Human papillomavirus immortalization and transformation functions.
By K. Münger, P. Howley. Virus Research, 2002
813 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/90ad12ff556e32ec2593a6a4b00823871aedabab
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In Epidemiology
In Molecular Biology
In Oncology
Citations in the corpus
- Cancer genes and the pathways they control (2004, background): “One of the most important—and most curious—discoveries of the 1990s was that virtually all DNA tumor viruses that cause tumors in experimental animals or humans encode proteins that inactivate both Rb and p53 (refs”
- Classification of papillomaviruses. (2004, background): “In short, three oncogenes , E5, E6, and E7, modulate the transformation process, two regulatory proteins, E1 and E2, modulate transcription and replication, and two structural proteins, L1 and L2, compose the viral capsid (for a review, see Munger and Howley, 2002).”
- Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells (2004, methodology): “To identify which pathway, p16 INK4a –Rb or p19 ARF –p53, governs stem cell function, we inhibited the function of Rb family members or p53 by infecting Atm -/- KSL cells with a retroviral vector expressing human papilloma virus type 16 E7 and E6, respectivel”
- Stem cell origin of cancer and differentiation therapy. (2004, background): “In squamous cell carcinoma of the uterine cervix associated with human papilloma virus infection, the initially infected and transformed cell is the basal stem cell, but productive infection requires keratinocyte differentiation [118,119].”