Differentiation therapy in poor risk myeloid malignancies: Results of companion phase II studies.

[1]  Liangfeng Han,et al.  Combined Treatment with Epigenetic, Differentiating, and Chemotherapeutic Agents Cooperatively Targets Tumor-Initiating Cells in Triple-Negative Breast Cancer. , 2016, Cancer research.

[2]  A. DeZern.  Nine years without a new FDA-approved therapy for MDS: how can we break through the impasse? , 2015, Hematology. American Society of Hematology. Education Program.

[3]  R. Hills,et al.  Arsenic trioxide and all-trans retinoic acid treatment for acute promyelocytic leukaemia in all risk groups (AML17): results of a randomised, controlled, phase 3 trial. , 2015, The Lancet. Oncology.

[4]  L. Campbell,et al.  Use of arsenic trioxide in remission induction and consolidation therapy for acute promyelocytic leukaemia in the Australasian Leukaemia and Lymphoma Group (ALLG) APML4 study: a non-randomised phase 2 trial. , 2015, The Lancet. Haematology.

[5]  Jace W. Jones,et al.  All-Trans Retinoic Acid Activity in Acute Myeloid Leukemia: Role of Cytochrome P450 Enzyme Expression by the Microenvironment , 2015, PloS one.

[6]  M. Lübbert,et al.  Epigenetic priming of non-small cell lung cancer cell lines to the antiproliferative and differentiating effects of all-trans retinoic acid , 2015, Journal of Cancer Research and Clinical Oncology.

[7]  P. Greenberg,et al.  Correlation of overall survival (OS) with bone marrow blast (BMBL) response in patients (pts) with myelodysplastic syndrome. , 2015 .

[8]  Jace W. Jones,et al.  Human bone marrow niche chemoprotection mediated by cytochrome p450 enzymes , 2015, Oncotarget.

[9]  T. Haferlach,et al.  Biomodulatory therapy induces complete molecular remission in chemorefractory acute myeloid leukemia , 2015, Haematologica.

[10]  J. Cen,et al.  Retinoic Acid Receptor-β Gene Reexpression and Biological Activity in SHI-1 Cells after Combined Treatment with 5-Aza-2′-Deoxycytidine and All-Trans Retinoic Acid , 2014, Acta Haematologica.

[11]  M. Zahurak,et al.  Granulocyte-macrophage colony stimulating factor (GM-CSF) enhances the clinical responses to interferon-α (IFN) in newly diagnosed chronic myeloid leukemia (CML). , 2014, Leukemia research.

[12]  J. Cen,et al.  All-trans retinoic acid enhances the effect of 5-aza-2′-deoxycytidine on p16INK4a demethylation, and the two drugs synergistically activate retinoic acid receptor β gene expression in the human erythroleukemia K562 cell line , 2014, Oncology letters.

[13]  Paola Fazi,et al.  Retinoic acid and arsenic trioxide for acute promyelocytic leukemia. , 2013, The New England journal of medicine.

[14]  S. Sukumar,et al.  Molecular Pathways: Current Role and Future Directions of the Retinoic Acid Pathway in Cancer Prevention and Treatment , 2013, Clinical Cancer Research.

[15]  J. Reynolds,et al.  All-trans-retinoic acid, idarubicin, and IV arsenic trioxide as initial therapy in acute promyelocytic leukemia (APML4). , 2012, Blood.

[16]  I. Gojo,et al.  New treatment approaches in acute myeloid leukemia: review of recent clinical studies. , 2012, Reviews on recent clinical trials.

[17]  M. Borowitz,et al.  A clinically relevant population of leukemic CD34(+)CD38(-) cells in acute myeloid leukemia. , 2012, Blood.

[18]  H. Wakelee,et al.  The effect of bexarotene on atorvastatin pharmacokinetics: results from a phase I trial of bexarotene plus chemotherapy in patients with advanced non-small cell lung cancer , 2012, Cancer Chemotherapy and Pharmacology.

[19]  Zhe Zhang,et al.  Differentiation therapy in poor risk myeloid malignancies: Results of a dose finding study of the combination bryostatin-1 and GM-CSF. , 2011, Leukemia research.

[20]  R. Roesler,et al.  Histone deacetylase inhibitors: a new perspective for the treatment of leukemia. , 2010, Leukemia research.

[21]  R. Arceci,et al.  Single cycle of arsenic trioxide-based consolidation chemotherapy spares anthracycline exposure in the primary management of acute promyelocytic leukemia. , 2010, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[22]  M. Carroll,et al.  A Phase I Study of Bexarotene, a Retinoic X Receptor Agonist, in Non-M3 Acute Myeloid Leukemia , 2008, Clinical Cancer Research.

[23]  P. Purushottamachar,et al.  Improved synthesis of histone deacetylase inhibitors (HDIs) (MS-275 and CI-994) and inhibitory effects of HDIs alone or in combination with RAMBAs or retinoids on growth of human LNCaP prostate cancer cells and tumor xenografts. , 2008, Bioorganic & medicinal chemistry.

[24]  E. Sausville,et al.  Phase 1 and pharmacologic study of MS-275, a histone deacetylase inhibitor, in adults with refractory and relapsed acute leukemias. , 2007, Blood.

[25]  R. Hills,et al.  A comparison of low‐dose cytarabine and hydroxyurea with or without all‐trans retinoic acid for acute myeloid leukemia and high‐risk myelodysplastic syndrome in patients not considered fit for intensive treatment , 2007, Cancer.

[26]  B. Cheson,et al.  Clinical application and proposal for modification of the International Working Group (IWG) response criteria in myelodysplasia. , 2006, Blood.

[27]  A. Burnett,et al.  Fludarabine and cytosine are less effective than standard ADE chemotherapy in high-risk acute myeloid leukemia, and addition of G-CSF and ATRA are not beneficial: results of the MRC AML-HR randomized trial. , 2006, Blood.

[28]  C. Huff,et al.  Effects of imatinib and interferon on primitive chronic myeloid leukaemia progenitors , 2005, British journal of haematology.

[29]  M. Osanai,et al.  Expression of the Retinoic Acid-Metabolizing Enzyme CYP26A1 Limits Programmed Cell Death , 2005, Molecular Pharmacology.

[30]  C. Huff,et al.  Requirement for myeloid growth factors in the differentiation of acute promyelocytic leukaemia , 2005, British journal of haematology.

[31]  S. Fröhling,et al.  Phase III study of all-trans retinoic acid in previously untreated patients 61 years or older with acute myeloid leukemia , 2004, Leukemia.

[32]  G. Bartolini,et al.  Retinoids and cancer: antitumor effect of ATRA and of a new derivative of retinoic acid, IIF, on colon carcinoma cell lines CaCo-2 and HT-29. , 2004, Anticancer research.

[33]  C. Bloomfield,et al.  Revised recommendations of the International Working Group for Diagnosis, Standardization of Response Criteria, Treatment Outcomes, and Reporting Standards for Therapeutic Trials in Acute Myeloid Leukemia. , 2003, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[34]  C. Huff,et al.  Anti‐tumour activity of interferon‐alpha in multiple myeloma: role of interleukin 6 and tumor cell differentiation , 2003, British journal of haematology.

[35]  Daniel G. Tenen,et al.  Disruption of differentiation in human cancer: AML shows the way , 2003, Nature Reviews Cancer.

[36]  Richard J. Jones,et al.  The role of growth factors in the activity of pharmacological differentiation agents. , 2002, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

[37]  P F Thall,et al.  Randomized phase II study of fludarabine + cytosine arabinoside + idarubicin +/- all-trans retinoic acid +/- granulocyte colony-stimulating factor in poor prognosis newly diagnosed acute myeloid leukemia and myelodysplastic syndrome. , 1999, Blood.

[38]  C. Eaves,et al.  Selective expansion of primitive normal hematopoietic cells in cytokine-supplemented cultures of purified cells from patients with chronic myeloid leukemia. , 1997, Blood.

[39]  M. Pfahl,et al.  Effects of novel retinoid X receptor-selective ligands on myeloid leukemia differentiation and proliferation in vitro. , 1996, Blood.

[40]  S. Grant,et al.  Effect of the protein kinase C activating agent bryostatin 1 on the clonogenic response of leukemic blast progenitors to recombinant granulocyte-macrophage colony-stimulating factor. , 1991, Leukemia.

[41]  R. Simon,et al.  Optimal two-stage designs for phase II clinical trials. , 1989, Controlled clinical trials.

[42]  R. Arceci.  The impact on outcome of the addition of all-trans retinoic acid to intensive chemotherapy in younger patients with nonacute promyelocytic acute myeloid leukemia: overall results and results in genotypic subgroups defined by mutations in NPM1, FLT3, and CEBPA , 2010 .