Expression of p53 and p16 in esophageal squamous cell carcinoma
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ABSTRACT:
PROVIDER: PRJEB76245 | ENA |
REPOSITORIES: ENA
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Project description:Head and neck squamous cell carcinomas are heterogeneous neoplasms that show clinical and biological differences in association with the human papillomavirus (HPV). To provide adequate therapeutic strategies, biological and clinical characterization is essential to stratify patients based on prognostic and predictive factors. Reports on HNSCC are scarce in Mexico, thus in the present study, we analyze 414 cases of HNSCC, including those of the oropharynx (OPSCC), larynx (LASCC), and oral cavity (OCSCC). We determined the presence of HPV and p16 expression. Global expression profiles were analyzed with Affymetrix HTA 2.0 microarray in 25 selected cases HPV+/p16+ versus HPV-/p16-. In our study we analyze 25 samples derived from HNSCC patients. 18 samples were HPV-/p16- and 7 HPV+/p16+. We compared the HPV-/p16- versus the HPV+/p16+ and identified differentially expressed RNAs with a fold change greater than 1.5 or less than -1.5. These data were used to obtain 98 genes that are differentially expressed in absence of HPV. The present study offers information regarding clinical and molecular characteristics of HNSCC, both associated and unassociated with HPV, in Mexican patients.
2021-12-01 | GSE181805 | GEO
Project description:Comparison between HPV+ / p16+ versus the HPV-/p16- from HNSCC patients
| PRJNA753515 | ENA
Project description:PTPRD is a tumor suppressor of glioma that is frequently co-deleted with CDKN2A/p16. We show that Ptprd and p16 cooperate to promote gliomagenesis in the RCAS PDGFB / Nestin tv-A glioma mouse model. We found unique gene expression changes within tumor cells of Ptprd+/-p16-/- vs. Ptprd+/+p16-/- and Ptprd-/-p16-/- tumor cells. Neonatal mice were injected with RCAS PDGFB GFP. At symptoms, or at 12 weeks post injection, GFP+DAPI- tumor cells were sorted for RNA extraction and hybridization on Affymetrix microarrays. The mouse strain used was a mixed background of C57/BL6 and FVB/N. Ptprd mice were from Uetani et al. 2000 and p16/Nestin-tvA mice were from Tchouganouva et al. 2007.
2014-06-02 | E-GEOD-55061 | biostudies-arrayexpress
Project description:PTPRD is a tumor suppressor of glioma that is frequently co-deleted with CDKN2A/p16. We show that Ptprd and p16 cooperate to promote gliomagenesis in the RCAS PDGFB / Nestin tv-A glioma mouse model. We found unique gene expression changes within tumor cells of Ptprd+/-p16-/- vs. Ptprd+/+p16-/- and Ptprd-/-p16-/- tumor cells.
2014-06-02 | GSE55061 | GEO
Project description:The objective was to investigate the toxic effect of Bortezomib on human esophageal carcinoma epithelial cells at gene expression level. Gene expression profilings between Bortezomib and vehicle treated cells were compared.
2017-04-10 | GSE97558 | GEO
Project description:This is the glycopeptide part of the above project. Purpose: No blood-based biomarkers to detect OPSCC early before symptoms develop or before clinically visible. Diagnosis is solely based on histology of a visible tumour. Most OPSCC patients are diagnosed at an advanced stage, which leads to significant morbidity and poor survival. If high-risk patients were identified with blood-based biomarkers before clear clinical manifestations, tumours could be detected and treated at an earlier stage. Causes of OPSCC include smoking, alcohol misuse, and human papillomavirus (HPV). Tumours are separated according to WHO recommendations into HPV+ OPSCC and HPV- OPSCC using the proxy histological marker p16. We additionally separated our patients into these groups to determine whether the serum glycopeptides would differ between HPV+ and HPV- tumours, as these are distinct clinical entities. Patients and Methods: Pre-treatment sera from 74 patients with OPSCC (including 26 p16- tumours and 48 p16+ tumours) and 12 controls were used, collected between the years 2012 and 2015 at the Department of Otorhinolaryngology – Head and Neck Surgery, Helsinki University Hospital, Helsinki, Finland. Samples were grouped as follows: early stage p16+ OPSCC (stage I only), early stage p16- OPSCC (stage I-II), p16+ (any stage), p16- (any stage), controls. In-parallel quantitative bulk serum proteomics and serum glycopeptidomics were performed. Results: We identified 78 bulk proteins in the serum, of which 33 significantly differed between early-stage p16- OPSCC and controls, 22 between early-stage p16+ OPSCC and controls, 1 between early-stage p16+ and early-stage p16- OPSCCs, and 30 between all p16+ and p16- OPSCCs. We identified glycopeptides from proteins including but not limited to alpha-1-antitrypsin, haptoglobin, and Immunoglobulin heavy constant alpha 1, and compared these with the protein expression levels in each comparison. Conclusions: We have identified novel serum glycopeptide biomarkers detect early-stage OPSCCs, to be evaluated further as a diagnostic panel to detect preclinical OPSCC in at-risk patients.
2024-01-26 | PXD016709 | Pride
Project description:This is the proteomics part of the above project. Purpose: No blood-based biomarkers to detect OPSCC early before symptoms develop or before clinically visible. Diagnosis is solely based on histology of a visible tumour. Most OPSCC patients are diagnosed at an advanced stage, which leads to significant morbidity and poor survival. If high-risk patients were identified with blood-based biomarkers before clear clinical manifestations, tumours could be detected and treated at an earlier stage. Causes of OPSCC include smoking, alcohol misuse, and human papillomavirus (HPV). Tumours are separated according to WHO recommendations into HPV+ OPSCC and HPV- OPSCC using the proxy histological marker p16. We additionally separated our patients into these groups to determine whether the serum glycopeptides would differ between HPV+ and HPV- tumours, as these are distinct clinical entities. Patients and Methods: Pre-treatment sera from 74 patients with OPSCC (including 26 p16- tumours and 48 p16+ tumours) and 12 controls were used, collected between the years 2012 and 2015 at the Department of Otorhinolaryngology – Head and Neck Surgery, Helsinki University Hospital, Helsinki, Finland. Samples were grouped as follows: early stage p16+ OPSCC (stage I only), early stage p16- OPSCC (stage I-II), p16+ (any stage), p16- (any stage), controls. In-parallel quantitative bulk serum proteomics and serum glycopeptidomics were performed. Results: We identified 78 bulk proteins in the serum, of which 33 significantly differed between early-stage p16- OPSCC and controls, 22 between early-stage p16+ OPSCC and controls, 1 between early-stage p16+ and early-stage p16- OPSCCs, and 30 between all p16+ and p16- OPSCCs. We identified glycopeptides from proteins including but not limited to alpha-1-antitrypsin, haptoglobin, and Immunoglobulin heavy constant alpha 1, and compared these with the protein expression levels in each comparison. Conclusions: We have identified novel serum glycopeptide biomarkers detect early-stage OPSCCs, to be evaluated further as a diagnostic panel to detect preclinical OPSCC in at-risk patients.
2024-01-26 | PXD016727 | Pride
Project description:The objective was to investigate the toxic effect of hydroxyl-modified Graphene quantum dots (GQD) on normal human esophageal epithelial cells at gene expression level. Gene expression profilings between GQD and vehicle treated cells were compared.
2017-03-17 | GSE96720 | GEO
Project description:Advancing age is the greatest risk factor for Alzheimer’s Disease (AD), as most AD patients are age 65 and older. However, the mechanistic contribution of aging to AD is unclear. Cellular senescence, one of the major hallmarks of aging, is recently implicated as an aggravator of AD pathogenesis. The critical senescence regulator p16 is increased in neurons of AD patients and mouse models. Eliminating p16-expressing senescent cells attenuates AD pathologies in AD mouse models. However, what p16 does in post-mitotic neurons and how p16 contributes to AD pathogenesis remains unknown. As clinical trials continually fail to improve cognitive decline in AD patients, it is increasingly important to develop a better human cell-based model system to advance our understanding of the impact of aging in AD pathogenesis. Induced pluripotent stem cell (iPSC) technology has revolutionized human disease modeling, enabling differentiation to relevant brain cell types for the study of AD pathogenesis in a human cell-based culture environment. AD iPSC-derived neurons exhibit higher levels of Amyloid beta secretion and tau phosphorylation compared to non-demented control iPSC-derived neurons. Nevertheless, iPSC-derived neurons are “fetal-like” and fail to recapitulate the aging process in AD pathogenesis. Thus, we have developed a robust human iPSC-based neuron model to investigate the contribution of p16 expression to cellular senescence and AD pathogenesis. We found that inducible p16 expression leads to senescence phenotypes in AD as well as non-demented control iPSC-derived neurons. The impact of p16 and induced senescence in neurons on the cellular pathologies of AD is investigated. Our study provides a novel approach to investigate aging-associated cellular changes that potentially influence AD patient-derived differentiated neurons to age and become more permissive to AD pathogenesis in culture.
2023-12-31 | GSE252132 | GEO