Project description:Equine Papillomavirus Type 2 (EcPV2) appears to be a causal factor for the development of genital especially penile squamous cell carcinomas (SCC) and as such have an important clinical impact on horses. However, the pathomechanisms associated with this cancer transformation are not known, yet. To analyze the host’s and viral transcriptome in EcPV2 affected horses, tissue samples were collected from horses with EcPV2-positive genital lesions as well as from healthy EcPV2-negative horses. Expression levels of host and viral genes were evaluated by RNA-Seq.
Project description:Mouse skin carcinogenesis experiments suggest upon carcinogen treatment and promotion on mouse skin there arise at least two populations of tumors. One population has a higher incidence of progression from benign papilloma to a squamous cell carcinoma. Further studies have shown that a certain carcinogenesis protocol can select for these high risk tumors. These microarray experiments aim to reveal the genetic signatures of the low risk and high risk papilloma. Keywords: Genetic Signatures
Project description:The head and neck / oral squamous cell carcinoma (HNOSCC) is a diverse group of cancers, which develop from many different anatomic sites and are associated with different risk factors and genetic characteristics. The oral tongue squamous cell carcinoma (OTSCC) is one of the most common types of HNOSCC. It is significantly more aggressive than other forms of HNOSCC, in terms of local invasion and spread. In this study, we aim to identify specific transcriptomic signatures that associated with OTSCC. Experiment Overall Design: 26 OTSCC samples and 12 control samples were analyzed using Affymetrix U133 Plus 2.0 array.
Project description:Genome-wide expression array measurements for 9 head and neck squamous cell carcinomas (HNSCC) stratified by worst pattern of invasion (WPOI) Jayakar et al. (2016). Apolipoprotein E promotes invasion in oral squamous cell carcinoma. Li et al. (2013). Validation of the risk model: high-risk classification and tumor pattern of invasion predict outcome for patients with low-stage oral cavity squamous cell carcinoma.
Project description:The head and neck / oral squamous cell carcinoma (HNOSCC) is a diverse group of cancers, which develop from many different anatomic sites and are associated with different risk factors and genetic characteristics. The oral tongue squamous cell carcinoma (OTSCC) is one of the most common types of HNOSCC. It is significantly more aggressive than other forms of HNOSCC, in terms of local invasion and spread. In this study, we aim to identify specific transcriptomic signatures that associated with OTSCC. Keywords: Disease/Control analysis
Project description:The human genome encodes two proteins closely related to transketolase (TKT), transketolase-like protein 1 and 2 (TKTL1 and TKTL2). TKTL1 shares 61% amino acid sequence identity with TKT. More and more evidence suggests a role for TKTL1 in proliferation or cell cycle regulation. Indeed, TKTL1 is overexpressed in various cancers and is correlated with poor prognosis in colon, urothelial, gastric, and lung cancers as well as in ocular adnexa carcinomas, rectum carcinomas, and laryngeal squamous cell carcinomas. Increased TKTL1 levels also correlate with esophageal squamous cell carcinoma metastasis and increased resistance against cisplatin chemotherapy in nasopharyngeal carcinomas. Moreover, TKTL1 overexpression promotes cell proliferation and enhanced tumor growth; in contrast, TKTL1 down regulation attenuates the proliferation of various types of cancer cells. However, the cellular functions and regulatory machineries of TKTL1 are still largely unknown. Through this proteomic analysis, we defined the protein-protein interaction map for the TKTL1 and uncovered the novel regulating function of TKTL1 in regulating TKT transketolase activity.
Project description:Both genetic and epigenetic aberrations are linked by intricate crosstalk, and can either individually or in synergy lead to the development of cancer. Accumulating evidence suggests that epigenetic changes such as alterations in DNA methylation play a crucial role in ESCC. We performed a Illumina Infinium HumanMethylation450 BeadChip to examine the global methylation signature of esophageal squamous cell carcinoma of Chinese patients. DNA methylation profiles of esophageal squamous cell carcinoma (4 samples), paired adjacent normal surrounding tissues (4 samples) and normal esophagus mucosa from healthy individuals (4 samples) were generated using Infinium methylation 450K BeadChips from Illumina (Illumina, San Diego, USA).
Project description:Genome-wide expression array measurements for 9 head and neck squamous cell carcinomas (HNSCC) stratified by worst pattern of invasion (WPOI) Jayakar et al. (2016). Apolipoprotein E promotes invasion in oral squamous cell carcinoma. Li et al. (2013). Validation of the risk model: high-risk classification and tumor pattern of invasion predict outcome for patients with low-stage oral cavity squamous cell carcinoma. Comparison of transcription profiles between OSCC tumors with a more invasive (WPOI 5) versus a less invasive (WPOI 3) pattern of invasion using two independent Illumina platforms.
Project description:Cervical intraepithelial neoplasia (CIN), also known as cervical dysplasia, is premalignant lesions of the cervical squamous cell carcinoma (CSCC) that shows abnormal growth of squamous cells in the cervix epithelium. Given the evidence suggesting that differences may exist between CIN and CSCC, we hypothesize that progression may be mediated by subpopulation selection or by acquisition of additional alterations, including gene mutations or chromosomal alterations. In this study, we analyzed cervical CIN, microinvasive carcinoma (MIC) and CSCC by whole-exome sequencing and array-comparative genomic hybridization (array-CGH) and found that CIN genomes harbored fewer mutations (especially fewer driver mutations) and copy number alterations (CNAs), suggesting that additional genomic alterations might burst onto the CIN genome at the final stage of CIN progression to CSCC or an early stage of CSCC.