Publications by authors named "Agueda Buitrago-Perez"
Human papillomavirus (HPV) is the causative agent of human cervical cancer and has been associated with oropharyngeal squamous cell carcinoma development. Although prophylactic vaccines have been developed, there is a need to develop new targeted therapies for individuals affected with malignant infected lesions in these locations, which must be tested in appropriate models. Cutaneous beta HPV types appear to be involved in skin carcinogenesis.
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- The study investigates how the removal of the Trp53 gene in mice leads to aggressive tumors, especially when the Rb gene is also ablated, mimicking certain human cancers.
- Gene expression analysis shows that these mouse tumors share similarities with human cancers that involve mutations in the TP53 gene, highlighting common features like increased cell cycle activity and chromosomal instability.
- The researchers identified a 20-gene signature that not only shows overexpression in mouse tumors but also helps predict poor outcomes in human cancers like breast cancer and multiple myeloma, suggesting these mouse models could be useful for finding cancer biomarkers and testing new therapies.
Article Synopsis
- Continuous renewal of skin cells in mice relies on pluripotent stem cells found in a niche called the bulge within hair follicles.
- Researchers isolated these bulge stem cells and found that many genes linked to the cell cycle are underexpressed in them compared to non-stem cells.
- Investigating the role of the E2F transcription factors revealed that the Rb-E2F pathway regulates stem cell activity, impacting processes like hair regrowth and wound healing.
The infection by mucosal human papillomavirus (HPV) is causally associated with tumor development in cervix and oropharynx. The mechanisms responsible for this oncogenic potential are mainly due to the product activities of two early viral oncogenes: E6 and E7. Although a large number of cellular targets have been described for both oncoproteins, the interaction with tumor suppressors p53 and retinoblastoma protein (pRb) emerged as the key functional activities.
View Article and Find Full Text PDFBackground: The specific ablation of Trp53 gene in mouse epidermis leads to the spontaneous development of aggressive squamous cell carcinoma, a process that is accelerated by the subsequent loss of Rb gene.
Materials And Methods: The possible mechanisms leading to spontaneous tumor formation in epidermis in the absence of Trp53 were studied focusing on hair cycle defects, inflammation and possible chromosomal instability (CIN).
Results: Loss of p53 induces tumorigenesis primarily by mediating early CIN and, to a minor extent, nuclear factor kappaB activation.