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Spatiotemporally Deciphering the Unknown Role of Persistent HPV Infection in Precancer to Cervical Cancer Progression: Integrating Single-Cell RNA-Sequencing Landscape and Spatial Transcriptomics Atlas [scRNA-seq]

ABSTRACT: Spatiotemporally Deciphering the Unknown Role of Persistent HPV Infection in Precancer to Cervical Cancer Progression: Integrating Single-Cell RNA-Sequencing Landscape and Spatial Transcriptomics Atlas [scRNA-seq]

PROVIDER: PRJNA860568 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20330700_1.fastq.gz	Fastqsanger.gz
	SRR20330700_2.fastq.gz	Fastqsanger.gz
	SRR20330701_1.fastq.gz	Fastqsanger.gz
	SRR20330701_2.fastq.gz	Fastqsanger.gz
	SRR20330702_1.fastq.gz	Fastqsanger.gz

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Spatiotemporally Deciphering the Unknown Role of Persistent HPV Infection in Precancer to Cervical Cancer Progression: Integrating Single-Cell RNA-Sequencing Landscape and Spatial Transcriptomics Atlas [Spatial Transcriptomics]

Project description:The mechanism underlying the cervical carcinogenesis mediated by persistent HPV infection remains elusive. Here we pioneeringly deciphered both temporal transition and spatial distribution of the cellular subsets during the disease progression from normal cervix, precancer lesions to cervical cancer by integrating scRNA-seq with ST. We not only identified three ‘HPV-related epithelial clusters’ unique to normal, HSIL and cervical cancer respectively, but also discovered node genes which potentially determined the disease progression. Moreover, we observed a gradual transition of multiple immune cells from positive immune response to dysregulation and exhaustion, to an immune-suppressive microenvironment during the malignant program. Besides, the cellular interaction analysis further verified a ‘homeostasis-balance-malignancy’ change within cervix microenvironment during disease escalation. Together, these findings not only deciphered mysterious persistent HPV infection spatiotemporally from the process of precancer to cervical cancer but also provided unprecedented possibilities for accurate diagnosis, precise treatment and prognosis evaluation for precancer and cervical cancer.

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Project description:Spatiotemporally Deciphering the Unknown Role of Persistent HPV Infection in Precancer to Cervical Cancer Progression: Integrating Single-Cell RNA-Sequencing Landscape and Spatial Transcriptomics Atlas [Spatial Transcriptomics]

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Spatiotemporally deciphering the mysterious mechanism of persistent HPV-induced malignant transition and immune remodelling from HPV-infected normal cervix, precancer to cervical cancer: Integrating single-cell RNA-sequencing and spatial transcriptome.

Project description:BackgroundThe mechanism underlying cervical carcinogenesis that is mediated by persistent human papillomavirus (HPV) infection remains elusive.AimsHere, for the first time, we deciphered both the temporal transition and spatial distribution of cellular subsets during disease progression from normal cervix tissues to precursor lesions to cervical cancer.Materials & methodsWe generated scRNA-seq profiles and spatial transcriptomics data from nine patient samples, including two HPV-negative normal, two HPV-positive normal, two HPV-positive HSIL and three HPV-positive cancer samples.ResultsWe not only identified three 'HPV-related epithelial clusters' that are unique to normal, high-grade squamous intraepithelial lesions (HSIL) and cervical cancer tissues but also discovered node genes that potentially regulate disease progression. Moreover, we observed the gradual transition of multiple immune cells that exhibited positive immune responses, followed by dysregulation and exhaustion, and ultimately established an immune-suppressive microenvironment during the malignant program. In addition, analysis of cellular interactions further verified that a 'homeostasis-balance-malignancy' change occurred within the cervical microenvironment during disease progression.DiscussionWe for the first time presented a spatiotemporal atlas that systematically described the cellular heterogeneity and spatial map along the four developmental steps of HPV-related cervical oncogenesis, including normal, HPV-positive normal, HSIL and cancer. We identified three unique HPV-related clusters, discovered critical node genes that determined the cell fate and uncovered the immune remodeling during disease escalation.ConclusionTogether, these findings provided novel possibilities for accurate diagnosis, precise treatment and prognosis evaluation of patients with precancer and cervical cancer.

| S-EPMC10040725 | biostudies-literature

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A trial to establish whether laser treatment of anal precancer prevents development of anal cancer in HIV-positive men who have sex with men

Project description:Background and study aims Anal cancer is a growing problem in the UK. Almost 90% of these cancers are caused by the human papillomavirus (HPV). HPV infection in a weakened immune system can lead to abnormal cell changes which are graded as anal intraepithelial neoplasia (AIN) 1-3, with AIN 2 and AIN 3 considered to be high-grade neoplasia (AIN 2/3). These changes are called precancers, but it is not known how many, over what time period will turn to cancer. Although many doctors and scientists think we need to treat AIN 2/3 (precancer), as is done in women for cervical precancer to prevent cancer, there is no proven treatment for anal precancer (AIN 2/3) that will prevent anal cancer. Laser treatment may be an effective strategy to prevent anal cancer. The main aim of the study is to assess the long-term effect (up to 5 years) of laser treatment in preventing anal cancer in HIV-positive men who have sex with men with anal precancer. Who can participate? HIV-positive men who have sex with men, who have anal precancer What does the study involve? Participants are randomly allocated to one of two groups. Participants in the treatment group undergo laser ablation of their perianal (external) or anal canal (internal) disease under local anaesthetic injections. If the disease volume (extent) is large the ablation may be done under general anaesthetic as a day case. Rarely, it may be necessary to treat extensive disease as a staged procedure over more than one treatment visit. Participants in the active surveillance group receive no treatment. All participants are followed up every 6 months with standard examinations. The number of cancers, the effect of treatment on preventing new precancer, quality of life, and the costs of treatment are compared between the groups.

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Identification and validation of a novel 3-gene methylation classifier for HPV-based cervical screening on self-samples

Project description:Background: Offering self-sampling of cervico-vaginal material for human papillomavirus (HPV) testing is an effective method to increase the coverage in cervical screening programmes. Molecular triage directly on HPV-positive self-samples for colposcopy referral opens the way to full molecular cervical screening. Here, we set out to identify a methylation classifier for detection of precancer (CIN3) or cancer, applicable to self-samples obtained by different devices. Findings: Genome-wide DNA methylation profiling of HPV-positive self-samples revealed 12 methylation targets for CIN3 detection. Multiplex quantitative methylation-specific PCR of these targets yielded a 3-gene methylation classifier (ASCL1, LHX8 and ST6GALNAC5), showing a very good clinical performance for CIN3 detection in both lavage (AUC=0.88; sensitivity=74%; specificity=79%) and brush (AUC=0.90; sensitivity=88%; specificity=81%) self-samples in the validation set. All self-samples from women with cervical cancer scored methylation-positive. Conclusion: By genome-wide DNA methylation profiling on self-samples, we identified a highly effective 3-gene methylation classifier for direct triage on self-samples from HPV-positive women.

2018-01-01 | GSE99511 | GEO

Gene expression of CD66 expressing cells in cervical precancer cell line

Project description:Gene Expression profiles of sorted CD66High and CD66Low cells were generated from CIN612-9E cells grown in Emedia. We have analyzed the gene expression pattern of CD66High and CD66Low cells from CIN612 9E. These cells are derived from a cervical precancer lesion (M. Bedell, J. Hudson, T. Golub et al, 1991, J. Virol) Two sets of experiments (biological replicates) were performed for CD66High and CD66Low cells.

2014-09-30 | E-GEOD-59322 | biostudies-arrayexpress

Gene expression profiling of HPV-active, HPV-inactive and HPV-negative oropharyngeal squamous cell carcinomas

Project description:Approximately 25% of all head and neck cancers (HNC), and up to 60% of oropharyngeal cancers (OPC) are associated with human papillomavirus (HPV), predominantly HPV16. HPV-associated OPC have better prognosis and a more favorable response to therapy as compared to HPV-negative tumors. Viral oncoproteins are capable of transforming primary human keratinocytes from either genital or oral epithelia in vitro and most likely play the same role in vivo, by disrupting cell-cycle regulatory pathways leading to a genetic progression to ano-genital cancer and OPC. However, the precise mechanisms by which HPV mediates malignant transformation of keratinocytes in the upper digestive tract epithelia are not entirely clear. HPV E7-mediated inactivation of pRb results in overexpression of p16INK4A, which is commonly used as a clinical surrogate marker for HPV positivity/activity. However, high p16INK4A alone has insufficient sensitivity and specificity as a biomarker of HPV positivity in different mucosal sub-sites of HNC. Therefore, increasing emphasis is being placed on the assessment of viral load and E7 oncogene expression, resulting in further classification of HPV positive OPC as HPV-active and HPV-inactive. Differences in risk factors, age of presentation, clinical behavior and gene expression profiles indicate that HPV-positive and HPV-negative tumors develop via different molecular mechanisms and are biologically distinct. This study aimed to compare the gene expression profiles of HPV-active, -inactive and -negative OPC and determine their biological differences. ANALYSIS 1: Three-condition, one-color experiment: HPV-active, HPV-inactive and HPV-negative oropharyngeal tumor samples. Biological replicates: 12 HPV Active tumors, 8 HPV Inactive tumors and 16 HPV Negative tumors.

2014-03-05 | E-GEOD-55542 | biostudies-arrayexpress

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