%0 Journal Article %~ PubMed %A Iland, Harry J %A Bradstock, Ken %A Supple, Shane G %A Catalano, Alberto %A Collins, Marnie %A Hertzberg, Mark %A Browett, Peter %A Grigg, Andrew %A Firkin, Frank %A Hugman, Amanda %A Reynolds, John %A Di Iulio, Juliana %A Tiley, Campbell %A Taylor, Kerry %A Filshie, Robin %A Seldon, Michael %A Taper, John %A Szer, Jeff %A Moore, John %A Bashford, John %A Seymour, John F %T All-trans-retinoic acid, idarubicin, and intravenous arsenic trioxide as initial therapy in acute promyelocytic leukemia (APML4). %B Blood %D 2012 %C United States %I American Society of Hematology %V 120 %N 8 %P 1570-1580 %@ 0006-4971 %X The treatment of acute promyelocytic leukemia has improved considerably following recognition of the effectiveness of all-trans-retinoic acid (ATRA), anthracycline-based chemotherapy, and arsenic trioxide (ATO). Here, we report the use of all 3 agents in combination (APML4 phase-II protocol). For induction, ATO was superimposed upon an ATRA and idarubicin backbone, with scheduling designed to exploit anti-leukemic synergy whilst minimizing cardiotoxicity and the severity of differentiation syndrome. Consolidation comprised 2 cycles of ATRA and ATO without chemotherapy, followed by 2 years of maintenance with ATRA, oral methotrexate and 6-mercaptopurine. Of 124 evaluable patients, there were 4 (3.2%) early deaths, 118 (95%) achieved hematological complete remission, and all 112 patients who commenced consolidation attained molecular complete remission. The 2-year rate for freedom from relapse is 97.5%, failure-free survival 88.1%, and overall survival 93.2%. These outcomes were not influenced by FLT3 mutation status, whereas failure-free survival was correlated with Sanz risk stratification (P[trend]=0.03). Compared with our previously reported ATRA/idarubicin-based protocol (APML3), APML4 patients had statistically significantly improved freedom from relapse (P=0.006) and failure-free survival (P=0.01). In conclusion, the use of ATO in both induction and consolidation achieved excellent outcomes despite a substantial reduction in anthracycline exposure. This trial was registered at www.anzctr.org.au (#ACTRN12605000070639). %Z FOR Codes: 111204 %0 Journal Article %~ PubMed %A Khoo, Teh-Liane %A Catalano, Alberto %A Supple, Shane %A Chong, Li %A Yeoh, Sue-Ching %A Yeung, Stephen %A Iland, Harry %T Hyperpigmentation of the hard palate associated with imatinib therapy for chronic myeloid leukemia with a genetic variation in the proto-oncogene c-KIT. %B Leukemia & Lymphoma %D 2012 %C Switzerland %I Informa Healthcare %V 54 %N 1 %P 186-188 %@ 1029-2403 %X %Z FOR Codes: 110202 110508 %0 Journal Article %~ PubMed %A Brown, C M S %A Larsen, S R %A Iland, H J %A Joshua, D E %A Gibson, J %T Leukaemias into the 21st century: part 1: the acute leukaemias. %B Internal Medicine Journal %D 2012 %C Australia %I Wiley-Blackwell Publishing Asia %V 42 %N 11 %P 1179-1186 %@ 1445-5994 %X %Z FOR Codes: 110202 111206 %0 Journal Article %~ PubMed %A Ling, Silvia C W %A Lau, Edwin K K %A Al-Shabeeb, Ammira %A Nikolic, Angela %A Catalano, Albert %A Iland, Harry %A Horvath, Noemi %A Ho, P Joy %A Harrison, Simon %A Fleming, Shaun %A Joshua, Douglas E %A Allen, John D %T Response of myeloma to the proteasome inhibitor bortezomib is correlated with the unfolded protein response regulator XBP-1. %B Haematologica %D 2012 %C Italy %I Fondazione Ferrata Storti %V 97 %N 1 %P 64-72 %@ 1592-8721 %X Multiple myeloma, a malignancy of the antibody-secreting plasma cells, remains incurable by current therapy. However, the proteasome inhibitor bortezomib and other new drugs are revolutionizing its treatment. It remains unclear why myelomas are peculiarly sensitive to bortezomib, or what causes primary or acquired resistance. The ''unfolded protein response'' is necessary for folding and assembly of immunoglobulin chains in both normal and malignant plasma cells, as well as for the disposal of incorrectly folded or unpaired chains via the ubiquitin-proteasome pathway. We tested the hypothesis that levels of transcription factor XBP-1, a major regulator of the unfolded protein response, predict response to bortezomib. %Z FOR Codes: 1112 %0 Journal Article %~ PubMed %A Iland, Harry %A Bradstock, Ken %A Seymour, John %A Hertzberg, Mark %A Grigg, Andrew %A Taylor, Kerry %A Catalano, John %A Cannell, Paul %A Horvath, Noemi %A Deveridge, Sandra %A Browett, Peter %A Brighton, Tim %A Chong, Li %A Springall, Francisca %A Ayling, Juliet %A Catalano, Alberto %A Supple, Shane %A Collins, Marnie %A Di Iulio, Juliana %A Reynolds, John %A , Australasian Leukaemia and Lymphoma Group %T Results of the APML3 trial incorporating all-trans-retinoic acid and idarubicin in both induction and consolidation as initial therapy for patients with acute promyelocytic leukemia. %B Haematologica %D 2012 %C Italy %I Fondazione Ferrata Storti %V 97 %N 2 %P 227-234 %@ 1592-8721 %X Initial therapy for patients with acute promyelocytic leukemia most often involves the combination of all-trans-retinoic acid with anthracycline-based chemotherapy. The role of non-anthracycline drugs in induction and consolidation is less well-established and varies widely between different cooperative group protocols. %Z FOR Codes: 111206 %0 Journal Article %~ PubMed %A de Zwaan, Sally E %A Iland, Harry J %A Damian, Diona L %T Treatment of refractory pyoderma gangrenosum with intravenous immunoglobulin. %B The Australasian Journal of Dermatology %D 2009 %C Australia %I Blackwell Publishing Asia %V 50 %N 1 %P 56-59 %@ 0004-8380 %X We report a patient with pyoderma gangrenosum successfully treated with intravenous immunoglobulin. He had previously been treated for 4 years with high-dose corticosteroids and had developed insulin-dependent diabetes mellitus. Multiple corticosteroid-sparing agents had failed or were contraindicated. He developed no adverse effects from intravenous immunoglobulin, which allowed reduction of his prednisone to 3 mg/day, and his ulcer has completely healed. %Z FOR Codes: 110304 %0 Journal Article %A Losco, Paul %A Brown, Ross %A Iland, Harry %A Uhr, Elaine %A Lee, Linda %A Joshua, Douglas %T An evaluation of the technical performance and clinical applications of the Beckman Coulter Access® Erythropoietin immunoassay %B Australian Journal of Medical Science %D 2007 %C Australia %I Australian Institute of Medical Scientists %V 28 %N 4 %P 139-144 %@ 1038-1643 %X %Z FOR Codes: 110202 %0 Journal Article %~ PubMed %A Young, G A R %A Iland, H J %T Clinical perspectives in lymphoma. %B Internal medicine journal %D 2007 %C Australia %I Blackwell Publishing Asia %V 37 %N 7 %P 478-484 %@ 1444-0903 %X The classification of both Hodgkin''s and non-Hodgkin''s lymphomas continues to evolve. The current World Health Organization classification incorporates data derived from advances in our understanding of the pathogenesis of these disorders together with their distinguishing immunophenotypic, genotypic, clinical and histopathological characteristics. As outcomes have improved, the main emphasis of treatment has been to incorporate a risk-adapted approach to reduce long-term toxicity without sacrificing efficacy through the use of varying combinations of chemotherapy, radiotherapy and immunotherapy. %Z FOR Codes: %0 Journal Article %~ PubMed %A Sanders, J %A Crawford, B %A Gibson, J %A Joy Ho, P %A Iland, H %A Joshua, D %T Is there a case for the early use of bisphosphonates in smouldering myeloma and MGUS? (Bisphosphonates in SMM & MGUS). %B International journal of laboratory hematology %D 2007 %C United Kingdom %I Blackwell Publishing Ltd. %V 29 %N 5 %P 395-397 %@ 1751-5521 %X %Z FOR Codes: %0 Journal Article %~ PubMed %A Catalano, Alberto %A Dawson, Mark A %A Somana, Karthiga %A Opat, Stephen %A Schwarer, Anthony %A Campbell, Lynda J %A Iland, Harry %T The PRKAR1A gene is fused to RARA in a new variant acute promyelocytic leukemia. %B Blood %D 2007 %C United States %I American Society of Hematology %V 110 %N 12 %P 4073-6 %@ 1528-0020 %X We report the molecular and cytogenetic characterization of a novel variant of acute promyelocytic leukemia (APL). The bone marrow showed 88% hypergranular promyelocytes, and the karyotype was 47,XY,+22 [5]/46,XY[30]. Fluorescence in situ hybridization (FISH) indicated disruption and deletion of the 5''-end of the RARA gene. Treatment with all-trans retinoic acid, idarubicin, and arsenic trioxide induced cytogenetic complete remission without morphologic evidence of residual leukemia. The diagnostic marrow was negative for PML-RARA transcripts by reverse transcription-polymerase chain reaction (RT-PCR), but an atypical product was observed. Sequencing showed partial homology to the PRKAR1A gene, encoding the regulatory subunit type I-alpha of cyclic adenosine monophosphate-dependent protein kinase. RT-PCR using specific primers for PRKAR1A and RARA amplified 2 transcript splice variants of a PRKAR1A-RARA fusion gene, and PRKAR1A and RARA FISH probes confirmed the fusion. This novel PRKAR1A-RARA gene rearrangement is the fifth variant APL in which the RARA partner gene has been identified and the second known rearrangement of PRKAR1A in a malignant disease. This trial was registered at www.actr.org.au with the Australian Clinical Trials Registry as number 12605000070639. %Z FOR Codes: %0 Journal Article %~ PubMed %A Ling, Silvia %A Joshua, Douglas E %A Gibson, John %A Young, Graham %A Iland, Harry %A Watson, Geoff %A Ho, P Joy %T Transformation and progression of Waldenström's macroglobulinemia following cladribine therapy in two cases: natural evolution or iatrogenic causation? %B American journal of hematology %D 2006 %C United States %I John Wiley & Sons, Inc. %V 81 %N 2 %P 110-4 %@ 0361-8609 %X We report two cases of Waldenström''s macroglobulinemia with an unusual aggressive transformation following treatment with cladribine (2-chlorodeoxyadenosine, 2-CdA), a purine analogue. The first patient developed transformation to a diffuse large-cell non-Hodgkin lymphoma, while the second developed extensive extramedullary involvement. Both patients displayed rapid progression following transformation and were refractory to chemotherapy. Both patients were pretreated with multiple courses of prednisone and chlorambucil, and transformation occurred shortly after therapy with cladribine. We propose that immune suppression from alkylating agents and purine analogues may have contributed to the unusual progression, resulting in a dismal outcome. %Z FOR Codes: