were co-expressed among 73(83.9%) of SCC, 15(22.1%) of TCC and 11(28.2%) of the cystitis group. The relationship between COX2 and iNOS immunostaining and Schistosomal ova positivity was statistically determined by P values 0.0565 and 0.1223 for Cox2 and iNOS, respectively.
Conclusion:
There are high rates of positive expression of COX2 and iNOS among Sudanese patients with Schistosomal-related bladder lesions. There might be strong association between high rates of bladder cancers and urinary Schistosomiasis in the Sudan since, the great majority of lesions were positive for COX2.</description>
        <link>http://www.infectagentscancer.com/content/8/1/9</link>
                <dc:creator>Hassan Elsiddig Hassan</dc:creator>
                <dc:creator>Ahmed Abdel Badie Mohamed</dc:creator>
                <dc:creator>Amel Omer Bakhiet</dc:creator>
                <dc:creator>Hussain Gadelkarim Ahmed</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:9</dc:source>
        <dc:date>2013-02-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-9</dc:identifier>
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        <prism:startingPage>9</prism:startingPage>
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        <item rdf:about="http://www.infectagentscancer.com/content/8/1/8">
        <title>Possible role of Toxoplasma gondii in brain cancer through modulation of host microRNAs</title>
        <description>Background:
The obligate intracellular protozoan parasite Toxoplasma gondii infects humans and other warm-blooded animals and establishes a chronic infection in the central nervous system after invasion. Studies showing a positive correlation between anti-Toxoplasma antibodies and incidences of brain cancer have led to the notion that Toxoplasma infections increase the risk of brain cancer. However, molecular events involved in Toxoplasma induced brain cancers are not well understood.Presentation of the hypothesisToxoplasma gains control of host cell functions including proliferation and apoptosis by channelizing parasite proteins into the cell cytoplasm and some of the proteins are targeted to the host nucleus. Recent studies have shown that Toxoplasma is capable of manipulating host micro RNAs (miRNAs), which play a central role in post-transcriptional regulation of gene expression. Therefore, we hypothesize that Toxoplasma promotes brain carcinogenesis by altering the host miRNAome using parasitic proteins and/or miRNAs.Testing the hypothesisThe miRNA expression profiles of brain cancer specimens obtained from patients infected with Toxoplasma could be analyzed and compared with that of normal tissues as well as brain cancer tissues from Toxoplasma uninfected individuals to identify dysregulated miRNAs in Toxoplasma-driven brain cancer cells. Identified miRNAs will be further confirmed by studying cancer related miRNA profiles of the different types of brain cells before and after Toxoplasma infection using cell lines and experimental animals.Expected outcomeThe miRNAs specifically associated with brain cancers that are caused by Toxoplasma infection will be identified.Implications of the hypothesisToxoplasma infection may promote initiation and progression of cancer by modifying the miRNAome in brain cells. If this hypothesis is true, the outcome of this research would lead to the development of novel biomarkers and therapeutic tools against Toxoplasma driven brain cancers.</description>
        <link>http://www.infectagentscancer.com/content/8/1/8</link>
                <dc:creator>Sivasakthivel Thirugnanam</dc:creator>
                <dc:creator>Namita Rout</dc:creator>
                <dc:creator>Munirathinam Gnanasekar</dc:creator>
                <dc:source>Infectious Agents and Cancer 2013, null:8</dc:source>
        <dc:date>2013-02-08T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1750-9378-8-8</dc:identifier>
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