Expression of the transcription factor CTCF in invasive breast cancer: a candidate gene located at 16q22.1

[1]  I. Ellis,et al.  The Nottingham prognostic index in primary breast cancer , 2005, Breast Cancer Research and Treatment.

[2]  R. Renkawitz,et al.  Dynamic association of the mammalian insulator protein CTCF with centrosomes and the midbody. , 2004, Experimental cell research.

[3]  R. Penzel,et al.  CTCF Gene Mutations in Invasive Ductal Breast Cancer , 2003, Breast Cancer Research and Treatment.

[4]  S. Pinder,et al.  Loss of CD59 expression in breast tumours correlates with poor survival , 2003, The Journal of pathology.

[5]  M. Ladanyi,et al.  Loss of imprinting of IGF2 and H19 in osteosarcoma is accompanied by reciprocal methylation changes of a CTCF-binding site. , 2003, Human molecular genetics.

[6]  Victor V Lobanenkov,et al.  CTCF functions as a critical regulator of cell-cycle arrest and death after ligation of the B cell receptor on immature B cells , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[7]  Victor V Lobanenkov,et al.  The novel BORIS + CTCF gene family is uniquely involved in the epigenetics of normal biology and cancer. , 2002, Seminars in cancer biology.

[8]  B. Tycko,et al.  Chromosome arm 16q in Wilms tumors: Unbalanced chromosomal translocations, loss of heterozygosity, and assessment of the CTCF gene , 2002, Genes, chromosomes & cancer.

[9]  I. Ellis,et al.  Pathological prognostic factors in breast cancer. I. The value of histological grade in breast cancer: experience from a large study with long-term follow-up. , 2002, Histopathology.

[10]  A. Feinberg,et al.  Tumor-associated zinc finger mutations in the CTCF transcription factor selectively alter tts DNA-binding specificity. , 2002, Cancer research.

[11]  D. Takai,et al.  Large scale mapping of methylcytosines in CTCF-binding sites in the human H19 promoter and aberrant hypomethylation in human bladder cancer. , 2001, Human molecular genetics.

[12]  R Ohlsson,et al.  CTCF is a uniquely versatile transcription regulator linked to epigenetics and disease. , 2001, Trends in genetics : TIG.

[13]  P. Neiman,et al.  Cell growth inhibition by the multifunctional multivalent zinc-finger factor CTCF. , 2001, Cancer research.

[14]  A. Feinberg,et al.  Loss of imprinting of insulin-like growth factor-II in Wilms' tumor commonly involves altered methylation but not mutations of CTCF or its binding site. , 2001, Cancer research.

[15]  P. Neiman,et al.  Functional Phosphorylation Sites in the C-Terminal Region of the Multivalent Multifunctional Transcriptional Factor CTCF , 2001, Molecular and Cellular Biology.

[16]  C. Mathew,et al.  Loss of heterozygosity mapping at chromosome arm 16q in 712 breast tumors reveals factors that influence delineation of candidate regions. , 2001, Cancer research.

[17]  T. Rebbeck,et al.  Differential expression of E-cadherin in lobular and ductal neoplasms of the breast and its biologic and diagnostic implications. , 2001, American journal of clinical pathology.

[18]  P. Rocca-Serra,et al.  High-resolution integrated map encompassing the breast cancer loss of heterozygosity region on human chromosome 16q22.1. , 2000, Genomics.

[19]  D. Rimm,et al.  Validation of Tissue Microarray Technology in Breast Carcinoma , 2000, Laboratory Investigation.

[20]  Victor V Lobanenkov,et al.  Functional association of CTCF with the insulator upstream of the H19 gene is parent of origin-specific and methylation-sensitive , 2000, Current Biology.

[21]  G. Felsenfeld,et al.  Methylation of a CTCF-dependent boundary controls imprinted expression of the Igf2 gene , 2000, Nature.

[22]  I. Ellis,et al.  Pathological prognostic factors in breast cancer. , 1999, Critical reviews in oncology/hematology.

[23]  I. Ellis,et al.  The prognosis of small primary breast cancers. , 1999, European journal of cancer.

[24]  J. Kononen,et al.  Tissue microarrays for high-throughput molecular profiling of tumor specimens , 1998, Nature Medicine.

[25]  P. Neiman,et al.  A widely expressed transcription factor with multiple DNA sequence specificity, CTCF, is localized at chromosome segment 16q22.1 within one of the smallest regions of overlap for common deletions in breast and prostate cancers , 1998, Genes, chromosomes & cancer.

[26]  Heinz Höfler,et al.  Mutations of the human E‐cadherin (CDH1) gene , 1998, Human mutation.

[27]  A. Vostrov,et al.  The zinc finger protein CTCF binds to the APBbeta domain of the amyloid beta-protein precursor promoter. Evidence for a role in transcriptional activation. , 1997, The Journal of biological chemistry.

[28]  Victor V Lobanenkov,et al.  Negative protein 1, which is required for function of the chicken lysozyme gene silencer in conjunction with hormone receptors, is identical to the multivalent zinc finger repressor CTCF , 1997, Molecular and cellular biology.

[29]  P. Neiman,et al.  An exceptionally conserved transcriptional repressor, CTCF, employs different combinations of zinc fingers to bind diverged promoter sequences of avian and mammalian c-myc oncogenes , 1996, Molecular and cellular biology.

[30]  M. Vijver,et al.  E‐cadherin is a tumour/invasion suppressor gene mutated in human lobular breast cancers. , 1995, The EMBO journal.

[31]  R. Barkardottir,et al.  High frequency of allelic imbalance at chromosome region 16q22‐23 in human breast cancer: Correlation with high pgr and low s phase , 1995, International journal of cancer.

[32]  S. Hirohashi,et al.  Point Mutation of the E–Cadherin Gene in Invasive Lobular Carcinoma of the Breast , 1994, Japanese journal of cancer research : Gann.

[33]  Tony Hunter,et al.  The regulation of transcription by phosphorylation , 1992, Cell.

[34]  R. Blamey,et al.  Pathological prognostic factors in breast cancer. II. Histological type. Relationship with survival in a large study with long‐term follow‐up , 1992, Histopathology.

[35]  E B Cox,et al.  Estrogen receptor analyses. Correlation of biochemical and immunohistochemical methods using monoclonal antireceptor antibodies. , 1985, Archives of pathology & laboratory medicine.