Ontology highlight
ABSTRACT:
PROVIDER: PRJNA477555 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7414990_1.fastq.gz | Fastqsanger.gz | |||
| SRR7414990_2.fastq.gz | Fastqsanger.gz | |||
| SRR7414991_1.fastq.gz | Fastqsanger.gz | |||
| SRR7414991_2.fastq.gz | Fastqsanger.gz | |||
| SRR7414992_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Purpose: There is substantial heterogeneity within the human papillomavirus (HPV) positive head and neck cancer (HNC) tumors that predispose them to different outcomes, however this subgroup is poorly characterized due to various historical reasons. Experimental Design: we perform unsupervised gene expression clustering on well-annotated HPV(+) HNC samples from two cohorts ( 84 total primary tumors), as well as 18 HPV(-) HNCs, to discover subtypes, and begin to characterize the differences between the subtypes in terms of their HPV characteristics, pathway activity, whole-genome somatic copy number variations and mutation frequencies. Results: We identified two distinctive HPV(+) subtypes by unsupervised clustering. Membership in the HPV(+) subtypes correlates with genic viral integration status, E2/E4/E5 expression levels and the ratio of spliced to full length HPV oncogene E6. The subtypes also show differences in copy number alterations, in particular the loss of chr16q and gain of chr3q, PIK3CA mutation, and in the expression of genes involved in several biological processes related to cancer, including immune response, oxidation-reduction process, and keratinocyte and mesenchymal differentiation. Conclusion: Our characterization of two subtypes of HPV(+) tumors provides valuable molecular level information in relation to the alternative paths to tumor development and to that of HPV(-) HNCs. Together, these results will shed light on stratifications of the HPV(+) HNCs and will help to guide personalized care for HPV(+) HNC patients.
2016-05-13 | GSE74949 | GEO
Project description:Chromatin alterations mediate mutations and gene expression changes in cancer. Chromatin immunoprecipitation followed by sequencing (ChIP-Seq) has been utilized to study genome-wide chromatin structure in human cancer cell lines, yet numerous technical challenges limit comparable analyses in primary tumors. Here we have developed a new whole-genome analytic pipeline to optimize ChIP-Seq protocols on patient-derived xenografts from human papillomavirus-related (HPV+) head and neck squamous cell carcinoma (HNSCC) samples. We further associated chromatin aberrations with gene expression changes from a larger cohort of the tumor and normal samples with RNA-Seq data. We detect differential histone enrichment associated with tumor-specific gene expression variation, sites of HPV integration in the human genome, and HPV-associated histone enrichment sites upstream of cancer driver genes, which play central roles in cancer-associated pathways. These comprehensive analyses enable unprecedented characterization of the complex network of molecular changes resulting from chromatin alterations that drive HPV-related tumorigenesis.
2018-03-20 | GSE112021 | GEO
Project description:Restif2007 - Vaccination invasion
This model is described in the article:
Vaccination and the dynamics
of immune evasion.
Restif O, Grenfell BT.
J R Soc Interface 2007 Feb; 4(12):
143-153
Abstract:
Vaccines exert strong selective pressures on pathogens,
favouring the spread of antigenic variants. We propose a simple
mathematical model to investigate the dynamics of a novel
pathogenic strain that emerges in a population where a previous
strain is maintained at low endemic level by a vaccine. We
compare three methods to assess the ability of the novel strain
to invade and persist: algebraic rate of invasion;
deterministic dynamics; and stochastic dynamics. These three
techniques provide complementary predictions on the fate of the
system. In particular, we emphasize the importance of
stochastic simulations, which account for the possibility of
extinctions of either strain. More specifically, our model
suggests that the probability of persistence of an invasive
strain (i) can be minimized for intermediate levels of vaccine
cross-protection (i.e. immune protection against the novel
strain) and (ii) is lower if cross-immunity acts through a
reduced infectious period rather than through reduced
susceptibility.
This
version of the model can be used for both the stochastic and the
deterministic simulations described in the article. For
deterministic interpretations with infinite population sizes, set
the population size
N = 1. The model does reproduces the deterministic
time course. The initial values are set to the steady state
values for a latent infection with strain 1 with an invading
infection of strain 2 (I2=1e-06), 100 percent vaccination with a
susceptibility reduction τ=0.7 at birth (p=1), and all other
parameters as in figure 3 of the publication.
To
be compatible with older software tools, the english letter names
instead of the greek symbols were used for parameter names:
parameter
symbol
name
transmission rate
β
beta
recovery rate
γ
gamma
birth/death rate
μ
mu
rate of loss of natural immunity
σ
sigma
rate of loss of vaccine immunity
σ
v
sigmaV
reduction of susceptibility by primary infection
θ
theta
reduction of infection period by primary infection
ν
nu
reduction of susceptibility by vaccination
τ
tau
reduction of infection period by vaccination
η
eta
Originally
created by libAntimony v1.4 (using libSBML 3.4.1)
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000294.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2024-09-02 | BIOMD0000000294 | BioModels
Project description:Purpose: There is substantial heterogeneity within the human papillomavirus (HPV) positive head and neck cancer (HNC) tumors that predispose them to different outcomes, however this subgroup is poorly characterized due to various historical reasons. Experimental Design: we perform unsupervised gene expression clustering on well-annotated HPV(+) HNC samples from two cohorts ( 84 total primary tumors), as well as 18 HPV(-) HNCs, to discover subtypes, and begin to characterize the differences between the subtypes in terms of their HPV characteristics, pathway activity, whole-genome somatic copy number variations and mutation frequencies. Results: We identified two distinctive HPV(+) subtypes by unsupervised clustering. Membership in the HPV(+) subtypes correlates with genic viral integration status, E2/E4/E5 expression levels and the ratio of spliced to full length HPV oncogene E6. The subtypes also show differences in copy number alterations, in particular the loss of chr16q and gain of chr3q, PIK3CA mutation, and in the expression of genes involved in several biological processes related to cancer, including immune response, oxidation-reduction process, and keratinocyte and mesenchymal differentiation. Conclusion: Our characterization of two subtypes of HPV(+) tumors provides valuable molecular level information in relation to the alternative paths to tumor development and to that of HPV(-) HNCs. Together, these results will shed light on stratifications of the HPV(+) HNCs and will help to guide personalized care for HPV(+) HNC patients. 36 head and neck primary tumors (18 HPV+ and 18 HPV-) and their matched blood samples were collected and genotyped by Illumina OmniExpress SNP array. RNA-seq was also performed on the same set of tumor samples.
2016-05-13 | E-GEOD-74927 | biostudies-arrayexpress
Project description:We combined ChIP-seq of chromatin marks and key islet transcription factor with RNA-seq in human islets to map cis-regulatory networks in this primary tissue. The output of this project provides a reference map to dissect genetic variants that alter the susceptibility for Type 2 diabetes, and assist efforts to generate new beta-cells by transcriptional programming strategies
2014-01-01 | E-MTAB-1919 | biostudies-arrayexpress
Project description:Global long non-coding RNA (lncRNA) expression profile in primary human keratinocytes post-expression of high-risk HPV-16 E6 oncoprotein Purpose: The goal of this study is to utlize high-throughput RNA sequencing (RNA-seq) to identify differentially expressed host lncRNAs with the presence of the high-risk HPV-16 E6 oncoprotein in primary human foreskin keratinocytes. Methods: Primary human foreskin keratinocytes (HEKa) stably expressing HPV-16 E6 compared to GFP control were analyzed, in triplicates, by RNA-seq (Illumina). qRT-PCR validation was performed using SYBR Green assays. Results: 151 up- and 100 down-regulated host lncRNAs were altered greater than 1.5-fold change in HEKa expressing HPV-16 E6 compared to GFP control cells. Altered expression of 16 genes (8 up- and 8 down-regulated) were confirmed by qRT-PCR, demonstrating the high-degree of sensitivity of the RNA-seq method. Conclusions: Our study represents the first global screening of host lncRNAs altered specifically by HPV-16 E6 oncoprotein expression.
2018-10-31 | GSE115334 | GEO
Project description:Tumor suppressor p53 and its related proteins, p63 and p73, can be synthesized as multiple isoforms lacking part of the N- or C-terminal regions. Specifically, high expression of the ΔNp73α isoform is notoriously associated with various human malignancies characterized by poor prognosis. This isoform is also accumulated by oncogenic viruses such as Epstein–Barr virus (EBV), as well as genus beta human papillomaviruses (HPV) that appear to be involved in carcinogenesis. To gain additional insight into ΔNp73α mechanisms, we have performed proteomics analyses using human keratinocytes transformed by the E6 and E7 proteins of the beta-HPV type 38 virus as an experimental model (38HK). We find that ΔNp73α associates with the E2F4/p130 repressor complex through a direct interaction with E2F4. This interaction is favored by the N-terminal truncation of p73 characteristic of ΔNp73 isoforms. Moreover, it is independent of the C-terminal splicing status, suggesting that it could represent a general feature of ΔNp73α isoforms (α, β, γ, δ, ε, ζ, θ, η, and η1). We show that the ΔNp73α-E2F4/p130 complex inhibits the expression of specific genes, including genes encoding for negative regulators of proliferation, both in 38HK and in HPV-negative cancer-derived cell lines. Such genes are not inhibited by E2F4/p130 in primary keratinocytes lacking ΔNp73α, indicating that the interaction with ΔNp73α rewires the E2F4 transcriptional program. In conclusion, we have identified and characterized a novel transcriptional regulatory complex with potential implications in oncogenesis.
2021-06-08 | GSE162816 | GEO
Project description:Gene expression profiling of 66 HPV-negative OSCC primary tumor was performed to identify gene expression that is related to lymph node metastasis and poor prognosis. These gene expression profiles were combined in silico with gene expression profiles of 84 OSCC primary tumors retrieved from GSE30788.
2017-08-10 | GSE85446 | GEO
Project description:Persistent infection by high-risk human papillomaviruses (HPVs) is associated with the development of cervical cancer and a subset of anogenital and head and neck squamous cell carcinomas. Abnormal expression of cellular microRNAs (miRNAs) plays an important role in the development of cancer, including HPV-related tumors. MiRNA expression profile was investigated by microrray analysis in the HPV-positive cervical cancer cell lines SiHa (HPV16-positive cell line derived from a cervical squamous cell carcinoma), CaSki (HPV16-positive cell line derived from a metastatic cervical epidermoid carcinoma), and HeLa (HPV18-positive cell line derived from a cervical adenocarcinoma) and compared with primary HFKs and C33a (HPV-negative cervical cell line).
2018-01-16 | E-MTAB-6361 | biostudies-arrayexpress
Project description:Investigate the transcriptomic differences between HPV-positive and HPV-negative primary cervical tumors.
2024-09-02 | GSE275914 | GEO