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http://dx.doi.org/10.7314/APJCP.2015.16.18.8041

Identification of HPV Integration and Genomic Patterns Delineating the Clinical Landscape of Cervical Cancer  

Akeel, Raid-Al (Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University)
Publication Information
Asian Pacific Journal of Cancer Prevention / v.16, no.18, 2016 , pp. 8041-8045 More about this Journal
Abstract
Cervical cancer is one of the most common cancers in women worldwide. During their life time the vast majority of women become infected with human papillomavirus (HPV), but interestingly only a small portion develop cervical cancer and in the remainder infection regresses to a normal healthy state. Beyond HPV status, associated molecular characterization of disease has to be established. However, initial work suggests the existence of several different molecular classes, based on the biological features of differentially expressed genes in each subtype. This suggests that additional risk factors play an important role in the outcome of infection. Host genomic factors play an important role in the outcome of such complex or multifactor diseases such as cervical cancer and are also known to regulate the rate of disease progression. The aim of this review was to compile advances in the field of host genomics of HPV positive and negative cervical cancer and their association with clinical response.
Keywords
Cervical cancer; HPV integration; genomic pattern;
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1 Allie K Adams, Trisha M Wise-Draper, Susanne I (2014). Wells human papillomavirus induced transformation in cervical and head and neck cancers. Cancers (Basel), 6; 1793-820.   DOI
2 Allen DG, White DJ, Hutchins AM, et al (2000). Progressive genetic aberrations detected by comparative genomic hybridization in squamous cell cervical cancer. Br J Cancer, 83, 1659-63.   DOI
3 Argiris A, Karamouzis MV, Raben D, Ferris RL (2008). Head and neck cancer. Lancet, 371, 1695-709.   DOI
4 Brady CA, Jiang D, Mello SS, et al (2011). Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppression. Cell, 145, 571-583.   DOI
5 Boren J, Brindle KM (2012). Apoptosis-induced mitochondrial dysfunction causes cytoplasmic lipid droplet formation. Cell Death Differ, 19, 1561-70.   DOI
6 Burtness B, Goldwasser MA, Flood W, Mattar B, Forastiere AA (2005). Eastern cooperative oncology g. phase iii randomized trial of cisplatin plus placebo compared with cisplatin plus cetuximab in metastatic/recurrent head and neck cancer: an eastern cooperative oncology group study. J Clin Oncol, 23, 8646-54.   DOI
7 Band V, De Caprio J, Delmolina L, Kulesa V, Sager R (1991). Loss of p53 protein in Human papillomavirus type 16 E6- immortalised human mammary epithelial cells. J Virol, 65, 6671-6.
8 Behtash N, Mehrdad N (2006). Cervical cancer: screening and prevention. Asian Pac J Cancer Prev, 7, 683-6
9 Bos JL (1989). ras oncogenes in human cancer: a review. Cancer Res, 49, 4682-9.
10 Bardelli A, Siena S (2010). Molecular mechanisms of resistance to cetuximab and panitumumab in colorectal cancer. J Clin Oncol, 28, 1254-61.   DOI
11 Blumenschein GRJr, Glisson BS, Lu C, et al (2012). Final results of a phase II study of sorafenib in combination with carboplatin and paclitaxel in patients with metastatic or recurrent SCCHN. J Clin Oncol, 30, 5592.
12 Brockstein BE (2011). Management of recurrent head and neck cancer: recent progress and future directions. Drugs, 71, 1551-9.   DOI
13 Chaturvedi AK, Anderson WF, Lortet-Tieulent J, et al (2013). Worldwide trends in incidence rates for oral cavity and oropharyngeal cancers. J Clin Oncol, 31, 4550-9.   DOI
14 Chaturvedi AK, Engels EA, Anderson WF, Gillison ML (2008). Incidence trends for human papillamavirus-related and -unrelated oral squamous cell carcinomas in the United States. J Clin Oncol, 26, 612-9.   DOI
15 Dotto GP (2009). Crosstalk of notch with p53 and p63 in cancer growth control. Nat Rev Cancer, 9, 587-95.   DOI
16 Engelman JA (2009). Targeting PI3K signalling in cancer: opportunities, challenges and limitations. Nat Rev Cancer, 9, 550-62.   DOI
17 De Bacco F, Luraghi P, Medico E, et al (2011). Induction of MET by ionizing radiation and its role in radioresistance and invasive growth of cancer. J Natl Cancer Inst, 103, 645-61.   DOI
18 Dayson N, Howley PM, Munger K, Harlow E (1989). The human papilloma virus-16 E7 oncoprotein is able to bind to the retinoblastoma gene product. Science, 243, 934-937.   DOI
19 Egloff AM, Grandis JR (2012). Molecular pathways: contextdependent approaches to notch targeting as cancer therapy. Clin Cancer Res, 18, 5188-95.   DOI
20 Hynes NE, Lane HA (2005). ERBB receptors and cancer: the complexity of targeted inhibitors. Nat Rev Cancer, 5, 341-354.   DOI
21 Harrington K, Berrier A, Robinson M, et al (2013). Randomised phase II study of oral lapatinib combined with chemoradiotherapy in patients with advanced squamous cell carcinoma of the head and neck: rationale for future randomised trials in human papilloma virus-negative disease. Eur J Cancer, 49, 1609-18.   DOI
22 Janku F, Wheler JJ, Naing A, et al (2013). PIK3CA mutation H1047R is associated with response to PI3K/AKT/mTOR signaling pathway inhibitors in early-phase clinical trials. Cancer Res, 73, 276-284.
23 Keiko Akagi, Jingfeng Li, Tatevik R Broutian, et al (2014). Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instability. Genome Res, 24, 185-99.   DOI
24 Knowles LM, Stabile LP, Egloff AM, et al (2009). HGF and c-Met participate in paracrine tumorigenic pathways in head and neck squamous cell cancer. Clin Cancer Res, 15, 3740-50.   DOI
25 Leonova KI, Brodsky L, Lipchick B, et al (2013). p53 cooperates with DNA methylation and a suicidal interferon response to maintain epigenetic silencing of repeats and noncoding RNAs. Proc Natl Acad Sci USA, 110, 89-98.   DOI
26 Kibe R, Zhang S, Guo D, et al (2012). IL-7Ralpha deficiency in p53null mice exacerbates thymocyte telomere erosion and lymphomagenesis. Cell Death Differ, 19, 1139-51.   DOI
27 Kolev V, Mandinova A, Guinea-Viniegra J, et al (2008). GFR signalling as a negative regulator of Notch1 gene transcription and function in proliferating keratinocytes and cancer. Nat Cell Biol, 10, 902-11   DOI
28 Krumbach R, Schuler J, Hofmann M, et al (2011). Primary resistance to cetuximab in a panel of patient-derived tumor xenograft models: activation of MET as one mechanism for drug resistance. Eur J Cancer, 47, 1231-43.   DOI
29 Lo Muzio L, Farina A, Rubini C, et al (2006). Effect of c-Metexpression on survival in head and neck squamous cell carcinoma. Tumor Biol, 27, 115-121.   DOI
30 Lando M, Holden M, Bergersen LC, et al (2009). Gene dosage, expression, and ontology analysis identifies driver genes in the carcinogenesis and chemoradioresistance of cervical cancer. PLoS Genet, 5, 1000719.   DOI
31 Molinolo AA, Marsh C, El Dinali M, et al (2012). mTOR as a molecular target in HPV-associated oral and cervical squamous carcinomas. Clin Cancer Res, 18, 2558-68.   DOI
32 Morton JP, Timpson P, Karim SA, et al (2010). Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer. Proc Natl Acad Sci USA, 107, 246-51   DOI
33 Sun S, Wang Z (2011). Head neck squamous cell carcinoma c-Met(+) cells display cancer stem cell properties and are responsible for cisplatin-resistance and metastasis. Int J Cancer, 129, 2337-48.   DOI
34 Pignon JP, le Maitre A, Maillard E, Bourhis J, Group M-NC (2009). Meta-analysis of chemotherapy in head and neck cancer (MACH-NC): an update on 93 randomised trials and 17, 346 patients. Radiother Oncol, 92, 4-14.   DOI
35 Qiu W, Schonleben F, Li X, et al (2006). PIK3CA mutations in head and neck squamous cell carcinoma. Clin Cancer Res, 12, 1441-6.   DOI
36 Seiwert TY, Jagadeeswaran R, Faoro L, et al (2009). The MET receptor tyrosine kinase is a potential novel therapeutic target for head and neck squamous cell carcinoma. Cancer Res, 69, 3021-31.
37 Seiwert T, Sarantopoulos J, Kallender H, et al (2013). Phase II trial of single-agent foretinib (GSK1363089) in patients with recurrent or metastatic squamous cell carcinoma of the head and neck. Invest New Drugs, 31, 417-24.
38 Scheffner M, Werness BA, Huibregtse JM, Levine AJ, Howley PM (1990). The E6 oncoprotein encoded by human papillomavirus types 16 and 18 promotes the degradation of p53. Cell, 63, 1129-36.   DOI
39 Talora C, Sgroi DC, Crum CP, Dotto GP (2002). Specific downmodulation of Notch1 signaling in cervical cancer cells is required for sustained HPV-E6/E7 expression and late steps of malignant transformation. Genes Dev, 16, 2252-63.   DOI
40 Ursula Winters, Richard Roden, Henry Kitchener, Peter Stern (2006). Progress in the development of a cervical cancer vaccine. Ther Clin Risk Manag, 2, 259-69.   DOI
41 Vogelstein B, Lane D, Levine AJ (2000). Surfing the p53 network. Nature, 408, 307-310.   DOI
42 Walboomers JM, Jacobs MV, Manos MM, et al (1999). Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol, 189, 12-19.   DOI
43 Vermorken JB, Stohlmacher-Williams J, Davidenko I, et al (2013). Cisplatin and fluorouracil with or without panitumumab in patients with recurrent or metastatic squamous-cell carcinoma of the head and neck (SPECTRUM): an openlabel phase 3 randomised trial. Lancet Oncol, 14, 697-710.   DOI
44 Walter V, Yin X, Wilkerson MD, et al (2013). Molecular subtypes in head and neck cancer exhibit distinct patterns of chromosomal gain and loss of canonicalcancer genes. PLoS One, 8, 56823.   DOI
45 Wilhelm SM, Adnane L, Newell P, et al (2008). Preclinical overview of sorafenib, a multikinase inhibitor that targets both Raf and VEGF and PDGF receptor tyrosine kinase signaling. Mol Cancer Ther, 7, 3129-40.   DOI
46 zur Hausen H (2002). Papillomaviruses and cancer: from basic studies to clinical application. Nat Rev Cancer, 2, 342-50   DOI
47 Zhao D, Wang SH, Feng Y, et al (2011). Intratumoral c-Met expression is associated with vascular endothelial growth factor C expression, lymphangiogenesis, and lymph node metastasis in oral squamous cell carcinoma: implications for use as a prognostic marker. Hum Pathol, 42, 1514-23.   DOI