The relationship of TP53 R72P polymorphism to disease outcome and TP53 mutation in myelodysplastic syndromes

[1]  Larry J. Smith,et al.  TP53 suppression promotes erythropoiesis in del(5q) MDS, suggesting a targeted therapeutic strategy in lenalidomide-resistant patients , 2013, Proceedings of the National Academy of Sciences.

[2]  L. Arenillas,et al.  Response to lenalidomide in myelodysplastic syndromes with del(5q): influence of cytogenetics and mutations , 2013, British journal of haematology.

[3]  A. Kohlmann,et al.  Robustness of amplicon deep sequencing underlines its utility in clinical applications. , 2013, The Journal of molecular diagnostics : JMD.

[4]  C. Preudhomme,et al.  P-023 Incidence and prognostic value of TP53 mutations in IPSS low and INT 1 (lower risk) MDS with del 5q , 2013 .

[5]  G. Mufti,et al.  TP53 mutations in myelodysplastic syndrome are strongly correlated with aberrations of chromosome 5, and correlate with adverse prognosis , 2013, British journal of haematology.

[6]  J. Clark,et al.  Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion , 2013, Oncogene.

[7]  A. Jankowska,et al.  Topography, clinical, and genomic correlates of 5q myeloid malignancies revisited. , 2012, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[8]  M. F. Andreoli-Risso,et al.  Lack of association between MDM2 SNP309 and TP53 Arg72Pro polymorphisms with clinical outcomes in myelodysplastic syndrome. , 2012, Neoplasma.

[9]  A. List,et al.  Role of lenalidomide in the treatment of myelodysplastic syndromes. , 2011, Seminars in oncology.

[10]  C. Owen,et al.  Familial myelodysplastic syndromes: a review of the literature , 2011, Haematologica.

[11]  Eva Hellström-Lindberg,et al.  TP53 mutations in low-risk myelodysplastic syndromes with del(5q) predict disease progression. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[12]  R. Siebert,et al.  TP53 codon 72 polymorphism in patients with chronic lymphocytic leukaemia: identification of a subgroup with mutated IGHV genes and poor clinical outcome , 2011, British journal of haematology.

[13]  J. Kutok,et al.  Haploinsufficiency for ribosomal protein genes causes selective activation of p53 in human erythroid progenitor cells. , 2011, Blood.

[14]  Yan Zhou,et al.  The Codon 72 Polymorphism of p53 Regulates Interaction with NF-κB and Transactivation of Genes Involved in Immunity and Inflammation , 2011, Molecular and Cellular Biology.

[15]  W. Lam,et al.  Genome-wide identification of human microRNAs located in leukemia-associated genomic alterations. , 2009, Blood.

[16]  C. Deisenroth,et al.  Ribosome biogenesis surveillance: probing the ribosomal protein-Mdm2-p53 pathway , 2010, Oncogene.

[17]  M. McArthur,et al.  Mouse models for the p53 R72P polymorphism mimic human phenotypes. , 2010, Cancer research.

[18]  A. Fersht,et al.  The tumor suppressor p53: from structures to drug discovery. , 2010, Cold Spring Harbor perspectives in biology.

[19]  J. Gotlib.  Ribosomes and Bone Marrow Failure Syndromes: Convergence With p53 , 2010 .

[20]  A. Warren,et al.  A p53-dependent mechanism underlies macrocytic anemia in a mouse model of human 5q− syndrome , 2009, Nature Medicine.

[21]  N. Cross,et al.  Gain of 1q21 Does Not Predict for Immediate Progression in MGUS. , 2009 .

[22]  Sheng Wei,et al.  Secondary Resistance to Lenalidomide in Del(5q) MDS Is Associated with CDC25C & PP2A Overexpression. , 2009 .

[23]  J. Byrd,et al.  A critical role for phosphatase haplodeficiency in the selective suppression of deletion 5q MDS by lenalidomide , 2009, Proceedings of the National Academy of Sciences.

[24]  T. Golub,et al.  Identification of RPS14 as a 5q- syndrome gene by RNA interference screen , 2007, Nature.

[25]  J. Fitzgibbon,et al.  Familial myelodysplasia and acute myeloid leukaemia – a review , 2007, British journal of haematology.

[26]  B. Ko,et al.  RUNX1 gene mutation in primary myelodysplastic syndrome – the mutation can be detected early at diagnosis or acquired during disease progression and is associated with poor outcome , 2007, British journal of haematology.

[27]  Thierry Soussi,et al.  Shaping genetic alterations in human cancer: the p53 mutation paradigm. , 2007, Cancer cell.

[28]  Xin Lu,et al.  The prolyl isomerase Pin1 orchestrates p53 acetylation and dissociation from the apoptosis inhibitor iASPP , 2007, Nature Structural &Molecular Biology.

[29]  G. Riegler,et al.  p53 codon 72 polymorphism in patients affected with ulcerative colitis , 2007, Journal of Gastroenterology.

[30]  G. Wahl,et al.  Mouse Mutants Reveal that Putative Protein Interaction Sites in the p53 Proline-Rich Domain Are Dispensable for Tumor Suppression , 2006, Molecular and Cellular Biology.

[31]  P. Greenberg,et al.  Lenalidomide in the myelodysplastic syndrome with chromosome 5q deletion. , 2006, The New England journal of medicine.

[32]  M. Zvelebil,et al.  iASPP preferentially binds p53 proline-rich region and modulates apoptotic function of codon 72–polymorphic p53 , 2006, Nature Genetics.

[33]  K. Soo,et al.  Evidence for Selective Expression of the p53 Codon 72 Polymorphs: Implications in Cancer Development , 2005, Cancer Epidemiology Biomarkers & Prevention.

[34]  L. Rimsza,et al.  Efficacy of lenalidomide in myelodysplastic syndromes. , 2005, The New England journal of medicine.

[35]  Zigang Dong,et al.  Post-translational modification of p53 in tumorigenesis , 2004, Nature Reviews Cancer.

[36]  T. Crook,et al.  Polymorphism in wild-type p53 modulates response to chemotherapy in vitro and in vivo , 2004, Oncogene.

[37]  D. Pim,et al.  p53 polymorphic variants at codon 72 exert different effects on cell cycle progression , 2004, International journal of cancer.

[38]  M. Cazzola,et al.  TP53 codon 72 polymorphism in patients with chronic myeloid leukemia. , 2004, Haematologica.

[39]  M. Murphy,et al.  The codon 72 polymorphic variants of p53 have markedly different apoptotic potential , 2003, Nature Genetics.

[40]  T. Naoe,et al.  Poor clinical significance of p53 gene polymorphism in acute myeloid leukemia. , 2000, Leukemia research.

[41]  A. Contente,et al.  Tumor-derived mutations within the DNA-binding domain of p53 that phenotypically resemble the deletion of the proline-rich domain , 2000, Oncogene.

[42]  Miranda Thomas,et al.  Two Polymorphic Variants of Wild-Type p53 Differ Biochemically and Biologically , 1999, Molecular and Cellular Biology.

[43]  G. Prendergast,et al.  The polyproline region of p53 is required to activate apoptosis but not growth arrest , 1997, Oncogene.

[44]  A. Levine,et al.  Identification of a novel p53 functional domain that is necessary for efficient growth suppression. , 1996, Proceedings of the National Academy of Sciences of the United States of America.