HPV positive neuroendocrine cervical cancer cells are dependent on Myc but not E6/E7 viral oncogenes
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S. Agarwal | T. Ried | C. Albanese | Yun-Ling Zheng | B. Haddad | R. Schlegel | D. Wangsa | Xuefeng Liu | M. Gillison | Hang Yuan | D. Symer | Aleksandra Dakić | Nancy Palechor-Ceron | D. Hartmann | Naidong Wang | Dan Zhou | E. Krawczyk | J. Blancato | Yukari Usuda | Faris A Alkhilaiwi | Siddartha Paul | Shuang Fang | S. Choudhary | Tung-Wei Hou
[1] A. Fersht,et al. Propagation of aggregated p53: Cross-reaction and coaggregation vs. seeding , 2015, Proceedings of the National Academy of Sciences.
[2] X. Fang,et al. Genome-wide profiling of HPV integration in cervical cancer identifies clustered genomic hot spots and a potential microhomology-mediated integration mechanism , 2015, Nature Genetics.
[3] E. Mardis,et al. AACR Cancer Progress Report 2014 , 2014, Clinical Cancer Research.
[4] Karen H. Vousden,et al. Mutant p53 in Cancer: New Functions and Therapeutic Opportunities , 2014, Cancer cell.
[5] Trevor J Pugh,et al. Landscape of genomic alterations in cervical carcinomas , 2013, Nature.
[6] T. Ried,et al. Genome-wide analysis of HPV integration in human cancers reveals recurrent, focal genomic instability , 2014, Genome research.
[7] A. Shad,et al. Use of reprogrammed cells to identify therapy for respiratory papillomatosis. , 2012, The New England journal of medicine.
[8] Lars Jansen,et al. Non-Random Integration of the HPV Genome in Cervical Cancer , 2012, PloS one.
[9] Chris Albanese,et al. ROCK inhibitor and feeder cells induce the conditional reprogramming of epithelial cells. , 2012, The American journal of pathology.
[10] P. Graves,et al. p53 mutants induce transcription of NF-κB2 in H1299 cells through CBP and STAT binding on the NF-κB2 promoter and gain of function activity. , 2012, Archives of biochemistry and biophysics.
[11] D. DiMaio,et al. Primary human cervical carcinoma cells require human papillomavirus E6 and E7 expression for ongoing proliferation. , 2012, Virology.
[12] P. Gehrig,et al. Neuroendocrine tumors of the gynecologic tract: A Society of Gynecologic Oncology (SGO) clinical document. , 2011, Gynecologic oncology.
[13] Cary A Moody,et al. Human papillomavirus oncoproteins: pathways to transformation , 2010, Nature Reviews Cancer.
[14] Magali Olivier,et al. TP53 mutations in human cancers: origins, consequences, and clinical use. , 2010, Cold Spring Harbor perspectives in biology.
[15] M. Olivier,et al. TP 53 Mutations in Human Cancers : Origins , Consequences , and Clinical Use , 2009 .
[16] Thomas Ried,et al. Spectral karyotyping analysis of human and mouse chromosomes , 2006, Nature Protocols.
[17] F. Radvanyi,et al. MYC activation associated with the integration of HPV DNA at the MYC locus in genital tumors , 2006, Oncogene.
[18] Kevin Gaston,et al. E2 Proteins from High- and Low-Risk Human Papillomavirus Types Differ in Their Ability To Bind p53 and Induce Apoptotic Cell Death , 2006, Journal of Virology.
[19] N. Yaegashi,et al. Small Cell Neuroendocrine Carcinomas of the Uterine Cervix: A Histological, Immunohistochemical, and Molecular Genetic Study , 2004, International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists.
[20] David I. Smith,et al. Preferential integration of human papillomavirus type 18 near the c-myc locus in cervical carcinoma , 2003, Oncogene.
[21] M. Hoeckel,et al. A comprehensive analysis of HPV integration loci in anogenital lesions combining transcript and genome-based amplification techniques , 2003, Oncogene.
[22] L. Clegg,et al. Endocrine tumors of the uterine cervix: incidence, demographics, and survival with comparison to squamous cell carcinoma. , 2003, Gynecologic oncology.
[23] Stella Pelengaris,et al. c-MYC: more than just a matter of life and death , 2002, Nature Reviews Cancer.
[24] J. Milner,et al. Selective silencing of viral gene expression in HPV-positive human cervical carcinoma cells treated with siRNA, a primer of RNA interference , 2002, Oncogene.
[25] D. DiMaio,et al. Repression of human papillomavirus oncogenes in HeLa cervical carcinoma cells causes the orderly reactivation of dormant tumor suppressor pathways. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[26] P. Howley,et al. Repression of the Integrated Papillomavirus E6/E7 Promoter Is Required for Growth Suppression of Cervical Cancer Cells , 2000, Journal of Virology.
[27] M. von Knebel Doeberitz,et al. Detection of high-risk cervical intraepithelial neoplasia and cervical cancer by amplification of transcripts derived from integrated papillomavirus oncogenes. , 1999, Cancer research.
[28] D. Ledbetter,et al. Multicolor Spectral Karyotyping of Human Chromosomes , 1996, Science.
[29] T. Iwasaka,et al. Correlation between HPV positivity and state of the p53 gene in cervical carcinoma cell lines. , 1993, Gynecologic oncology.
[30] H. Westphal,et al. Analysis of the p53 gene in human uterine carcinoma cell lines. , 1991, Cancer research.
[31] K. Münger,et al. The state of the p53 and retinoblastoma genes in human cervical carcinoma cell lines. , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[32] T. Crook,et al. p53 point mutation in HPV negative human cervical carcinoma cell lines. , 1991, Oncogene.
[33] Pamela Cushing,et al. Pathways to Transformation , 1998, Nature.