• EBV
• HBV
• HCV
• HIV
• lymphoma
• pathogenesis
• virus

• Humans
• Lymphoma/etiology
• Oncogenic Viruses
• Herpesvirus 8, Human

• Department of Science and Technology of Jilin Province

• Humans
• Neoplasms/therapy
• Neoplasms/pathology
• Histocompatibility Antigens Class I/metabolism
• Immunotherapy/methods
• T-Lymphocytes/pathology

• Causal pie
• Epidemiology
• Etiology
• Immunosuppressed
• Immunosuppression
• Oncogenic
• Sebaceous carcinoma
• Skin cancer
• Sufficient-component
• Transplant
• Virus

• Animals
• Breast Neoplasms
• Female
• Humans
• Mammary Tumor Virus, Mouse/genetics
• Mice
• Retroviridae Infections

• CRISPR associated protein 9 (Cas9)
• Cancer treatment
• Clustered regularly interspaced short palindromic repeats (CRISPR)
• Genome editing

• CRISPR-Cas Systems/genetics
• Gene Editing
• Genome
• Humans
• Neoplasms/genetics
• Neoplasms/therapy

• bacteriome
• colorectal cancer
• metastasis
• phages
• viruses

• Colorectal Neoplasms/genetics
• Epstein-Barr Virus Infections
• Herpesvirus 4, Human
• Humans
• Microbiota
• Risk Factors

• Alfried Krupp von Bohlen und Halbach‐Stiftung
• Deutsche Krebshilfe
• Deutsche Forschungsgemeinschaft

• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Area Under Curve
• Breast/pathology
• Breast/virology
• Breast Neoplasms/diagnosis
• Breast Neoplasms/pathology
• Breast Neoplasms/virology
• Case-Control Studies
• Colombia
• Female
• Humans
• Leukemia Virus, Bovine/genetics
• Leukemia Virus, Bovine/isolation & purification
• Logistic Models
• Middle Aged
• Polymerase Chain Reaction
• Prognosis
• RNA, Viral/analysis
• RNA, Viral/blood
• RNA, Viral/metabolism
• ROC Curve
• Risk Factors
• Young Adult

• Departamento Administrativo de Ciencia, Tecnología e Innovación
• Fulbright Association
• HOSPITAL UNIVERSITARIO MAYOR MÉDERI – Universidad del Rosario

• Epstein–Barr virus
• John Cunningham virus
• Merkel cell polyomavirus
• human papillomavirus
• jaagsiekte sheep virus
• lung cancer
• oncogenic virus

Persistence of human papillomavirus (HPV) infections is associated with squamous cell carcinomas of different human anatomic sites. Several studies have suggested a potential role for HPV infection, particularly HPV16 genotype, in rectal cancer carcinogenesis.. The aim of this study was to assess the frequency of oncogenic HPV 16 viral DNA sequences in rectal carcinomas cases retrieved from the pathology archive of Braga Hospital, North Portuga.

TaqMan-based type-specific real-time PCR for HPV 16 was performed using primers and probe targeting HPV16 E7 region.

Most of the rectal cancer patients (88.5%, n = 206 patients), were symptomatic at diagnosis. The majority of the lesions (55.3%, n = 129) presented malignancies of polypoid/vegetant phenotype. 26.8% (n = 63) had synchronic metastasis at diagnosis. 26.2% (n = 61) patients had clinical indication for neoadjuvant therapy. Most patients with rectal cancer were stage IV (19.7% patients), followed by stage IIA (19.3%) and stage I (18.5%). All cases of the present series tested negative for HPV16.

The total of negative tests for HPV 16 infection is a robust argument to support the assumption that HPV 16 infection, despite of previous evidences, is not involved in rectal cancer carcinogenesis and progression.

• Carcinogenesis
• Human papillomavirus 16
• Rectal cancer

• Adult
• Aged
• Aged, 80 and over
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/pathology
• Colorectal Neoplasms/virology
• Female
• Gene Expression Regulation, Neoplastic
• Humans
• Male
• Middle Aged
• Neoplasm Proteins/biosynthesis
• Papillomaviridae/metabolism
• Papillomavirus Infections/metabolism
• Papillomavirus Infections/pathology

The JC polyomavirus (JCV) has been repeatedly but discordantly detected in healthy colonic mucosa, adenomatous polyps, and colorectal cancer (CRC), and proposed to contribute to oncogenesis. The controversies may derive from differences in JCV targets, patient’s cohorts, and methods. Studies of simultaneous detection, quantification, and characterization of JCV presence/expression in paired samples of normal/altered tissues of the same patient are lacking. Therefore, we simultaneously quantified JCV presence (DNA) and expression (mRNA and protein) of T-antigen (T-Ag), Viral Protein 1 (Vp1), and miR-J1-5p in paired normal/altered tissues of CRC or polyps, and from controls. JCV signatures were found in most samples. They increased in patients, but were higher in normal mucosa than in corresponding polyp or CRC lesions. JCV non-coding control region (NCCR) DNA rearrangements increased in CRC patients, also in normal mucosa, thus before the onset of the lesion. A new ∆98bp NCCR DNA rearrangement was detected. T-Ag levels were higher in normal mucosa than in adenoma and adenocarcinoma lesions, but decreased to levels of controls in established CRC lesions. In CRC, miR-J1-5p expression decreased with CRC progression. Vp1 expression was not detected. The data indicate a JCV link with the disease, but possible JCV contributes to oncogenesis should occur at pre-polyp stages.

• JC polyomavirus
• NCCR non-coding control region
• T-antigen
• adenomatous polyps
• colorectal cancer
• oncogenesis

• NF-κB
• hepatitis B virus
• hepatitis C virus
• hepatocellular carcinoma
• inflammation

• Aetiopathology
• Cáncer orofaríngeo
• Etiopatogenia
• Habits
• Health
• Hábitos
• Oropharyngeal cancer
• Prevención
• Prevention
• Salud

• Indoleamine-pyrrole 2,3-dioxygenase
• aryl hydrocarbon receptor
• immune cytokine
• kynurenine
• tumor dormancy
• tumor-repopulating cells

• Colorectal cancer
• Cytokine
• Enterovirus 71
• Th17

• Adult
• Aged
• Aged, 80 and over
• Antigens, Viral/genetics
• Antigens, Viral/immunology
• Antigens, Viral/physiology
• Colorectal Neoplasms/immunology
• Colorectal Neoplasms/metabolism
• Colorectal Neoplasms/virology
• Cytokines/immunology
• Cytokines/metabolism
• Enterovirus A, Human/genetics
• Enterovirus A, Human/immunology
• Enterovirus A, Human/physiology
• Enterovirus Infections/immunology
• Enterovirus Infections/metabolism
• Enterovirus Infections/virology
• Female
• Host-Pathogen Interactions/immunology
• Humans
• Male
• Middle Aged
• Neoplasm Staging
• Pilot Projects
• Th17 Cells/immunology
• Th17 Cells/metabolism

• Breast cancer
• Human papillomavirus
• PCR
• Prevalence

• Adult
• Breast Neoplasms/complications
• Breast Neoplasms/virology
• Case-Control Studies
• Female
• Human papillomavirus 16
• Humans
• Middle Aged
• Papillomavirus Infections/complications
• Papillomavirus Infections/epidemiology
• Prevalence
• Spain/epidemiology

Almost one fifth of human cancers worldwide are associated with infectious agents, either bacteria or viruses, and this makes the possible association between infections and tumors a relevant research issue. We focused our attention on the human Polyomavirus JC (JCPyV), that is a small, naked DNA virus, belonging to the Polyomaviridae family. It is the recognized etiological agent of the Progressive Multifocal Leukoencephalopathy (PML), a fatal demyelinating disease, occurring in immunosuppressed individuals.

JCPyV is able to induce cell transformation in vitro when infecting non-permissive cells, that do not support viral replication and JCPyV inoculation into small animal models and non human primates drives to tumor formation. The molecular mechanisms involved in JCPyV oncogenesis have been extensively studied: the main oncogenic viral protein is the large tumor antigen (T-Ag), that is able to bind, among other cellular factors, both Retinoblastoma protein (pRb) and p53 and to dysregulate the cell cycle, but also the early proteins small tumor antigen (t-Ag) and Agnoprotein appear to cooperate in the process of cell transformation.

Consequently, it is not surprising that JCPyV genomic sequences and protein expression have been detected in Central Nervous System (CNS) tumors and colon cancer and an association between this virus and several brain and non CNS-tumors has been proposed. However, the significances of these findings are under debate because there is still insufficient evidence of a casual association between JCPyV and solid cancer development.

In this paper we summarized and critically analyzed the published literature, in order to describe the current knowledge on the possible role of JCPyV in the development of human tumors.

• Central nervous system tumors
• Colon cancer
• JC virus

Studies of human polyomavirus (HPyV) infection and lung cancer are limited and those regarding the association of human papillomavirus (HPV) infection and lung cancer have produced inconsistent results.

We conducted a nested case–control study to assess the association between incident lung cancer of various histologies and evidence of prior infection with HPyVs and HPVs. We selected serum from 183 cases and 217 frequency matched controls from the Yunnan Tin Miner’s Cohort study, which was designed to identify biomarkers for early detection of lung cancer. Using multiplex liquid bead microarray (LBMA) antibody assays, we tested for antibodies to the VP1 structural protein and small T antigen (ST-Ag) of Merkel cell, KI, and WU HPyVs. We also tested for antibodies against HPV L1 structural proteins (high-risk types 16, 18, 31, 33, 52, and 58 and low-risk types 6 and 11) and E6 and E7 oncoproteins (high risk types 16 and 18). Measures of antibody reactivity were log transformed and analyzed using logistic regression.

We found no association between KIV, WUV, and MCV antibody levels and incident lung cancer (P-corrected for multiple comparisons >0.10 for all trend tests). We also found no association with HPV-16, 18, 31, 33, 52, and 58 seropositivity (P-corrected for multiple comparisons >0.05 for all).

Future studies of infectious etiologies of lung cancer should look beyond HPyVs and HPVs as candidate infectious agents.

The online version of this article (doi:10.1186/s12885-016-2381-3) contains supplementary material, which is available to authorized users.

• Human papillomavirus
• Human polyomavirus
• KI polyomavirus
• Lung cancer
• Merkel cell polyomavirus
• WU polyomavirus

Epstein-Barr virus (EBV) has been detected in the tumor cells of several cancers, including some cases of lung carcinoma (LC). However, the genomic characteristics and diversity of EBV strains associated with LC are poorly understood. In this study, we sequenced the EBV genomes isolated from four primary LC tumor biopsy samples, designated LC1 to LC4. Comparative analysis demonstrated that LC strains were more closely related to GD1 strain. Compared to GD1 reference genome, a total of 520 variations in all, including 498 substitutions, 12 insertions, and 10 deletions were found. Latent genes were found to harbor the most numbers of nonsynonymous mutations. Phylogenetic analysis showed that all LC strains were closely related to Asian EBV strains, whereas different from African/American strains. LC2 genome was distinct from the other three LC genomes, suggesting at least two parental lineages of EBV among the LC genomes may exist. All LC strains could be classified as China 1 and V-val subtype according to the amino acid sequence of LMP1 and EBNA1, respectively. In conclusion, our results showed the genomic diversity among EBV genomes isolated from LC, which might facilitate to uncover the previously unknown variations of pathogenic significance.

“The forgotten organ”, the human microbiome, comprises a community of microorganisms that colonizes various sites of the human body. Through coevolution of bacteria, archaea and fungi with the human host over thousands of years, a complex host-microbiome relationship emerged in which many functions, including metabolism and immune responses, became codependent. This coupling becomes evident when disruption in the microbiome composition, termed dysbiosis, is mirrored by the development of pathologies in the host. Among the most serious consequences of dysbiosis, is the development of cancer. As many as 20% of total cancers worldwide are caused by a microbial agent. To date, a vast majority of microbiome-cancer studies focus solely on the microbiome of the large intestine and the development of gastrointestinal cancers. Here, we will review the available evidence implicating microbiome involvement in the development and progression of non-gastrointestinal cancers, while distinguishing between viral and bacterial drivers of cancer, as well as “local” and “systemic”, “cancer-stimulating” and “cancer-suppressing” effects of the microbiome. Developing a system-wide approach to cancer-microbiome studies will be crucial in understanding how microbiome influences carcinogenesis, and may enable to employ microbiome-targeting approaches as part of cancer treatment.

• Microbiome
• Non-gastrointestinal cancers
• Carcinogenesis
• Dysbiosis
• Microbial agent

• Biomarker
• In vitro diagnostics
• Protein microarray
• Translational research

• Autoimmune Diseases/diagnosis
• Autoimmune Diseases/metabolism
• Biomarkers/metabolism
• Communicable Diseases/diagnosis
• Communicable Diseases/metabolism
• Humans
• Neoplasms/diagnosis
• Neoplasms/metabolism
• Protein Array Analysis/methods
• Protein Binding
• Proteome/metabolism
• Proteomics/methods
• Translational Research, Biomedical/methods

• U01 CA117374 NCI NIH HHS
• 5U01CA117374 NCI NIH HHS

• hiv
• lung neoplasms
• carcinoma, non-small cell lung
• aids-related kaposi sarcoma
• lymphoma, non-hodgkin

• Anti-HIV Agents/therapeutic use
• HIV Infections/complications
• HIV Infections/drug therapy
• Humans
• Lung Neoplasms/epidemiology
• Lung Neoplasms/etiology
• Lung Neoplasms/pathology
• Lymphoma, AIDS-Related/epidemiology
• Lymphoma, AIDS-Related/etiology
• Mass Screening/methods
• Sarcoma, Kaposi/epidemiology
• Sarcoma, Kaposi/etiology
• Tomography, X-Ray Computed

• K07 CA180782 NCI NIH HHS

• Anti-HIV Agents/therapeutic use
• Early Detection of Cancer
• Female
• HIV Infections/complications
• HIV Infections/drug therapy
• Humans
• Male
• Neoplasms/prevention & control
• Neoplasms/virology
• Primary Prevention

• Adult
• Algeria/epidemiology
• Breast Neoplasms/epidemiology
• Breast Neoplasms/virology
• Female
• Herpesviridae
• Herpesviridae Infections/epidemiology
• Human papillomavirus 16
• Humans
• Middle Aged
• Papillomavirus Infections/epidemiology
• Polyomavirus
• Polyomavirus Infections/epidemiology
• Tumor Virus Infections/epidemiology

• 001 World Health Organization

• Large T antigen
• Merkel cell carcinoma
• polyomavirus

Up to 20% of cancers worldwide are thought to be associated with microbial pathogens, including bacteria and viruses. The widely used methods of viral infection detection are usually limited to a few a priori suspected viruses in one cancer type. To our knowledge, there have not been many broad screening approaches to address this problem more comprehensively.

In this study, we performed a comprehensive screening for viruses in nine common cancers using a multistep computational approach. Tumor transcriptome and genome sequencing data were available from The Cancer Genome Atlas (TCGA). Nine hundred fifty eight primary tumors in nine common cancers with poor prognosis were screened against a non-redundant database of virus sequences. DNA sequences from normal matched tissue specimens were used as controls to test whether each virus is associated with tumors.

We identified human papilloma virus type 18 (HPV-18) and four human herpes viruses (HHV) types 4, 5, 6B, and 8, also known as EBV, CMV, roseola virus, and KSHV, in colon, rectal, and stomach adenocarcinomas. In total, 59% of screened gastrointestinal adenocarcinomas (GIA) were positive for at least one virus: 26% for EBV, 21% for CMV, 7% for HHV-6B, and 20% for HPV-18. Over 20% of tumors were co-infected with multiple viruses. Two viruses (EBV and CMV) were statistically significantly associated with colorectal cancers when compared to the matched healthy tissues from the same individuals (p = 0.02 and 0.03, respectively). HPV-18 was not detected in DNA, and thus, no association testing was possible. Nevertheless, HPV-18 expression patterns suggest viral integration in the host genome, consistent with the potentially oncogenic nature of HPV-18 in colorectal adenocarcinomas. The estimated counts of viral copies were below one per cell for all identified viruses and approached the detection limit.

Our comprehensive screening for viruses in multiple cancer types using next-generation sequencing data clearly demonstrates the presence of viral sequences in GIA. EBV, CMV, and HPV-18 are potentially causal for GIA, although their oncogenic role is yet to be established.