Prognostic impact of INK4A deletion in Ewing sarcoma
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G. Wei | M. Ladanyi | C. Antonescu | A. Huvos | E. de Álava | J. Healey | P. Meyers | D. Leung
[1] M. Ladanyi,et al. Prognostic impact of P53 status in Ewing sarcoma , 2000, Cancer.
[2] M. Ladanyi,et al. Alterations of cell cycle regulators in localized synovial sarcoma: A multifactorial study with prognostic implications. , 2000, The American journal of pathology.
[3] P. Sorensen,et al. EWS-FLI1 and EWS-ERG gene fusions are associated with similar clinical phenotypes in Ewing's sarcoma. , 1999, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[4] M. Ladanyi,et al. Differential transactivation by alternative EWS-FLI1 fusion proteins correlates with clinical heterogeneity in Ewing's sarcoma. , 1999, Cancer research.
[5] P. Ambros,et al. Prognostic impact of deletions at 1p36 and numerical aberrations in Ewing tumors , 1999, Genes, chromosomes & cancer.
[6] R. DePinho,et al. The INK4A/ARF locus and its two gene products. , 1999, Current opinion in genetics & development.
[7] F. Mertens,et al. Cytogenetic aberrations in Ewing sarcoma: are secondary changes associated with clinical outcome? , 1999, Medical and pediatric oncology.
[8] G. Wei,et al. CDK4 gene amplification in osteosarcoma: Reciprocal relationship with INK4A gene alterations and mapping of 12q13 amplicons , 1999, International journal of cancer.
[9] A. Huvos,et al. The Histological Response to Chemotherapy as a Predictor of the Oncological Outcome of Operative Treatment of Ewing Sarcoma* , 1998, The Journal of bone and joint surgery. American volume.
[10] W. Gerald,et al. EWS-FLI1 fusion transcript structure is an independent determinant of prognosis in Ewing's sarcoma. , 1998, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[11] Ken Chen,et al. The Ink4a Tumor Suppressor Gene Product, p19Arf, Interacts with MDM2 and Neutralizes MDM2's Inhibition of p53 , 1998, Cell.
[12] H. Kovar. Progress in the Molecular Biology of Ewing Tumors , 1998, Sarcoma.
[13] R. Perez-soler,et al. Adenovirus-mediated p16 transfer to glioma cells induces G1 arrest and protects from paclitaxel and topotecan: implications for therapy. , 1998, International journal of oncology.
[14] F. Sigaux,et al. Genomic alterations of the p19ARF encoding exons in T-cell acute lymphoblastic leukemia. , 1998, Blood.
[15] J. Fletcher,et al. Frequency and implications of chromosome 8 and 12 gains in Ewing sarcoma. , 1998, Cancer genetics and cytogenetics.
[16] F. Perler,et al. Protein Splicing of Inteins and Hedgehog Autoproteolysis: Structure, Function, and Evolution , 1998, Cell.
[17] R. Kratzke,et al. Adenovirus-mediated delivery of p16 to p16-deficient human bladder cancer cells confers chemoresistance to cisplatin and paclitaxel. , 1997, Clinical cancer research : an official journal of the American Association for Cancer Research.
[18] H. Kovar,et al. Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors , 1997, Oncogene.
[19] S. Ferrari,et al. Chemotherapy-induced tumor necrosis as a prognostic factor in localized Ewing's sarcoma of the extremities. , 1997, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[20] D. Quelle,et al. Cancer-associated mutations at the INK4a locus cancel cell cycle arrest by p16INK4a but not by the alternative reading frame protein p19ARF. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[21] K. Siebenrock,et al. Comparison of soft tissue Ewing's sarcoma and peripheral neuroectodermal tumor. , 1996, Clinical orthopaedics and related research.
[22] A. Llombart‐Bosch,et al. Small round blue cell tumors in bone: prognostic factors correlated to Ewing's sarcoma and neuroectodermal tumors. , 1996, Seminars in diagnostic pathology.
[23] O. Delattre,et al. Does expression of different EWS chimeric transcripts define clinically distinct risk groups of Ewing tumor patients? , 1996, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[24] H. Koeffler,et al. Alterations of the p15, p16,and p18 genes in osteosarcoma. , 1996, Cancer genetics and cytogenetics.
[25] W. Gerald,et al. Very-high-dose short-term chemotherapy for poor-risk peripheral primitive neuroectodermal tumors, including Ewing's sarcoma, in children and young adults. , 1995, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[26] E. Hovig,et al. Homozygous deletion frequency and expression levels of the CDKN2 gene in human sarcomas--relationship to amplification and mRNA levels of CDK4 and CCND1. , 1995, British Journal of Cancer.
[27] W. Gerald,et al. MDM2 and CDK4 gene amplification in Ewing's sarcoma , 1995, The Journal of pathology.
[28] J. Pelletier,et al. Clonal expansion and attenuated apoptosis in Wilms' tumors are associated with p53 gene mutations. , 1995, Cancer research.
[29] C. Larsson,et al. The human NOTCH1, 2, and 3 genes are located at chromosome positions 9q34, 1p13-p11, and 19p13.2-p13.1 in regions of neoplasia-associated translocation. , 1994, Genomics.
[30] T. Triche,et al. The Ewing family of tumors--a subgroup of small-round-cell tumors defined by specific chimeric transcripts. , 1994, The New England journal of medicine.
[31] N. Nowak,et al. Anaplastic Wilms' tumour, a subtype displaying poor prognosis, harbours p53 gene mutations , 1994, Nature Genetics.
[32] G. Thomas,et al. p53 mutations in human tumors with chimeric EWS/FLI/1 genes , 1994, International journal of cancer.
[33] M. Skolnick,et al. A cell cycle regulator potentially involved in genesis of many tumor types. , 1994, Science.
[34] P. Sorensen,et al. A second Ewing's sarcoma translocation, t(21;22), fuses the EWS gene to another ETS–family transcription factor, ERG , 1994, Nature Genetics.
[35] G. Hannon,et al. A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4 , 1993, Nature.
[36] R. Hanada,et al. Mutations of the p53 gene are involved in Ewing's sarcomas but not in neuroblastomas. , 1993, Cancer research.
[37] H. Kovar,et al. Narrow spectrum of infrequent p53 mutations and absence of MDM2 amplification in Ewing tumours. , 1993, Oncogene.
[38] A. Aurias,et al. Chromosomes in Ewing's sarcoma. II. Nonrandom additional changes, trisomy 8 and der(16)t(1;16). , 1988, Cancer genetics and cytogenetics.
[39] P. Pynsent,et al. Overexpression of p53 protein in primary Ewing’s sarcoma of bone: relationship to tumour stage, response and prognosis , 1999, British Journal of Cancer.
[40] O. Myklebost,et al. Recurrent gains of 1q, 8 and 12 in the Ewing family of tumours by comparative genomic hybridization. , 1997, British Journal of Cancer.
[41] D. Louis,et al. CDKN2/p16 or RB alterations occur in the majority of glioblastomas and are inversely correlated. , 1996, Cancer research.
[42] T. Triche,et al. Is neuro-ectodermal differentiation of Ewing's sarcoma of bone associated with an unfavourable prognosis? , 1995, European journal of cancer.