Prevalence and 3-year persistence of human papillomavirus serotypes in asymptomatic patients in Northern Mexico.

Objective: To investigate clinical outcomes and 3-year persistence of human papillomavirus (HPV) infections among women in Mexico.

Methods: A prospective study enrolled sexually active women attending primary healthcare clinics in metropolitan Monterrey, Mexico, between June 3 and August 30, 2002. Baseline data were collected and participants underwent HPV screening.

Methylation of human papillomavirus 16, 18, 31, and 45 L2 and L1 genes and the cellular DAPK gene: Considerations for use as biomarkers of the progression of cervical neoplasia.

During progression of cervical cancer, human papillomavirus genomes and cellular tumor suppressor genes can become methylated. Toward a better understanding of these biomarkers, we studied 104 samples with HPV16, 18, 31, and 45 representing five pathological categories from asymptomatic infection to cancer. We grouped all samples by HPV type and pathology and measured the overall methylation of informative amplicons of HPV late genes and the cellular DAPK gene.

Muscarinic cholinergic signaling in cervical cancer cells affects cell motility via ERK1/2 signaling.

Aims: The etiology of cervical cancer depends primarily on infection with human papillomaviruses, but tobacco smoking is the most important behavioral risk factor for this cancer. Therefore, we have previously confirmed involvement of nicotinic acetylcholine receptors (nAChRs) in cervical cancer biology. In order to comprehensively evaluate the role of cholinergic signaling in cervical cells, we have addressed additional participation of muscarinic acetylcholine receptors (mAChRs).

Laser capture microdissection of cervical human papillomavirus infections: copy number of the virus in cancerous and normal tissue and heterogeneous DNA methylation.

Research on the pathogenicity of human papillomaviruses (HPVs) during cervical carcinogenesis often relies on the study of homogenized tissue or cultured cells. This approach does not detect molecular heterogeneities within the infected tissue. It is desirable to understand molecular properties in specific histological contexts.

Cholinergic signaling through nicotinic acetylcholine receptors stimulates the proliferation of cervical cancer cells: an explanation for the molecular role of tobacco smoking in cervical carcinogenesis?

We have analyzed the expression of mRNAs encoding nicotinic acetylcholine receptors (nAChRs) in CaSki, SiHa and HeLa cell lines, which are derived from two squamous and one adenocarcinoma of the cervix, respectively. We detected with reverse transcription-polymerase chain reaction mRNAs for ten of the 16 nAChR subunits, namely strong signals for alpha-5, alpha-7, alpha-9, beta-1 and epsilon, and weak signals for alpha-4, beta-2, beta-4, gamma and delta. We confirmed the translation of alpha-5 and beta-1, corresponding to the two strongest RNA signals, in SiHa and HeLa cells by Western blotting, and the localization of these proteins to the plasma membrane by immunofluorescence.

Human papillomavirus-16 and -18 in penile carcinomas: DNA methylation, chromosomal recombination and genomic variation.

Penile carcinomas are frequently associated with high risk human papillomavirus (HPV) types. Because little is known about the molecular biology of this association, we investigated three properties of HPV genomes in penile carcinomas from Brazilian patients: (i) HPV DNA methylation, (ii) junctions between HPV and cellular DNA and (iii) genomic variation. In cervical carcinogenesis, recombination between HPV and chromosomal DNA is frequent and likely necessary for progression, and DNA hypermethylation-specifically of the L1 gene-is a biomarker for cancerous progression.

Effects of cellular differentiation, chromosomal integration and 5-aza-2'-deoxycytidine treatment on human papillomavirus-16 DNA methylation in cultured cell lines.

Human papillomavirus-16 (HPV-16) genomes in cell culture and in situ are affected by polymorphic methylation patterns, which can repress the viral transcription. In order to understand some of the underlying mechanisms, we investigated changes of the methylation of HPV-16 DNA in cell cultures in response to cellular differentiation, to recombination with cellular DNA, and to an inhibitor of methylation. Undifferentiated W12E cells, derived from a precancerous lesion, contained extrachromosomal HPV-16 DNA with a sporadically methylated enhancer-promoter segment.

Human papillomavirus-16 DNA methylation patterns support a causal association of the virus with oral squamous cell carcinomas.

Infection with human papillomavirus-16 (HPV-16) is the cause of most anogenital carcinomas. This virus is also detected in about 20% of all head and neck squamous cell carcinomas. While there is strong evidence for a causal etiological role in the case of tonsillar carcinomas, causal association with malignant lesions of the oral cavity is not yet conclusive.

Methylation of the human papillomavirus-18 L1 gene: a biomarker of neoplastic progression?

Epigenetic transcriptional regulation plays an important role in the life cycle of human papillomaviruses (HPVs) and the carcinogenic progression of anogenital HPV associated lesions. We performed a study designed to assess the methylation status of the HPV-18 genome, specifically of the late L1 gene, the adjacent long control region (LCR), and part of the E6 oncogene in cervical specimens with a range of pathological diagnoses. In asymptomatic infections and infections with precancerous (precursor) lesions, HPV-18 DNA was mostly unmethylated, with the exception of four samples where hypermethylation of L1 was detected.

Genome variation of human papillomavirus types: phylogenetic and medical implications.

Human papillomaviruses (HPVs) are described as "types" based on their genome sequences and identified by a number. For example, HPV-6 is associated with genital warts, and HPV-16 with anogenital cancers. The genomes of many HPV types have been reisolated, sequenced and compared to reference "prototypes" countless times by laboratories throughout the world.

Worldwide genomic diversity of the high-risk human papillomavirus types 31, 35, 52, and 58, four close relatives of human papillomavirus type 16.

Among the more than one hundred formally described human papillomavirus (HPV) types, 18 are referred to as high-risk HPV types due to their association with anogenital cancer. Despite pathogenic similarities, these types form three remotely related taxonomic groups. One of these groups is called HPV species 9 and is formed by HPV-16, the most common and best-studied type, together with HPV-31, -33, -35, -52, -58, and -67.

Worldwide genomic diversity of the human papillomaviruses-53, 56, and 66, a group of high-risk HPVs unrelated to HPV-16 and HPV-18.

Among more than 200 human papillomavirus (HPV) types presumed to exist, 18 "high-risk" HPV types are frequently found in anogenital cancer. The best studied types are HPV-16 and 18, which are only distantly related to one another and form two separate phylogenetic branches, each including six closely related types. HPV-30, 53, 56, and 66 form a third phylogenetic branch unrelated to HPV-16 and 18.

Papillomavirus subtypes are natural and old taxa: phylogeny of human papillomavirus types 44 and 55 and 68a and -b.

A human papillomavirus (HPV) type is defined as an HPV isolate whose L1 gene sequence is at least 10% different from that of any other type, while a subtype is 2 to 10% different from any HPV type. In order to analyze the phylogeny behind the subtype definition, we compared 49 isolates of HPV type 44 (HPV-44) and its subtype HPV-55, previously misclassified as a separate type, and 41 isolates of the subtype pair HPV-68a and -b, sampled from cohorts in four continents. The subtypes of each pair are separated by deep dichotomic branching, and three of the four subtypes have evolved large phylogenetic clusters of genomic variants forming a "star" phylogeny, with some branches specific for ethnically defined cohorts.

Conserved methylation patterns of human papillomavirus type 16 DNA in asymptomatic infection and cervical neoplasia.

DNA methylation contributes to the chromatin conformation that represses transcription of human papillomavirus type16 (HPV-16), which is prevalent in the etiology of cervical carcinoma. In an effort to clarify the role of this phenomenon in the regulation and carcinogenicity of HPV-16, 115 clinical samples were studied to establish the methylation patterns of the 19 CpG dinucleotides within the long control region and part of the L1 gene by bisulfite modification, PCR amplification, DNA cloning, and sequencing. We observed major heterogeneities between clones from different samples as well as between clones from individual samples.

The human papillomavirus-18 genome is efficiently targeted by cellular DNA methylation.

Human papillomaviruses (HPVs) infect epithelia, including the simple and the squamous epithelia of the cervix, where they can cause cancer and precursor lesions. The molecular events leading from asymptomatic HPV infections to neoplasia are poorly understood. There is evidence that progression is modulated by transcriptional mechanisms that control HPV gene expression.

Genomic diversity of human papillomavirus-16, 18, 31, and 35 isolates in a Mexican population and relationship to European, African, and Native American variants.

Cervical cancer, mainly caused by infection with human papillomaviruses (HPVs), is a major public health problem in Mexico. During a study of the prevalence of HPV types in northeastern Mexico, we identified, as expected from worldwide comparisons, HPV-16, 18, 31, and 35 as highly prevalent. It is well known that the genomes of HPV types differ geographically because of evolution linked to ethnic groups separated in prehistoric times.

[Y chromosome micro-deletion identification in infertile males].

Unlabelled: Identifying the genetic causes of male infertility is very important, considering they account for 30-50% of reproductive problems among couples. Genetic abnormalities, among which Y chromosome microdeletions are found, are commonly detected in patients with non-obstructive azoospermia (0-4.3%).