All Stories

  1. Insights into the Pathogenesis of Anaplastic Large-Cell Lymphoma through Genome-wide DNA Methylation Profiling
  2. μ-Crystalline as hormone antagonist in prostate cancer
  3. Challenging perspectives on the cellular origins of lymphoma
  4. Abstract 671: Assessing the origins of anaplastic large cell lymphoma in murine models via forced lineage specificity of NPM-ALK expression in T cells
  5. Anaplastic large cell lymphoma in paediatric and young adult patients
  6. Anaplastic large cell lymphoma arises in thymocytes and requires transient TCR expression for thymic egress
  7. Anti-ALK Antibodies in Patients with ALK-Positive Malignancies Not Expressing NPM-ALK
  8. Excess of NPM-ALK oncogenic signaling promotes cellular apoptosis and drug dependency
  9. ID: 263
  10. Erratum: STAT3 regulated ARF expression suppresses prostate cancer metastasis
  11. Abstract 2920: Excess of cytoplasmic NPM-ALK driven oncogenic signaling is toxic and promotes cellular apoptosis and drug dependency
  12. STAT3 regulated ARF expression suppresses prostate cancer metastasis
  13. Oncogenic role of miR ‐155 in anaplastic large cell lymphoma lacking the t(2;5) translocation
  14. Twenty years of modelling NPM-ALK-induced lymphomagenesis
  15. Twenty years of modelling NPM-ALK-induced lymphomagenesis
  16. ALCL and breast implants
  17. Anaplastic large cell lymphoma-propagating cells are detectable by side population analysis and possess an expression profile reflective of a primitive origin
  18. Malignant Transformation of CD4+ T Lymphocytes Mediated by Oncogenic Kinase NPM/ALK Recapitulates IL-2-Induced Cell Signaling and Gene Expression Reprogramming
  19. PDGFR blockade is a rational and effective therapy for NPM-ALK–driven lymphomas
  20. Anaplastic large cell lymphoma: the current state of play from a European prospective as presented at the second annual meeting of the European Research Initiative on ALCL, 27–28 June 2011
  21. Assessment of the transforming potential of novel anaplastic lymphoma kinase point mutants
  22. Oncogenic tyrosine kinase NPM-ALK induces expression of the growth-promoting receptor ICOS
  23. Determining the contribution of NPM1 heterozygosity to NPM-ALK-induced lymphomagenesis
  24. The lymphoma-associated NPM-ALK oncogene elicits a p16INK4a/pRb-dependent tumor-suppressive pathway
  25. Aberrant Anaplastic Lymphoma Kinase Activity Induces a p53 and Rb-Dependent Senescence-Like Arrest in the Absence of Detectable p53 Stabilization
  26. Jailbreak: Oncogene-induced senescence and its evasion
  27. Identification of differential and functionally active miRNAs in both anaplastic lymphoma kinase (ALK) + and ALK − anaplastic large-cell lymphoma
  28. Genomic profiling of pediatric ALK-positive anaplastic large cell lymphoma: A Children's Cancer and Leukaemia Group Study
  29. NPM-ALK inhibits the p53 tumor suppressor pathway in an MDM2 and JNK-dependent manner
  30. NPM-ALK modulates the p53 tumour suppressor pathway in a JNK and PI 3-Kinase dependent manner: MDM-2 is a potential therapeutic target for the treatment of ALK-expressing malignancies
  31. The NPM-ALK tyrosine kinase mimics TCR signalling pathways, inducing NFAT and AP-1 by RAS-dependent mechanisms
  32. What have we learnt from mouse models of NPM-ALK-induced lymphomagenesis?
  33. Vav-promoter regulated oncogenic fusion protein NPM-ALK in transgenic mice causes B-cell lymphomas with hyperactive Jun kinase
  34. Signal Transduction Pathways Mediated by the Nucleophosmin-Anaplastic Lymphoma Kinase
  35. Assays to predict the genotoxicity of the chromosomal mutagen etoposide — focussing on the best assay
  36. The effects of dose, route of administration, drug scheduling and MDR-1 gene transfer on the genotoxicity of etoposide in bone marrow
  37. Genotoxicity studies on the azo dye Direct Red 2 using the in vivo mouse bone marrow micronucleus test