PubMed · 14849927
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
T M SONNEBORN. Cellular transformations.. https://pubmed.ncbi.nlm.nih.gov/14849927/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Human papillomaviruses are the causative agents of cervical cancer. Previous studies have shown that loss of the viral E2 protein during malignant progression is an important feature of HPV-induced malignancy due to the resulting uncontrolled expression of the viral oncoproteins E6 and E7. We now show however that the viral E2 and E6 proteins are both capable of regulating each other's activity. When coexpressed, E2 and E6 induce marked changes in the pattern of each other's expression, with preferential accumulation in nuclear speckles. The two proteins interact directly, resulting in changes in the substrate specificities of E6 and the biochemical activities of E2. Thus, while E6 efficiently degrades its PDZ domain-containing substrates in the absence of E2, this activity is greatly diminished when E2 is present. Likewise, E2 alone drives both viral DNA replication and viral gene expression. However, in the presence of E6, viral DNA replication is inhibited while the transcriptional activity of E2 is elevated. These studies define a far more complex pattern of interaction between E2 and E6 than was previously thought and redefines the possible consequences of loss of E2 with respect to uncontrolled E6 activity and consequent malignant progression.
Epithelial mesenchymal transition has been postulated as a versatile mechanism which facilitates cellular repositioning and redeployment during embryonic development, tissue reconstruction after injury, carcinogenesis, and tumor metastasis. The hypothesis originates from parallels drawn between the morphology and behavior of locomotory and sedentary cells in vitro and in various normal and pathologic processes in vivo. This review analyzes data from several studies on embryonic development, wound healing, and the pathology of human tumors, including work from our own laboratory, to assess the validity of the proposal. It is concluded that there is no convincing evidence for conversion of epithelial cells into mesenchymal cell lineages in vivo and that the biological repertoire of normal and malignant cells is sufficient to account for the events and processes observed, without needing to invoke radical changes in cell identity.
STUDY DESIGN: Spinal ependymoma is a benign central nervous system tumor described as an intramedullary lesion more frequently located at the conus medullaris. It has been described exceptionally in the literature as an intradural extramedullary tumor. OBJECTIVE: Presentation of an extremelly rare location and evolution of extremedullary ependymoma and discussion of its probable origin, differential diagnosis, treatment options, and follow-up. SUMMARY OF BACKGROUND DATA: This case demonstrates an unusual location of a benign ependymal tumor in the extramedullary space with a total resection, which recurred in a lower level with a malignant transformation with the same extramedullary location. METHODS: The authors present the case of a 47-year-old woman with a subacute spinal cord dysfunction and an intradural extramedullary D2-D3 tumor mimicking meningioma or neurinoma. At surgery, an encapsulated intradural extramedullary mass was found, but neither dural attachment nor medullary infiltration was present. RESULTS: After complete resection, anatomic-pathologic studies confirmed that the lesion was a benign classic ependymoma. Good neurologic outcome was achieved, and no residual tumor was present at magnetic resonance imaging (MRI) control performed at 3 and 9 months later. One year after surgery, a new intradural extramedullary tumor was found at the D4 level without recurrence at D2. The patient was operated on again, but at this time the histologic study showed an anaplastic ependymoma with a proliferation index of 25% measured by Ki-67. Whole central nervous system radiotherapy was performed. CONCLUSION: All of the previously reported cases of spinal intradural extramedullary ependymomas carried out a benign course. The case we are reporting is the first one in which malignant transformation occurred. This tumor should be taken into account in the differential diagnosis of intradural extramedullary lesions. Moreover, close follow-up is recommended for this unusual location of ependymomas.