Integrative genomics analysis of chromosome 5p gain in cervical cancer reveals target over-expressed genes, including Drosha

[1]  Ralph J Deberardinis,et al.  Brick by brick: metabolism and tumor cell growth. , 2008, Current opinion in genetics & development.

[2]  Leonard D. Goldstein,et al.  Global microRNA profiles in cervical squamous cell carcinoma depend on Drosha expression levels , 2007, The Journal of pathology.

[3]  J. Rader,et al.  Profiling microdissected epithelium and stroma to model genomic signatures for cervical carcinogenesis accommodating for covariates. , 2007, Cancer research.

[4]  N. Coleman,et al.  Gain and overexpression of the oncostatin M receptor occur frequently in cervical squamous cell carcinoma and are associated with adverse clinical outcome , 2007, The Journal of pathology.

[5]  C. Croce,et al.  Oncogenic All1 fusion proteins target Drosha-mediated microRNA processing , 2007, Proceedings of the National Academy of Sciences.

[6]  K. Basso,et al.  Gene dosage alterations revealed by cDNA microarray analysis in cervical cancer: Identification of candidate amplified and overexpressed genes , 2007, Genes, chromosomes & cancer.

[7]  Ekaterina S Jordanova,et al.  Combined array-comparative genomic hybridization and single-nucleotide polymorphism-loss of heterozygosity analysis reveals complex genetic alterations in cervical cancer , 2007, BMC Genomics.

[8]  Y. Fujii,et al.  RNASEN Regulates Cell Proliferation and Affects Survival in Esophageal Cancer Patients , 2006, Clinical Cancer Research.

[9]  C J L M Meijer,et al.  Increased gene copy numbers at chromosome 20q are frequent in both squamous cell carcinomas and adenocarcinomas of the cervix , 2006, The Journal of pathology.

[10]  H. Horvitz,et al.  MicroRNA expression profiles classify human cancers , 2005, Nature.

[11]  R. Shiekhattar,et al.  The Microprocessor complex mediates the genesis of microRNAs , 2004, Nature.

[12]  Carlos L Arteaga,et al.  Tyrosine kinase inhibitors: why does the current process of clinical development not apply to them? , 2004, Cancer cell.

[13]  Cheng Li,et al.  dChipSNP: significance curve and clustering of SNP-array-based loss-of-heterozygosity data , 2004, Bioinform..

[14]  David I. Smith,et al.  Acquisition of High-Level Chromosomal Instability Is Associated with Integration of Human Papillomavirus Type 16 in Cervical Keratinocytes , 2004, Cancer Research.

[15]  P. Rao,et al.  Chromosomal amplifications, 3q gain and deletions of 2q33-q37 are the frequent genetic changes in cervical carcinoma , 2004, BMC Cancer.

[16]  M. Mansukhani,et al.  Frequent Promoter Methylation of CDH1, DAPK, RARB, and HIC1 Genes in Carcinoma of Cervix Uteri: Its Relationship to Clinical Outcome , 2003, Molecular Cancer.

[17]  M. Mansukhani,et al.  Mapping common deleted regions on 5p15 in cervical carcinoma and their occurrence in precancerous lesions , 2002, Molecular Cancer.

[18]  H. Hausen.  Papillomaviruses and cancer: from basic studies to clinical application , 2002, Nature Reviews Cancer.

[19]  H. zur Hausen.  Papillomaviruses and cancer: from basic studies to clinical application , 2002, Nature reviews. Cancer.

[20]  J. Mestan,et al.  Skp2 is oncogenic and overexpressed in human cancers , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[21]  C. Li,et al.  Model-based analysis of oligonucleotide arrays: expression index computation and outlier detection. , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[22]  G. Evans,et al.  Identification of a 6-cM minimal deletion at 11q23.1-23.2 and exclusion of PPP2R1B gene as a deletion target in cervical cancer. , 2000, Cancer research.

[23]  N. B. Atkin.  Significance of chromosome 5 and 17 changes in the development of carcinoma of the cervix uteri , 2000, Cytogenetic and Genome Research.

[24]  F. Mitelman,et al.  Recurrent chromosome aberrations in cancer. , 2000, Mutation research.

[25]  M. Schwab.  Oncogene amplification in solid tumors. , 1999, Seminars in cancer biology.

[26]  C. Lundsteen,et al.  Comparative genomic hybridization reveals a recurrent pattern of chromosomal aberrations in severe dysplasia/carcinoma in situ of the cervix and in advanced‐stage cervical carcinoma , 1999, Genes, chromosomes & cancer.

[27]  S. Davey,et al.  HRAD1 and MRAD1 encode mammalian homologues of the fission yeast rad1(+) cell cycle checkpoint control gene. , 1998, Nucleic acids research.

[28]  Z. Estrov,et al.  Oncostatin M-specific receptor expression and function in regulating cell proliferation of normal and malignant mammary epithelial cells. , 1998, Cytokine.

[29]  J. D. Benson,et al.  Two classes of human papillomavirus type 16 E1 mutants suggest pleiotropic conformational constraints affecting E1 multimerization, E2 interaction, and interaction with cellular proteins , 1997, Journal of virology.

[30]  E. Schröck,et al.  Advanced‐stage cervical carcinomas are defined by a recurrent pattern of chromosomal aberrations revealing high genetic instability and a consistent gain of chromosome arm 3q , 1997, Genes, chromosomes & cancer.

[31]  R. Chaganti,et al.  Genetic alterations at 5p15: a potential marker for progression of precancerous lesions of the uterine cervix. , 1995, Journal of the National Cancer Institute.

[32]  P. Rao,et al.  i(5p) and del(6q) are nonrandom abnormalities in carcinoma cervix uteri. Cytogenetics of two newly developed cell lines. , 1994, Cancer genetics and cytogenetics.

[33]  A. Ostör.  Natural history of cervical intraepithelial neoplasia: a critical review. , 1993, International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists.

[34]  L. Koutsky,et al.  Natural history and epidemiological features of genital HPV infection. , 1992, IARC scientific publications.

[35]  D. K. Das,et al.  Risk factors related to biological behaviour of precancerous lesions of the uterine cervix. , 1990, British Journal of Cancer.

[36]  L. G. Koss,et al.  Cervical Cancer , 1981, Current Topics in Pathology.