R W Johnstone

Summary

Affiliation: University of Melbourne
Country: Australia

Publications

  1. ncbi request reprint Apoptosis: a link between cancer genetics and chemotherapy
    Ricky W Johnstone
    Cancer Immunology Division, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Smorgon Family Building, St Andrews Place, East Melbourne, 3002 Victoria, Australia
    Cell 108:153-64. 2002
  2. ncbi request reprint Suberanilohydroxamic Acid. Aton Pharma
    Ricky W Johnstone
    Gene Regulation Laboratory, Cancer Immunology Division, Peter MacCallum Cancer Centre, East Melbourne, VIC 3200, Australia
    IDrugs 7:674-82. 2004
  3. ncbi request reprint Histone-deacetylase inhibitors: novel drugs for the treatment of cancer
    Ricky W Johnstone
    Cancer Immunology Program, Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Smorgon Family Building, St Andrews Place, East Melbourne, 3002 Victoria, Australia
    Nat Rev Drug Discov 1:287-99. 2002
  4. ncbi request reprint P-glycoprotein does not protect cells against cytolysis induced by pore-forming proteins
    R W Johnstone
    Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, St Andrews Place, East Melbourne 3002, Victoria, Australia
    J Biol Chem 276:16667-73. 2001
  5. ncbi request reprint Mutational analysis of P-glycoprotein: suppression of caspase activation in the absence of ATP-dependent drug efflux
    K M Tainton
    Cancer Immunology Program, The Peter MacCallum Cancer Centre, Trescowthick Research Laboratories, East Melbourne, Victoria, Australia
    Cell Death Differ 11:1028-37. 2004
  6. ncbi request reprint P-glycoprotein protects leukemia cells against caspase-dependent, but not caspase-independent, cell death
    R W Johnstone
    The Austin Research Institute, Austin Hospital, Heidelberg, Victoria, Australia
    Blood 93:1075-85. 1999
  7. pmc The histone deacetylase inhibitor and chemotherapeutic agent suberoylanilide hydroxamic acid (SAHA) induces a cell-death pathway characterized by cleavage of Bid and production of reactive oxygen species
    A A Ruefli
    Cancer Immunology Division, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Saint Andrews Place, East Melbourne, Victoria 3002, Australia
    Proc Natl Acad Sci U S A 98:10833-8. 2001
  8. doi request reprint Blocking granule-mediated death by primary human NK cells requires both protection of mitochondria and inhibition of caspase activity
    K A Sedelies
    Cancer Cell Death Laboratory, Cancer Immunology Program, Peter MacCallum Cancer Centre, Locked Bag 1, A Beckett Street, Melbourne, Victoria 8006, Australia
    Cell Death Differ 15:708-17. 2008
  9. pmc Functional analysis of the leukemia protein ELL: evidence for a role in the regulation of cell growth and survival
    R W Johnstone
    The Peter MacCallum Cancer Institute, Gene Regulation Laboratory, Cancer Immunology Division, East Melbourne, 3002 Victoria, Australia
    Mol Cell Biol 21:1672-81. 2001
  10. ncbi request reprint Critical role of the transcription factor AP-1 for the constitutive and interferon-induced expression of IFI 16
    C J P Clarke
    Trescowthick Research Laboratories, Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria 3002, Australia
    J Cell Biochem 89:80-93. 2003

Collaborators

Detail Information

Publications51

  1. ncbi request reprint Apoptosis: a link between cancer genetics and chemotherapy
    Ricky W Johnstone
    Cancer Immunology Division, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Smorgon Family Building, St Andrews Place, East Melbourne, 3002 Victoria, Australia
    Cell 108:153-64. 2002
    ....
  2. ncbi request reprint Suberanilohydroxamic Acid. Aton Pharma
    Ricky W Johnstone
    Gene Regulation Laboratory, Cancer Immunology Division, Peter MacCallum Cancer Centre, East Melbourne, VIC 3200, Australia
    IDrugs 7:674-82. 2004
    ..Aton Pharma Inc, under license from the Memorial Sloan-Kettering Cancer Center, is developing suberanilohydroxamic acid (SAHA), a cytodifferentiating agent and histone deacetylase inhibitor, as a potential cancer chemopreventive...
  3. ncbi request reprint Histone-deacetylase inhibitors: novel drugs for the treatment of cancer
    Ricky W Johnstone
    Cancer Immunology Program, Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Smorgon Family Building, St Andrews Place, East Melbourne, 3002 Victoria, Australia
    Nat Rev Drug Discov 1:287-99. 2002
    ..The remarkable tumour specificity of these compounds, and their potency in vitro and in vivo, underscore the potential of HDAC inhibitors as exciting new agents for the treatment of cancer...
  4. ncbi request reprint P-glycoprotein does not protect cells against cytolysis induced by pore-forming proteins
    R W Johnstone
    Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, St Andrews Place, East Melbourne 3002, Victoria, Australia
    J Biol Chem 276:16667-73. 2001
    ..Based on these results, we conclude that P-gp does not affect cell lysis induced by pore-forming proteins...
  5. ncbi request reprint Mutational analysis of P-glycoprotein: suppression of caspase activation in the absence of ATP-dependent drug efflux
    K M Tainton
    Cancer Immunology Program, The Peter MacCallum Cancer Centre, Trescowthick Research Laboratories, East Melbourne, Victoria, Australia
    Cell Death Differ 11:1028-37. 2004
    ..The structure-function analyses described herein provide novel insight into the mechanisms of action of P-gp in mediating MDR...
  6. ncbi request reprint P-glycoprotein protects leukemia cells against caspase-dependent, but not caspase-independent, cell death
    R W Johnstone
    The Austin Research Institute, Austin Hospital, Heidelberg, Victoria, Australia
    Blood 93:1075-85. 1999
    ..This study has confirmed a potential novel physiological function for P-glycoprotein and it now remains to dissect the molecular mechanisms involved in the inhibition of capsase-dependent cell death by P-glycoprotein...
  7. pmc The histone deacetylase inhibitor and chemotherapeutic agent suberoylanilide hydroxamic acid (SAHA) induces a cell-death pathway characterized by cleavage of Bid and production of reactive oxygen species
    A A Ruefli
    Cancer Immunology Division, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, Saint Andrews Place, East Melbourne, Victoria 3002, Australia
    Proc Natl Acad Sci U S A 98:10833-8. 2001
    ..These data provide evidence of a mechanism of cell death mediated by transcriptional events that result in the cleavage of Bid, disruption of the mitochondrial membrane, and production of reactive oxygen species to induce cell death...
  8. doi request reprint Blocking granule-mediated death by primary human NK cells requires both protection of mitochondria and inhibition of caspase activity
    K A Sedelies
    Cancer Cell Death Laboratory, Cancer Immunology Program, Peter MacCallum Cancer Centre, Locked Bag 1, A Beckett Street, Melbourne, Victoria 8006, Australia
    Cell Death Differ 15:708-17. 2008
    ....
  9. pmc Functional analysis of the leukemia protein ELL: evidence for a role in the regulation of cell growth and survival
    R W Johnstone
    The Peter MacCallum Cancer Institute, Gene Regulation Laboratory, Cancer Immunology Division, East Melbourne, 3002 Victoria, Australia
    Mol Cell Biol 21:1672-81. 2001
    ..These novel results indicate that ELL can regulate cell growth and survival and may explain how ELL translocations result in the development of human malignancies...
  10. ncbi request reprint Critical role of the transcription factor AP-1 for the constitutive and interferon-induced expression of IFI 16
    C J P Clarke
    Trescowthick Research Laboratories, Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria 3002, Australia
    J Cell Biochem 89:80-93. 2003
    ..These experiments define the transcriptional mechanisms of IFI 16 gene regulation and provide evidence suggesting that AP-1 activation may be an important event in IFN signaling...
  11. pmc Initiation of apoptosis by granzyme B requires direct cleavage of bid, but not direct granzyme B-mediated caspase activation
    V R Sutton
    Cancer Immunology Laboratory, Peter MacCallum Cancer Institute, Melbourne 8006, Australia
    J Exp Med 192:1403-14. 2000
    ..Overall, our results indicate that mitochondrial perturbation by Bid is necessary to achieve a lethal threshold of caspase activity and cell death due to granzyme B...
  12. pmc Preclinical screening of histone deacetylase inhibitors combined with ABT-737, rhTRAIL/MD5-1 or 5-azacytidine using syngeneic Vk*MYC multiple myeloma
    G M Matthews
    Gene Regulation Laboratory, Cancer Therapeutics, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria, Australia
    Cell Death Dis 4:e798. 2013
    ..Taken together, our studies provide evidence that the transplanted Vk*MYC model of MM is a useful screening tool for anti-MM drugs and should aid in the prioritization of novel drug testing in the clinic...
  13. pmc Fas ligand-mediated lysis of self bystander targets by human papillomavirus-specific CD8+ cytotoxic T lymphocytes
    M J Smyth
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Heidelberg 3084, Victoria, Australia
    J Virol 72:5948-54. 1998
    ....
  14. ncbi request reprint P-glycoprotein inhibits caspase-8 activation but not formation of the death inducing signal complex (disc) following Fas ligation
    A A Ruefli
    Peter MacCallum Cancer Institute, St Andrew s Place, East Melbourne, Victoria, Australia
    Cell Death Differ 9:1266-72. 2002
    ..These studies demonstrate that P-gp inhibits Fas-induced caspase-8 activation but not formation of the DISC and that this activity of P-gp is dependent on ATP hydrolysis...
  15. pmc The drug efflux protein, P-glycoprotein, additionally protects drug-resistant tumor cells from multiple forms of caspase-dependent apoptosis
    M J Smyth
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Studley Road, Heidelberg, 3084, Victoria, Australia
    Proc Natl Acad Sci U S A 95:7024-9. 1998
    ..These observations suggest that, in addition to effluxing drugs, P-gp may play a specific role in regulating some caspase-dependent apoptotic pathways...
  16. pmc Granzyme B triggers a prolonged pressure to die in Bcl-2 overexpressing cells, defining a window of opportunity for effective treatment with ABT-737
    V R Sutton
    Cancer Cell Death Laboratory, Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, Victoria 8006, Australia
    Cell Death Dis 3:e344. 2012
    ..This defines a therapeutic window in which ABT-737 and CL synergise to cause maximum death of cancer cells that are resistant to either treatment alone, which will be essential in defining optimum treatment regimens...
  17. ncbi request reprint Functional interaction between p53 and the interferon-inducible nucleoprotein IFI 16
    R W Johnstone
    The Peter MacCallum Cancer Institute, Cancer Immunology Division, East Melbourne, Victoria, Australia
    Oncogene 19:6033-42. 2000
    ..These findings demonstrate a possible link between gene induction following interferon stimulation and p53-mediated cellular events...
  18. ncbi request reprint Multiple physiological functions for multidrug transporter P-glycoprotein?
    R W Johnstone
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Austin Hospital, Studley Road, Heidelberg 3084, Victoria, Australia
    Trends Biochem Sci 25:1-6. 2000
    ....
  19. ncbi request reprint A role for P-glycoprotein in regulating cell death
    R W Johnstone
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Australia, Victoria
    Leuk Lymphoma 38:1-11. 2000
    ..There is now a lively debate regarding the possible role of P-gp in regulating cell differentiation, proliferation and survival...
  20. pmc HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses
    J E Bolden
    Cancer Therapeutics Program, Gene Regulation Laboratory, The Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne 3002, Victoria, Australia
    Cell Death Dis 4:e519. 2013
    ..This study provides new insight into the transcriptional effects of HDACi in human donor-matched normal and transformed cells, and implicates specific molecules and pathways in the tumor-selective cytotoxic activity of these compounds...
  21. doi request reprint Efficacy of CHK inhibitors as single agents in MYC-driven lymphoma cells
    P T Ferrao
    Molecular Oncology Laboratory and Cancer Therapeutics Program, Research Division, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne, Victoria, Australia
    Oncogene 31:1661-72. 2012
    ..We propose that inhibitors of CHK can act in a synthetically lethal manner in cancers with replication stress as a result of these cancers being reliant on CHK proteins for an effective DDR and cell survival...
  22. ncbi request reprint Filamin (280-kDa actin-binding protein) is a caspase substrate and is also cleaved directly by the cytotoxic T lymphocyte protease granzyme B during apoptosis
    K A Browne
    Cancer Immunology Laboratory, Peter MacCallum Cancer Institute, Locked Bag 1, A Beckett Street, Melbourne 8006, Australia
    J Biol Chem 275:39262-6. 2000
    ..Thus, filamin is a functionally important substrate for granzyme B, as its cleavage may account at least partly for caspase-independent cell death mediated by the granzyme...
  23. pmc Analysis of the apoptotic and therapeutic activities of histone deacetylase inhibitors by using a mouse model of B cell lymphoma
    R K Lindemann
    Cancer Immunology Program, The Peter MacCallum Cancer Institute, Trescowthick Research Laboratories, St Andrews Place, East Melbourne, Victoria 3002, Australia
    Proc Natl Acad Sci U S A 104:8071-6. 2007
    ..Our studies provide important information regarding the mechanisms of action of HDACi that have broad implications regarding stratification of patients receiving HDACi therapy alone or in combination with other anticancer agents...
  24. ncbi request reprint The human interferon-inducible protein, IFI 16, is a repressor of transcription
    R W Johnstone
    The Austin Research Institute, Austin Hospital, Studley Road, Heidelberg 3084, Victoria, Australia
    J Biol Chem 273:17172-7. 1998
    ..Thus, IFI 16 is a transcriptional repressor, with a modular structure typical of many known transcription regulators...
  25. ncbi request reprint Isotypic variants of the interferon-inducible transcriptional repressor IFI 16 arise through differential mRNA splicing
    R W Johnstone
    The John Connell Laboratory, The Austin Research Institute, Heidelberg, Australia
    Biochemistry 37:11924-31. 1998
    ..Finally, IFI 16 isoforms can homo- and heterodimerize, and we have mapped the dimerization domain to the amino terminus which contains an imperfect leucine zipper domain...
  26. ncbi request reprint Structural organization, tissue expression, and chromosomal localization of Ciao 1, a functional modulator of the Wilms' tumor suppressor, WT1
    R W Johnstone
    Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA
    Immunogenetics 49:900-5. 1999
  27. ncbi request reprint Role of TNF in lymphocyte-mediated cytotoxicity
    M J Smyth
    Cellular Cytotoxicity Laboratory, Austin Research Institute, Austin
    Microsc Res Tech 50:196-208. 2000
    ..This review describes the key molecular details of the action of TNF and discusses the evidence for TNF-mediated cytotoxicity being critical to lymphocyte function and immunoregulation...
  28. pmc A functional genomics screen identifies PCAF and ADA3 as regulators of human granzyme B-mediated apoptosis and Bid cleavage
    D Brasacchio
    1 Sir Peter MacCallum Department of Oncology, The University of Melbourne, Parkville, Vic, Australia 2 Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Vic, Australia
    Cell Death Differ 21:748-60. 2014
    ..We conclude that PCAF and ADA3 regulate Bid processing via PACS2, to modulate the mitochondrial cell death pathway in response to hGrzB. ..
  29. ncbi request reprint Mechanisms of interferon mediated anti-viral resistance
    C J Clarke
    Peter MacCallum Cancer Institute, St Andrews Place, East Melbourne, Victoria 3002, Australia
    Curr Drug Targets Immune Endocr Metabol Disord 1:117-30. 2001
    ..This review explains the current model of IFN action, during viral infections and the potential for well-established and emerging groups of IFN inducible genes as therapeutic targets is highlighted...
  30. doi request reprint Thalidomide-analogue biology: immunological, molecular and epigenetic targets in cancer therapy
    J Shortt
    Gene Regulation Laboratory, Cancer Therapeutics Program, Peter MacCallum Cancer Centre, Locked Bag 1, A Beckett St, Melbourne, Victoria, Australia
    Oncogene 32:4191-202. 2013
    ..It is anticipated that elucidation of important IMiD targets will allow the rational development of new-generation therapeutics with the potential to separate thalidomide-analogue efficacy from clinical toxicity...
  31. pmc Translation inhibitors induce cell death by multiple mechanisms and Mcl-1 reduction is only a minor contributor
    L M Lindqvist
    The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia
    Cell Death Dis 3:e409. 2012
    ..Indeed, loss of clonogenic survival proved to be independent of the Bax/Bak-mediated apoptosis altogether. Our findings warn of potential toxicity as these translation inhibitors are cytotoxic to many differentiated non-cycling cells...
  32. ncbi request reprint Multiple deficiencies underlie NK cell inactivity in lymphotoxin-alpha gene-targeted mice
    M J Smyth
    Cellular Cytotoxicity Laboratory, The Austin Research Institute, Heidelberg, Victoria, Australia
    J Immunol 163:1350-3. 1999
    ..5- to 3-fold in LT-alpha-deficient mice, as compared with wild-type mice. Combined defects in NK cell development and effector function contribute to compromised NK cell antitumor function in LT-alpha-deficient mice...
  33. doi request reprint Histone deacetylase inhibitors in lymphoma and solid malignancies
    Walid Rasheed
    Division of Haematology and Medical Oncology, Peter MacCallum Cancer Centre, Locked Bag 1, A Beckett St, Melbourne, Victoria 8006, Australia
    Expert Rev Anticancer Ther 8:413-32. 2008
    ..In this review we discuss the recent advances in the clinical development of HDACi and their current therapeutic role in lymphoma and solid malignancies...
  34. doi request reprint Characterisation of the novel apoptotic and therapeutic activities of the histone deacetylase inhibitor romidepsin
    Andrea Newbold
    Cancer Immunology Program, Peter MacCallum Cancer Centre, Trescowthick Research Laboratories, St Andrews Place, East Melbourne, Victoria 3002, Australia
    Mol Cancer Ther 7:1066-79. 2008
    ..These data provide strong support that HDACi of different chemical classes may have subtle yet potentially important differences in their molecular and biological activities...
  35. doi request reprint Histone deacetylase inhibitor panobinostat induces clinical responses with associated alterations in gene expression profiles in cutaneous T-cell lymphoma
    Leigh Ellis
    Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
    Clin Cancer Res 14:4500-10. 2008
    ..Herein, we report the safety and activity of the histone deacetylase inhibitor panobinostat (LBH589) in cutaneous T-cell lymphoma (CTCL) and identify genes commonly regulated by panobinostat...
  36. pmc Combination therapy of established cancer using a histone deacetylase inhibitor and a TRAIL receptor agonist
    Ailsa J Frew
    Cancer Immunology Program, The Peter MacCallum Cancer Centre, Trescowthick Research Laboratories, St Andrews Place, East Melbourne 3002, Victoria, Australia
    Proc Natl Acad Sci U S A 105:11317-22. 2008
    ..These data demonstrate that combination therapies involving HDACi and activators of the TRAIL pathway can be efficacious for the treatment of cancer in experimental mouse models...
  37. ncbi request reprint Epigenetic changes to the MDR1 locus in response to chemotherapeutic drugs
    Emma K Baker
    Epigenetics in Human Health and Disease Laboratory, The Alfred Medical Research and Education Precinct, Baker Medical Research Institute, Commercial Road, Prahran, Victoria 3181, Australia
    Oncogene 24:8061-75. 2005
    ..Our results demonstrate that chemotherapeutic drugs can actively induce epigenetic changes within the MDR1 promoter, and enhance the MDR phenotype...
  38. ncbi request reprint Suberoylanilide hydroxamic acid (SAHA) overcomes multidrug resistance and induces cell death in P-glycoprotein-expressing cells
    Astrid A Ruefli
    Cancer Immunology Division, The Peter MacCallum Cancer Institute, East Melbourne, Victoria, Australia
    Int J Cancer 99:292-8. 2002
    ..These data provide evidence that P-gp inhibits caspase activation after chemotherapeutic drug treatment and demonstrates that SAHA may be of value for the treatment of P-gp-expressing MDR cancers...
  39. ncbi request reprint Novel mechanisms of apoptosis induced by histone deacetylase inhibitors
    Melissa J Peart
    Cancer Immunology Program, The Peter MacCallum Cancer Institute, East Melbourne 3002, Victoria, Australia
    Cancer Res 63:4460-71. 2003
    ....
  40. ncbi request reprint Histone-deacetylase inhibitors for the treatment of cancer
    Ralph K Lindemann
    Gene Regulation Laboratory, Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Australia
    Cell Cycle 3:779-88. 2004
    ..Herein, we provide an update on the transcription-dependent and -independent events that may be important for the anti-tumor activities of HDACi and discuss the use of these compounds in combination with other chemotherapeutic drugs...
  41. pmc Identification and functional significance of genes regulated by structurally different histone deacetylase inhibitors
    Melissa J Peart
    The Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne 3002, Victoria, Australia
    Proc Natl Acad Sci U S A 102:3697-702. 2005
    ....
  42. ncbi request reprint Histone deacetylase inhibitors in cancer therapy: is transcription the primary target?
    Ricky W Johnstone
    The Peter MacCallum Cancer Centre, East Melbourne 3002, Victoria, Australia
    Cancer Cell 4:13-8. 2003
  43. ncbi request reprint Histone deacetylase inhibitors in cancer therapy
    Walid K Rasheed
    Department of Haematology and Medical Oncology, Peter MacCallum Cancer Centre, Locked Bag 1, A Beckett St, Melbourne, Victoria 8006, Australia
    Expert Opin Investig Drugs 16:659-78. 2007
    ..Although still early in drug development, there is a picture that is starting to develop as to the common toxicities and which tumors seem to be the most susceptible to this class of drugs...
  44. ncbi request reprint Anticancer activities of histone deacetylase inhibitors
    Jessica E Bolden
    Cancer Immunology Program, Peter MacCallum Cancer Centre, St Andrews Place, East Melbourne 3002, Victoria, Australia
    Nat Rev Drug Discov 5:769-84. 2006
    ....
  45. ncbi request reprint Expression of IFI 16 in epithelial cells and lymphoid tissues
    Wu Wei
    Peter MacCallum Cancer Institute, St Andrews Place, 3002 East Melbourne, Victoria, Australia
    Histochem Cell Biol 119:45-54. 2003
    ..In contrast to the perceived role of HIN-200 proteins as suppressors of cell growth, maximal expression of IFI 16 was in cells with high proliferative potential...
  46. ncbi request reprint Role of IFI 16, a member of the interferon-inducible p200-protein family, in prostate epithelial cellular senescence
    Hong Xin
    Departments of Pathology and Radiation Oncology, Stritch School of Medicine, Loyola University Medical Center, 2160 South First Avenue, Mail Code 114B, Maywood, IL 60153, USA
    Oncogene 22:4831-40. 2003
    ..Collectively, our observations support the idea that increased levels of IFI 16 in PrECs contribute to senescence-associated irreversible cell growth arrest...
  47. ncbi request reprint Histone deacetylase inhibitors potently repress CXCR4 chemokine receptor expression and function in acute lymphoblastic leukaemia
    Roman Crazzolara
    Tyrolean Cancer Research Institute TCRI at the University of Innsbruck, Department of Paediatrics, Innsbruck University Hospital, Innsbruck, Austria
    Br J Haematol 119:965-9. 2002
    ..Repression of CXCR4 transcription by inhibitors of histone deacetylases might therefore represent a promising novel approach in the treatment of acute leukaemias...
  48. doi request reprint The TRAIL apoptotic pathway in cancer onset, progression and therapy
    Ricky W Johnstone
    Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria 3002, Australia
    Nat Rev Cancer 8:782-98. 2008
    ..Herein we review what is known about the molecular control of TRAIL-mediated apoptosis, the role of TRAIL in carcinogenesis and the potential therapeutic utility of recombinant TRAIL and agonistic antibodies against TRAILR1 and TRAILR2...
  49. ncbi request reprint From cancer immunosurveillance to cancer immunotherapy
    John Stagg
    Cancer Immunology Program, Sir Donald and Lady Trescowthick Laboratories, Peter MacCallum Cancer Centre, East Melbourne, Vic, Australia
    Immunol Rev 220:82-101. 2007
    ....
  50. pmc Small molecule obatoclax (GX15-070) antagonizes MCL-1 and overcomes MCL-1-mediated resistance to apoptosis
    Mai Nguyen
    Department of Biochemistry and McGill Cancer Center, McGill University, Montreal, QC, Canada
    Proc Natl Acad Sci U S A 104:19512-7. 2007
    ..In both cases, this resistance was overcome by obatoclax. These findings support a rational clinical development opportunity for the compound in cancer indications or treatments where MCL-1 contributes to resistance to cell killing...
  51. doi request reprint The role of p202 in regulating hematopoietic cell proliferation and differentiation
    Louise E Ludlow
    Gene Regulation Laboratory, Peter MacCallum Cancer Centre, East Melbourne VIC 3002, Australia
    J Interferon Cytokine Res 28:5-11. 2008
    ..Thus, p202 plays a role in regulating the proliferative capacity of hematopoietic cells...