Papillomaviruses and cancer: from basic studies to clinical application

By H. Hausen. Nature Reviews. Cancer, 2002

4,097 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c177ad676d52241446a332a6eb8af2c5fe799fc2

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Citations in the corpus

Multifaceted polo-like kinases: drug targets and antitargets for cancer therapy (2010, background): “In addition, it has been shown that the HPV E7 protein from high-risk HPV types impairs the repressive function of the retinoblastoma protein (Rb”
Identification of a Third Human Polyomavirus (2007, background): “Nevertheless, many of these viruses may occasionally produce severe disease (21, 32, 34, 37).”
Human papillomavirus oncoproteins: pathways to transformation (2010, background): “From infection to tumour initiation Failure of the immune system to clear persistent HPV infections can lead to the development of cervical cancer after several decade”
Integration of interferon-α/β signalling to p53 responses in tumour suppression and antiviral defence (2003, background): “Persistent infection with oncogenic HPV types represents a major risk factor for the development of cervical cancer, in which E6 is known to have a critical role (together with another oncoprotein, E7 (ref”
The molecular biology of head and neck cancer (2011, background): “HPV is a strictly epitheliotropic, circular double-stranded DNA virus that is known to be the primary cause of cervical cance”
A novel algorithm for reliable detection of human papillomavirus in paraffin embedded head and neck cancer specimen (2007, background): “These oncoproteins directly inactivate p53 and pRb, respectively, and promote cell cycle entry and DNA synthesis as well as blockade of apoptosis, cellular conditions favoring viral replication.(11)”
miR-21: a small multi-faceted RNA (2008, background): “Infection with HPV16 or 18 is a major risk factor for developing cervical cancer, and common fragile sites are preferential targets for HPV16 integrations in cervical tumours [35].”
Cell cycle regulation: p53-p21-RB signaling (2022, background): “More importantly, essentially all tumors of the cervix uteri are a consequence of HPV infection [11, 12].”