Frank Traganos

Summary

Affiliation: New York Medical College
Country: USA

Publications

  1. ncbi request reprint Cycling without cyclins
    Frank Traganos
    Brander Cancer Research Institute, New York Medical College, Hawthorne, New York, USA
    Cell Cycle 3:32-4. 2004
  2. ncbi request reprint Activation of ATM and histone H2AX phosphorylation induced by mitoxantrone but not by topotecan is prevented by the antioxidant N-acetyl-L-cysteine
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cancer Biol Ther 5:959-64. 2006
  3. ncbi request reprint Sequential phosphorylation of Ser-10 on histone H3 and ser-139 on histone H2AX and ATM activation during premature chromosome condensation: relationship to cell-cycle phase and apoptosis
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10532, USA
    Cytometry A 69:222-9. 2006
  4. ncbi request reprint Assessment of ATM phosphorylation on Ser-1981 induced by DNA topoisomerase I and II inhibitors in relation to Ser-139-histone H2AX phosphorylation, cell cycle phase, and apoptosis
    Akira Kurose
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10532, USA
    Cytometry A 68:1-9. 2005
  5. ncbi request reprint Effects of hydroxyurea and aphidicolin on phosphorylation of ataxia telangiectasia mutated on Ser 1981 and histone H2AX on Ser 139 in relation to cell cycle phase and induction of apoptosis
    Akira Kurose
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA
    Cytometry A 69:212-21. 2006
  6. pmc ATM activation accompanies histone H2AX phosphorylation in A549 cells upon exposure to tobacco smoke
    Toshiki Tanaka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    BMC Cell Biol 8:26. 2007
  7. pmc Phosphorylation of p53 on Ser15 during cell cycle caused by Topo I and Topo II inhibitors in relation to ATM and Chk2 activation
    Hong Zhao
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 7:3048-55. 2008
  8. pmc DNA damage response induced by exposure of human lung adenocarcinoma cells to smoke from tobacco- and nicotine-free cigarettes
    Ellen D Jorgensen
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY, USA
    Cell Cycle 9:2170-6. 2010
  9. ncbi request reprint Induction of ATM activation, histone H2AX phosphorylation and apoptosis by etoposide: relation to cell cycle phase
    Toshiki Tanaka
    Brander Cancer Research Institute, Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 6:371-6. 2007
  10. pmc Kinetics of the UV-induced DNA damage response in relation to cell cycle phase. Correlation with DNA replication
    Hong Zhao
    Department of Pathology, Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 77:285-93. 2010

Collaborators

Detail Information

Publications64

  1. ncbi request reprint Cycling without cyclins
    Frank Traganos
    Brander Cancer Research Institute, New York Medical College, Hawthorne, New York, USA
    Cell Cycle 3:32-4. 2004
    ..That, in turn, would imply a fair amount redundancy exists in the system which may call into question current cancer treatment strategies designed to target some of these "dispensable" cell cycle control molecules...
  2. ncbi request reprint Activation of ATM and histone H2AX phosphorylation induced by mitoxantrone but not by topotecan is prevented by the antioxidant N-acetyl-L-cysteine
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cancer Biol Ther 5:959-64. 2006
    ....
  3. ncbi request reprint Sequential phosphorylation of Ser-10 on histone H3 and ser-139 on histone H2AX and ATM activation during premature chromosome condensation: relationship to cell-cycle phase and apoptosis
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10532, USA
    Cytometry A 69:222-9. 2006
    ....
  4. ncbi request reprint Assessment of ATM phosphorylation on Ser-1981 induced by DNA topoisomerase I and II inhibitors in relation to Ser-139-histone H2AX phosphorylation, cell cycle phase, and apoptosis
    Akira Kurose
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10532, USA
    Cytometry A 68:1-9. 2005
    ....
  5. ncbi request reprint Effects of hydroxyurea and aphidicolin on phosphorylation of ataxia telangiectasia mutated on Ser 1981 and histone H2AX on Ser 139 in relation to cell cycle phase and induction of apoptosis
    Akira Kurose
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA
    Cytometry A 69:212-21. 2006
    ..The present study was undertaken to reveal whether H2AX is phosphorylated in cells exposed to HU or APH and whether its phosphorylation is mediated by ATM...
  6. pmc ATM activation accompanies histone H2AX phosphorylation in A549 cells upon exposure to tobacco smoke
    Toshiki Tanaka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    BMC Cell Biol 8:26. 2007
    ..We have recently reported that brief exposure of human pulmonary adenocarcinoma A549 cells or normal human bronchial epithelial cells (NHBE) to cigarette smoke (CS) induced phosphorylation of H2AX...
  7. pmc Phosphorylation of p53 on Ser15 during cell cycle caused by Topo I and Topo II inhibitors in relation to ATM and Chk2 activation
    Hong Zhao
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 7:3048-55. 2008
    ..The respective kinetics of p53-Ser15 phosphorylation versus ATM and Chk2 activation suggest that in response to DNA damage by TPT or MXT, Chk2 rather than ATM mediates p53 phosphorylation...
  8. pmc DNA damage response induced by exposure of human lung adenocarcinoma cells to smoke from tobacco- and nicotine-free cigarettes
    Ellen D Jorgensen
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY, USA
    Cell Cycle 9:2170-6. 2010
    ..Since DSBs are potentially carcinogenic our data indicate that smoking tobacco and nicotine-free cigarettes is at least as hazardous as smoking cigarettes containing tobacco and nicotine...
  9. ncbi request reprint Induction of ATM activation, histone H2AX phosphorylation and apoptosis by etoposide: relation to cell cycle phase
    Toshiki Tanaka
    Brander Cancer Research Institute, Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 6:371-6. 2007
    ..mitoxantrone, may contribute to formation of DSBs and to triggering of apoptosis...
  10. pmc Kinetics of the UV-induced DNA damage response in relation to cell cycle phase. Correlation with DNA replication
    Hong Zhao
    Department of Pathology, Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 77:285-93. 2010
    ....
  11. pmc Analysis of individual molecular events of DNA damage response by flow- and image-assisted cytometry
    Zbigniew Darzynkiewicz
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY, USA
    Methods Cell Biol 103:115-47. 2011
    ..The new microfluidic Lab-on-a-Chip platforms for interrogation of individual cells offer a novel approach for DDR cytometric analysis...
  12. pmc Cytometric assessment of DNA damage by exogenous and endogenous oxidants reports aging-related processes
    Hong Zhao
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 71:905-14. 2007
    ..Cytometric analysis of CHP and CAA provides the means to measure the effectiveness of exogenous factors, which either through lowering aerobic metabolism or neutralizing radicals may protect DNA from such damage...
  13. pmc Oxidative stress induces cell cycle-dependent Mre11 recruitment, ATM and Chk2 activation and histone H2AX phosphorylation
    Hong Zhao
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 7:1490-5. 2008
    ..g., maximal pixel) offers unique advantage in studies of the response of different cell constituents in relation to cell cycle position...
  14. pmc New biomarkers probing depth of cell senescence assessed by laser scanning cytometry
    Hong Zhao
    Department of Pathology, Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 77:999-1007. 2010
    ....
  15. ncbi request reprint 2-deoxy-D-glucose reduces the level of constitutive activation of ATM and phosphorylation of histone H2AX
    Toshiki Tanaka
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10532, USA
    Cell Cycle 5:878-82. 2006
    ..Therefore, the assay of CHP by multiparameter cytometry provides the means to measure effects of antioxidants and metabolic inhibitors on endogenous oxidative DNA damage in relation to cell cycle phase...
  16. pmc Cell fixation in zinc salt solution is compatible with DNA damage response detection by phospho-specific antibodies
    Hong Zhao
    Department of Pathology, Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 79:470-6. 2011
    ..Analysis of cells by flow cytometry revealed that ZBF fixation of lymphoblastoid TK6 cells led to about 60 and 33% higher intensity of the side and forward light scatter, respectively, compared to formaldehyde fixed cells...
  17. pmc Cytometry of ATM activation and histone H2AX phosphorylation to estimate extent of DNA damage induced by exogenous agents
    Toshiki Tanaka
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 71:648-61. 2007
    ....
  18. pmc Induction of DNA damage signaling by oxidative stress in relation to DNA replication as detected using "click chemistry"
    Hong Zhao
    Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    Cytometry A 79:897-902. 2011
    ....
  19. pmc Induction of DNA damage response by the supravital probes of nucleic acids
    Hong Zhao
    Department of Pathology, Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 75:510-9. 2009
    ..The data indicate that supravital use of Ho 42, DRAQ5, and DCV induces various degrees of DDR, including activation of ATM, Chk2 and p53, which may have significant consequences on regulatory cell cycle pathways and apoptosis...
  20. ncbi request reprint Constitutive histone H2AX phosphorylation on Ser-139 in cells untreated by genotoxic agents is cell-cycle phase specific and attenuated by scavenging reactive oxygen species
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, NY 10595, USA
    Int J Oncol 29:495-501. 2006
    ....
  21. ncbi request reprint Nitrogen oxide-releasing aspirin induces histone H2AX phosphorylation, ATM activation and apoptosis preferentially in S-phase cells: involvement of reactive oxygen species
    Toshiki Tanaka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York, USA
    Cell Cycle 5:1669-74. 2006
    ..Because neither induction of H2AX phosphorylation nor apoptosis were observed at equimolar concentrations of ASA, the NO moiety attached to ASA appeared to mediate these effects...
  22. ncbi request reprint Phosphorylation of histone H2AX on Ser 139 and activation of ATM during oxidative burst in phorbol ester-treated human leukocytes
    Toshiki Tanaka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 5:2671-5. 2006
    ..The observed H2AX phosphorylation in lymphocytes may reflect their DNA damage by the superoxide ions propagating from the neighboring granulocytes and/or monocytes...
  23. ncbi request reprint Assessment of histone H2AX phosphorylation induced by DNA topoisomerase I and II inhibitors topotecan and mitoxantrone and by the DNA cross-linking agent cisplatin
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10532, USA
    Cytometry A 58:99-110. 2004
    ..The purpose of this study was to further characterize the drug-induced (DI) IF of gammaH2AX, and in particular to distinguish it from AA gammaH2AX IF triggered by DNA breaks that occur in the course of AA DNA fragmentation...
  24. pmc DNA damage response induced by tobacco smoke in normal human bronchial epithelial and A549 pulmonary adenocarcinoma cells assessed by laser scanning cytometry
    Hong Zhao
    New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 75:840-7. 2009
    ..The cytometric assessment of CS-induced DDR provides a means to estimate the genotoxicity of CS and to explore the mechanisms of the response as a function of cell cycle phase and cell type...
  25. pmc Constitutive histone H2AX phosphorylation and ATM activation, the reporters of DNA damage by endogenous oxidants
    Toshiki Tanaka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 5:1940-5. 2006
    ....
  26. pmc Assessment of DNA double-strand breaks and gammaH2AX induced by the topoisomerase II poisons etoposide and mitoxantrone
    Daniel J Smart
    Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    Mutat Res 641:43-7. 2008
    ..ETOP data are consistent with the threshold concept for TOPO II poison-induced genotoxicity and this should be considered in the safety assessment of chemicals displaying an affinity for TOPO II and genotoxic/clastogenic effects...
  27. pmc DNA damage response as a biomarker in treatment of leukemias
    H Dorota Halicka
    Brander Cancer Research Institute, Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    Cell Cycle 8:1720-4. 2009
    ..The present findings, however, demonstrate the feasibility of assessment of DDR during the treatment of leukemias with drugs targeting DNA...
  28. ncbi request reprint Phosphorylation of RIalpha by cyclin-dependent kinase CDK 2/cyclin E modulates the dissociation of the RIalpha-RFC40 complex
    Rakhee S Gupte
    Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 5:653-60. 2006
    ..Taken together, these findings suggest that CDK2/Cyclin E may function as downstream modulator that regulates the dissociation of the RIalpha-RFC40 complex and subsequently the association of the RFC40-RFC37 complex...
  29. pmc Cytometric detection of chromatin relaxation, an early reporter of DNA damage response
    H Dorota Halicka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    Cell Cycle 8:2233-7. 2009
    ..The method offers a rapid and simple means of detecting genotoxic insult on cells...
  30. pmc Down-regulation of androgen-receptor and PSA by phytochemicals
    Sophie Chen
    Department of Medicine, New York Medical College, Valhalla, NY 10595, USA
    Int J Oncol 32:405-11. 2008
    ..In each case, these compounds have independent activities which may partly contribute to the biological activity of PC-SPES...
  31. doi request reprint Kinetics of histone H2AX phosphorylation and Chk2 activation in A549 cells treated with topotecan and mitoxantrone in relation to the cell cycle phase
    Hong Zhao
    Brander Cancer Research Institute, Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 73:480-9. 2008
    ....
  32. ncbi request reprint Histone H2AX phosphorylation after cell irradiation with UV-B: relationship to cell cycle phase and induction of apoptosis
    H Dorota Halicka
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA
    Cell Cycle 4:339-45. 2005
    ..Induction of gammaH2AX in G(1), G(2) and M is likely a response to the primary DSBs generated during UV exposure and/or DNA repair. It is unclear why the latter process was more pronounced in HeLa than in HL-60 cells...
  33. pmc Relationship of DNA damage signaling to DNA replication following treatment with DNA topoisomerase inhibitors camptothecin/topotecan, mitoxantrone, or etoposide
    Hong Zhao
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 81:45-51. 2012
    ..The confocal analysis of the association between DNA replication sites and the sites of DSBs (γH2AX foci) opens a new approach for mechanistic studies of the involvement of DNA replication in induction of DNA damage...
  34. pmc Attenuation of constitutive DNA damage signaling by 1,25-dihydroxyvitamin D3
    H Dorota Halicka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    Aging (Albany NY) 4:270-8. 2012
    ....
  35. ncbi request reprint Cyclic AMP regulates the expression and nuclear translocation of RFC40 in MCF7 cells
    Rakhee S Gupte
    Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA
    Exp Cell Res 312:796-806. 2006
    ..3%, substantiating the decrease in DNA replication rate. Taken together, these findings suggest that cAMP functions as an upstream modulator that regulates the expression and nuclear translocation of RFC40...
  36. pmc Genome protective effect of metformin as revealed by reduced level of constitutive DNA damage signaling
    H Dorota Halicka
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY 10595, USA
    Aging (Albany NY) 3:1028-38. 2011
    ....
  37. ncbi request reprint Histone H2AX phosphorylation induced by selective photolysis of BrdU-labeled DNA with UV light: relation to cell cycle phase
    Xuan Huang
    Brander Cancer Research Institute at New York Medical College, 19 Bradhurst Avenue, Hawthorne, NY 10532, USA
    Cytometry A 62:1-7. 2004
    ..The present study explored whether the detection of gammaH2AX IF can serve as a marker of the presence of the DNA precursor bromodeoxyuridine (BrdU) that is incorporated into DNA...
  38. pmc Fluoroquinolones lower constitutive H2AX and ATM phosphorylation in TK6 lymphoblastoid cells via modulation of the intracellular redox status
    H Dorota Halicka
    Brander Cancer Research Institute, New York Medical College, Valhalla, NY 10595, USA
    Pharmacol Rep 61:711-8. 2009
    ..We presume that FQs mediate this effect via a combination of ROS-scavenging and mitochondrial suppression and therefore may protect against the onset or may slow the progression of numerous oxidative pathophysiological conditions...
  39. pmc gammaH2AX: A potential DNA damage response biomarker for assessing toxicological risk of tobacco products
    Anthony P Albino
    Vector Tobacco Inc, Public Health, 712 Fifth Avenue, 52nd Floor, New York, NY 10019, USA
    Mutat Res 678:43-52. 2009
    ..We conclude that gammaH2AX induction shows promise as a genotoxic bioassay offering specific advantages over the traditional assays for the evaluation of conventional and nonconventional tobacco products...
  40. pmc Cytometric assessment of DNA damage in relation to cell cycle phase and apoptosis
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, NY 10532, USA
    Cell Prolif 38:223-43. 2005
    ..Detection of DNA damage in tumour cells during radio- or chemotherapy may provide an early marker predictive of response to treatment...
  41. pmc Ciprofloxacin-induced G2 arrest and apoptosis in TK6 lymphoblastoid cells is not dependent on DNA double-strand break formation
    Daniel J Smart
    Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cancer Biol Ther 7:113-9. 2008
    ..The subsequent induction of apoptosis appears to be facilitated by functional p53. CPFX may therefore have a potential use as a chemotherapeutic agent in the treatment of lymphoblast-derived cancer...
  42. ncbi request reprint RIalpha influences cellular proliferation in cancer cells by transporting RFC40 into the nucleus
    Rakhee S Gupte
    Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, New York 10595, USA
    Cancer Biol Ther 4:429-37. 2005
    ..These findings provide evidence for a previously unknown mechanism for the nuclear transport of RFC40 and also for a novel mechanism for cellular proliferation...
  43. ncbi request reprint Mechanism of antitumor drug action assessed by cytometry
    Frank Traganos
    Brander Cancer Research Institute, New York Medical College, Hawthorne, New York 10532, USA
    Methods Cell Biol 75:257-305. 2004
  44. pmc Cell cycle arrest and apoptosis induced by human Polo-like kinase 3 is mediated through perturbation of microtubule integrity
    Qi Wang
    Department of Medicine and Brander Cancer Research Institute, New York Medical College, Hwathorne, 10532, USA
    Mol Cell Biol 22:3450-9. 2002
    ....
  45. pmc Persistent DNA damage caused by low levels of mitomycin C induces irreversible cell senescence
    Elise McKenna
    Brander Cancer Research Institute, Department of Pathology, New York Medical College, Valhalla, NY, USA
    Cell Cycle 11:3132-40. 2012
    ..It is reasonable to expect that tumors having constitutive activation of oncogenes triggering mTOR signaling may be particularly predisposed to undergoing senescence following prolonged treatment with low doses of DNA damaging drugs...
  46. ncbi request reprint Induction of DNA double-strand breaks in A549 and normal human pulmonary epithelial cells by cigarette smoke is mediated by free radicals
    Anthony P Albino
    Vector Research Ltd, New York, NY 10019, USA
    Int J Oncol 28:1491-505. 2006
    ..The detection of gammaH2AX to assess the induction of CS-induced DSBs and their relationship to cell cycle phase provides a convenient tool to explore approaches to protect cells from this type of genotoxic damage...
  47. ncbi request reprint The cytostatic and cytotoxic effects of oridonin (Rubescenin), a diterpenoid from Rabdosia rubescens, on tumor cells of different lineage
    Sophie Chen
    NovaSpes Research Lab, Hawthorne, NY 10532, USA
    Int J Oncol 26:579-88. 2005
    ..The present data suggest that further studies are warranted to assess the potential of oridonin in cancer prevention and/or treatment...
  48. pmc Impaired DNA damage response--an Achilles' heel sensitizing cancer to chemotherapy and radiotherapy
    Zbigniew Darzynkiewicz
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, NY, USA
    Eur J Pharmacol 625:143-50. 2009
    ..Antitumor strategies are being designed to treat cancers having particular defects in their DDR, concurrent with protecting normal cells...
  49. pmc Cytometry of DNA replication and RNA synthesis: Historical perspective and recent advances based on "click chemistry"
    Zbigniew Darzynkiewicz
    Brander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York 10595, USA
    Cytometry A 79:328-37. 2011
    ..Several examples are presented that illustrate incorporation of EdU or EU in cells subjected to DNA damage detected as histone H2AX phosphorylation that have been analyzed by flow or laser scanning cytometry...
  50. pmc The 2,6-disubstituted purine reversine induces growth arrest and polyploidy in human cancer cells
    Tze Chen Hsieh
    Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA
    Int J Oncol 31:1293-300. 2007
    ..These results suggest that RV may induce polyploidy and increase in cell size by up-regulating p21(WAF1) and cyclin D3/CDK6, while simultaneously suppressing the expression of cyclin B and CDK1...
  51. ncbi request reprint N-acetylcysteine conjugate of phenethyl isothiocyanate enhances apoptosis in growth-stimulated human lung cells
    Yang Ming Yang
    Division of Carcinogenesis, American Health Foundation Cancer Center, Institute for Cancer Prevention, Valhalla, New York, USA
    Cancer Res 65:8538-47. 2005
    ..The observation that PEITC-NAC induces apoptosis predominantly in growth-promoted cells, such as neoplastic cells, suggests a selective mechanism by which PEITC-NAC inhibits lung carcinogenesis...
  52. ncbi request reprint Physical and functional interactions between mitotic kinases during polyploidization and megakaryocytic differentiation
    Xuan Huang
    Division of Molecular Carcinogenesis, Department of Medicine, New York Medical College, Valhalla, New York 10595, USA
    Cell Cycle 3:946-51. 2004
    ..Taken together, our study suggests that Plk3 and Aurora A kinases may lie in the same regulatory pathway and that Plk3 and Aurora A as well as BubR1 may play an important role in polyploidization and megakaryocytic differentiation...
  53. ncbi request reprint DNA damage induced by DNA topoisomerase I- and topoisomerase II-inhibitors detected by histone H2AX phosphorylation in relation to the cell cycle phase and apoptosis
    Xuan Huang
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York, USA
    Cell Cycle 2:614-9. 2003
    ..The data also indicate that regardless whether treated with inhibitors of topo1 or topo2, at comparable levels of dsDNA breaks, the cells replicating DNA have a higher proclivity to undergo apoptosis compared to G1 or G2/M cells...
  54. ncbi request reprint Cytometry of cell cycle regulatory proteins
    Zbigniew Darzynkiewicz
    Cancer Research Institute, New York Medical College, Valhalla, N Y 10593, USA
    Prog Cell Cycle Res 5:533-42. 2003
    ..Particular attention is given to the use of multiparameter cytometry in analysis of the mechanism by which antitumor drugs affect cell cycle progression and induce cell cycle phase-specific apoptosis...
  55. ncbi request reprint Polo-like kinases and centrosome regulation
    Wei Dai
    Brander Cancer Institute, Department of Medicine, New York Medical College, Valhalla, New York, NY 10595, USA
    Oncogene 21:6195-200. 2002
  56. ncbi request reprint Arsenic trioxide arrests cells early in mitosis leading to apoptosis
    H Dorota Halicka
    Brander Cancer Research Institute, New York Medical College, Hawthorne, New York 10532, USA
    Cell Cycle 1:201-9. 2002
    ..Our data suggest that the antileukemic activities of arsenic may be a result of mitotic arrest which culminates in apoptosis...
  57. ncbi request reprint Differential effect of heme oxygenase-1 in endothelial and smooth muscle cell cycle progression
    Giovanni Li Volti
    Department of Medicine, New York Medical College, 10595, Valhalla, NY, USA
    Biochem Biophys Res Commun 296:1077-82. 2002
    ..Nevertheless, these findings suggest that cell-specific targeting of HO-1 expression may provide a novel therapeutic strategy for the treatment of cardiovascular diseases...
  58. pmc Noncatalytic requirement for cyclin A-cdk2 in p27 turnover
    Xin Hua Zhu
    Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Mol Cell Biol 24:6058-66. 2004
    ..Together these lines of evidence suggest that cyclin A-cdk2 plays an ancillary noncatalytic role in the ubiquitination of p27 by the SCF(skp2) complex...
  59. ncbi request reprint Histone deacetylase inhibitors all induce p21 but differentially cause tubulin acetylation, mitotic arrest, and cytotoxicity
    Mikhail V Blagosklonny
    Brander Cancer Research Institute, New York Medical College, Valhalla, New York 10595, USA
    Mol Cancer Ther 1:937-41. 2002
    ..We conclude that HDIs have differential effects on non-histone deacetylases and that rapid acetylation of tubulin caused by TSA is a marker of nontranscriptional effects of TSA...
  60. ncbi request reprint Proteasome-dependent downregulation of p21(Waf1/Cip1) induced by reactive oxygen species
    Suqing Xie
    Department of Medicine, New York Medical College, Valhalla, NY 10595, USA
    J Interferon Cytokine Res 22:957-63. 2002
    ..Taken together, our studies indicate that oxidative stress induces rapid, but reversible, downregulation of functional p21 by accelerating its protein turnover...
  61. ncbi request reprint Effects of PC-SPES on proliferation and expression of AR/PSA in androgen-responsive LNCaP cells are independent of estradiol
    Tze Chen Hsieh
    Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla 10595, USA
    Anticancer Res 22:2051-60. 2002
    ..These studies show that the antiproliferative and gene modulatory effects of PC-SPES in androgen-dependent human prostate cancer cells are mechanistically and functionally distinct from effects attributable to estradiol...
  62. ncbi request reprint Angiotensin II stimulates nitric oxide production in pulmonary artery endothelium via the type 2 receptor
    Susan Olson
    Dept of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY 10595, USA
    Am J Physiol Lung Cell Mol Physiol 287:L559-68. 2004
    ..This endothelial, type 2 receptor-dependent increase in nitric oxide may serve to counterbalance the angiotensin II-dependent vasoconstriction in smooth muscle cells, ultimately regulating pulmonary vascular tone...
  63. ncbi request reprint Nitric oxide-donating nonsteroidal anti-inflammatory drugs inhibit the growth of various cultured human cancer cells: evidence of a tissue type-independent effect
    Khosrow Kashfi
    American Health Foundation, Valhalla, New York, USA
    J Pharmacol Exp Ther 303:1273-82. 2002
    ..These results raise the possibility that NO-NSAIDs possess chemopreventive and/or chemotherapeutic activity against a wide variety of human cancers...
  64. ncbi request reprint NO-donating nonsteroidal antiinflammatory drugs (NSAIDs) inhibit colon cancer cell growth more potently than traditional NSAIDs: a general pharmacological property?
    Raymond K Yeh
    American Health Foundation Cancer Center, Institute for Cancer Prevention, Valhalla, NY 06595, USA
    Biochem Pharmacol 67:2197-205. 2004
    ..Our findings suggest that the enhanced potency imparted on NSAIDs by this structural modification represents a pharmacological property that may be a general one for this class of compounds...