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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-.

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LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].

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Gemtuzumab Ozogamicin

Last Update: March 9, 2018.



Gemtuzumab ozogamicin is a humanized monoclonal antibody conjugate which is used in the therapy of acute myelogenous leukemia. Gemtuzumab ozogamicin has been linked to transient serum enzyme elevations during therapy and not uncommon instances of acute sinusoidal obstruction syndrome which can be severe and even fatal.


Gemtuzumab (jem tooz’ ue mab) ozogamicin (oh” zoe ga mye’ sin) is a humanized monoclonal IgG4 antibody to the human CD33 cell surface marker which is highly expressed on acute myelogenous leukemia cells. The monoclonal antibody is conjugated to a cytotoxic molecule, ozogamicin. When gemtuzumab binds to CD33, it is internalized and the ozogamicin is released by the action of lysosomal enzymes on the linker molecule that joins the monoclonal antibody and cytotoxic molecule. The intracellular ozogamicin results in apoptotic cell death. This monoclonal antibody conjugate has been shown to be effective in inducing remissions in refractory acute myelogenous leukemia in patients over the age of 60 years and was given accelerated approval for this indication in the United States in 2000. A subsequent randomized controlled trial, however, showed that the mortality rate was higher with gemtuzumab ozogamicin than with conventional therapy and the monoclonal antibody conjugate was withdrawn from use in 2010. Further studies suggested that a modified dosing schedule [total of 9 mg/m2 given over days 1 and 4 or days 1, 4 and 7 was effective in prolonging event-free survival in patients with acute myelogenous leukemia and had a lower rate of severe hepatic injury than regimens using the 9 mg/m2 dose over one day. Accordingly, gemtuzumab ozogamicin was approved and reintroduced as a therapy of acute myelogenous leukemia in 2017. Gemtuzumab ozogamicin is available in powder for reconstitution in single dose vials of 4.5 mg under the brand name Mylotarg. The typical recommended dose regimen for induction is 3 mg/m2 on days 1, 4 and 7 by intravenous infusion over 2 hours. Gemtuzumab ozogamicin can be given by itself or in combination with daunorubicin and cytarabine. Doses for continuation are generally a single dose of 3 mg/meter squared with each course. Common side effects included infusion reactions with fever, nausea, chills, hypotension and shortness of breath and subsequent adverse events of neutropenia and thrombocytopenia. Less common, but serious side effects included anaphylactic reactions, severe neutropenia, infections and acute hepatic failure. Gemtumuzumab ozogamicin should be administered only by physicians with training and expertise in cancer chemotherapy and management of its potential adverse effects.


In publications on the large scale trials of gemtuzumab ozogamicin, up to half of patients had serum ALT or AST elevations during therapy which were greater than 5 times the upper limit of normal (ULN) in 10% to 16%. Hyperbilirubinemia was also common during gemtuzumab therapy. More importantly, a variable proportion (ranging from 2% to 35%) of patients developed clinically apparent sinusoidal obstruction syndrome (SOS). Symptoms of nausea, right upper quadrant pain, weight gain and abdominal distension (from ascites) arose within 5 to 20 days of the infusion and were followed by progressive rise in bilirubin, serum aminotransferase and alkaline phosphatase levels. Recent studies using lower and fractionated regimens of administration of gemtuzumab ozogamicin have reported rates of sinusoidal obstruction syndrome of 5% (6/131) compared to 0% with standard chemotherapy. In general, SOS that is severe enough to cause clinical symptoms and signs has an extremely poor prognosis, with a mortality rate as high as 70%, most patients dying of multiorgan failure. Risk factors for developing SOS after gemtuzumab ozogamicin therapy included allogenic hematopoietic cell transplantation, use of other antineoplastic agents and presence of preexisting liver disease. There are no proven means of prevention or treatment of SOS due to gemtuzumab ozogamicin, although pretreatment with ursodiol and acute management with defibrotide are often employed.

Likelihood score: A (well known cause of clinically significant liver injury, typically the result of sinusoidal obstruction syndrome).

Mechanism of Injury

The cause of the serum enzyme elevations during gemtuzumab ozogamicin therapy is not known, but it is likely due to direct toxicity of the conjugate. The propensity of gemtuzumab ozogamicin to cause sinusoidal obstruction syndrome is perhaps due to the fact that hepatic sinusoidal endothelial cells express CD33 on the cell surface and the antibody conjugate may be taken up preferentially by these cells, resulting in their damage and release of apoptotic fragments into sinusoids causing obstruction.

Outcome and Management

The serum aminotransferase elevations that occur during gemtuzumab ozogamicin therapy are generally transient, mild and asymptomatic and do not require dose modification or delay in therapy. Elevations above 5 times the upper limit of normal should lead to more careful monitoring and suspension of further infusions, at least until levels return to normal or near normal levels. Patients receiving gemtuzumab ozogamicin should be carefully monitored before, during and after each course of therapy and treatment discontinued if symptoms, signs of laboratory evidence of sinusoidal obstruction syndrome arise.

Drug Class: Antineoplastic Agents, Monoclonal Antibodies



Gemtuzumab Ozogamicin – Mylotarg®


Antineoplastic Agents


Product labeling at DailyMed, National Library of Medicine, NIH


Gemtuzumab Ozogamicin 356547-88-1 Monoclonal AntibodyNot Available


References updated: 09 March 2018

Abbreviations used: AML, acute myelogenous leukemia; SOS, sinusoidal obstruction syndrome; HCT, hematopoietic cell transplantation.

  • DeLeve LD. Gemtuzumab ozogamicin. Liver sinusoidal endothelial cells and liver injury. In, Kaplowitz N, DeLeve LD, eds. Drug-induced liver disease. 3rd ed. Amsterdam: Elsevier, 2011, pp. 142-3. (
    Review of agents that damage liver sinusoidal cells, including gemtuzumab ozogamicin, mentions that CD33 which is present on leukemic blast cells is also present on liver sinusoidal endothelial cells).
  • Chabner BA, Barnes J, Neal J, Olson E, Mujagiv H, Sequist L, Wilson W, et al. Targeted therapies: tyrosine kinase inhibitors, monoclonal antibodies, and cytokines. In, Brunton LL, Chabner BA, Knollman BC, eds. Goodman & Gilman's the pharmacological basis of therapeutics. 12th ed. New York: McGraw-Hill, 2011, pp. 1731-53.
    (Textbook of pharmacology and therapeutics).
  • Gemtuzumab for relapsed acute myeloid leukemia. Med Lett Drugs Ther 2000; 42: 67-8. [PubMed: 10908423]
    (Concise review of the mechanism of action, efficacy and safety of gemtuzumab in acute myeloid leukemia [AML]; mentions that it has been associated with hyperbilirubinemia, serum enzyme elevations and one case of hepatic failure).
  • Neumeister P, Eibl M, Zinke-Cerwenka W, Scarpatetti M, Sill H, Linkesch W. Hepatic veno-occlusive disease in two patients with relapsed acute myeloid leukemia treated with anti-CD33 calicheamicin (CMA-676) immunoconjugate. Ann Hematol 2001; 80: 119-20. [PubMed: 11261323]
    (2 patients with sinusoidal obstruction syndrome [SOS] after an initial dose of gemtuzumab ozogamicin; a 50 year old man with refractory AML developed jaundice 2 weeks after a single infusion [bilirubin 27 mg/dL], with hepatomegaly and ascites dying 2 weeks later; and, a 45 year old woman with refractory AML developed jaundice 8 days after initial infusion [bilirubin 32 mg/dL], with ascites, renal failure and death 4 weeks later).
  • Bross PF, Beitz J, Chen G, Chen XH, Duffy E, Kieffer L, Roy S, et al. Approval summary: gemtuzumab ozogamicin in relapsed acute myeloid leukemia. Clin Cancer Res 2001; 7: 1490-6. [PubMed: 11410481]
    (Review of the preclinical and clinical trials of gemtuzumab ozogamicin for refractory AML that formed the basis of its accelerated approval by the FDA, mentions that 45 of 142 patients developed severe liver test abnormalities, 12 of whom had elevations in both bilirubin and ALT).
  • Giles FJ, Kantarjian HM, Kornblau SM, Thomas DA, Garcia-Manero G, Waddelow TA, David CL, et al. Mylotarg (gemtuzumab ozogamicin) therapy is associated with hepatic venoocclusive disease in patients who have not received stem cell transplantation. Cancer 2001; 92: 406-13. [PubMed: 11466696]
    (Among 119 patients with AML treated with gemtuzumab ozogamicin, 14 [12%] developed SOS with abrupt onset of weight gain, abdominal distension and pain [bilirubin 2.2-33.6 mg/dL, peak ALT 43-1789 U/L], being a major cause of death in 5, and probably contributory in 3 and possibly in 4 more patients).
  • Tack DK, Letendre L, Kamath PS, Tefferi A. Development of hepatic veno-occlusive disease after Mylotarg infusion for relapsed acute myeloid leukemia. Bone Marrow Transplant 2001; 28: 895-7. [PubMed: 11781652]
    (67 year old woman with refractory AML after hematopoietic cell transplanation [HCT] developed SOS arising 6 days after intravenous gemtuzumab ozogamicin, with ascites and jaundice [peak bilirubin 15.8 mg/dL]).
  • Gordon LI. Gemtuzumab Ozogamicin (Mylotarg) and hepatic veno-occlusive disease: take two acetaminophen, and... Bone Marrow Transplant 2001; 28: 811-2. [PubMed: 11781639]
    (Editorial in response to Tack [2001] reviewing the pathogenesis of SOS and the possible role of free radicals and potential for acetaminophen to contribute to the injury).
  • Rajvanshi P, Shulman HM, Sievers EL, McDonald GB. Hepatic sinusoidal obstruction after gemtuzumab ozogamicin (Mylotarg) therapy. Blood 2002; 99: 2310-4. [PubMed: 11895761]
    (Among 23 patients with relapsed, refractory AML treated with gemtuzumab ozogamicin, liver injury suggestive of SOS developed in 11, 7 of whom died of hepatic failure 8 to 47 days after the infusion).
  • Leopold LH, Berger MS, Feingold J. Acute and long-term toxicities associated with gemtuzumab ozogamicin (Mylotarg) therapy of acute myeloid leukemia. Clin Lymphoma 2002; 2 Suppl 1: S29-34. [PubMed: 11970768]
    (Review of adverse side effects of gemtuzumab ozogamicin therapy mentions mild ALT and AST [Grade 1 and 2] elevations in 26% and elevations ≥5 times ULN in 16% and clinically apparent SOS in 2-12% of patients, risk factors for this complication being HCT, concurrent cytotoxic therapies, higher and more frequent doses and underlying liver disease).
  • McDonald GB. Management of hepatic sinusoidal obstruction syndrome following treatment with gemtuzumab ozogamicin (Mylotarg). Clin Lymphoma 2002; 2 Suppl 1: S35-9. [PubMed: 11970769]
    (Review of management of SOS).
  • Giles F, Garcia-Manero G, Cortes J, Thomas D, Kantarjian H, Estey E. Ursodiol does not prevent hepatic venoocclusive disease associated with Mylotarg therapy. Haematologica 2002; 87: 1114-6. [PubMed: 12368170]
    (Among 85 patients with refractory AML or myelodysplastic syndromes treated with gemtuzumab ozogamicin and given ursodiol starting the day before infusion and continuing for 21 days, ten [12%] developed SOS, a rate similar to that reported before use of ursodiol [Giles 2001]).
  • O'Boyle KP, Murigeppa A, Jain D, Dauber L, Dutcher JP, Wiernik PH. Probable veno-occlusive disease after treatment with gemtuzumab ozogamicin in a patient with acute myeloid leukemia and a history of liver transplantation for familial hemochromatosis. Med Oncol 2003; 20: 379-84. [PubMed: 14716035]
    (69 year old man with a history of liver transplantation and AML developed rising AST and bilirubin levels 7 days and died 13 days after an infusion of gemtuzumab ozogamicin).
  • Nabhan C, Rundhaugen L, Jatoi M, Riley MB, Boehlke L, Peterson LC, Tallman MS. Gemtuzumab ozogamicin (MylotargTM) is infrequently associated with sinusoidal obstructive syndrome/veno-occlusive disease. Ann Oncol 2004; 15: 1231-6. [PubMed: 15277263]
    (Among 47 patients with AML treated with gemtuzumab as a single agent, 23 [48%] had elevation of liver tests, but only one [2%] developed clinically apparent SOS).
  • Amadori S, Suciu S, Willemze R, Mandelli F, Selleslag D, Stauder R, Ho A, et al.; EORTC leukemia group; GIMEMA leukemia group. Sequential administration of gemtuzumab ozogamicin and conventional chemotherapy as first line therapy in elderly patients with acute myeloid leukemia: a phase II study (AML-15) of the EORTC and GIMEMA leukemia groups. Haematologica 2004; 89: 950-6. [PubMed: 15339678]
    (Among 57 patients with AML treated with gemtuzumab ozogamicin on days 1 and 15, severe myelosuppression was universal and SOS occurred in 3, which was fatal in 2 patients).
  • Perry R, Penk Kapoor N, Shah AJ, Kapoor N, Shah AJ. Gemtuzumab ozogamicin exposure and portal fibrosis. Pediatr Blood Cancer 2005; 45: 82-3. [PubMed: 15880448]
    (An 8 year old girl and 5 year old boy with acute leukemia developed clinical evidence of SOS after several courses of gemtuzumab ozogamicin therapy, and liver biopsies showed periportal fibrosis).
  • Arceci RJ, Sande J, Lange B, Shannon K, Franklin J, Hutchinson R, Vik TA, et al. Safety and efficacy of gemtuzumab ozogamicin in pediatric patients with advanced CD33+ acute myeloid leukemia. Blood 2005; 106: 1183-8. [PubMed: 15886328]
    (Among 29 children with relapsed or refractory AML treated with gemtuzumab ozogamicin, 21% developed ALT or AST elevations and one SOS).
  • Larson RA, Sievers EL, Stadtmauer EA, Löwenberg B, Estey EH, Dombret H, Theobald M, et al. Final report of the efficacy and safety of gemtuzumab ozogamicin (Mylotarg) in patients with CD33-positive acute myeloid leukemia in first recurrence. Cancer 2005; 104: 1442-52. [PubMed: 16116598]
    (277 patients with relapsed AML treated with gemtuzumab ozogamicin, 28% developed ALT levels ≥5 times ULN and 29% bilirubin levels ≥3 times ULN and 0.9% SOS).
  • Lannoy D, Decaudin B, Grozieux de Laguérenne A, Barrier F, Pignon JM, Wetterwald M, et al. Gemtuzumab ozogamicin-induced sinusoidal obstructive syndrome treated with defibrotide: a case report. J Clin Pharm Ther 2006; 31: 389-92. [PubMed: 16882110]
    (65 year old man with AML treated with gemtuzumab ozogamicin developed SOS 23 days after the first dose and died of multiorgan failure several weeks later).
  • McKoy JM, Angelotta C, Bennett CL, Tallman MS, Wadleigh M, Evens AM, Kuzel TM, et al. Gemtuzumab ozogamicin-associated sinusoidal obstructive syndrome (SOS): an overview from the research on adverse drug events and reports (RADAR) project. Leuk Res 2007; 31: 599-604. [PubMed: 16959316]
    (Analysis of the FDAs Medwatch database revealed 99 reports of SOS in adult and 6 in pediatric patients treated with gemtuzumab ozogamicin; review of clinical trials and observational studied found highest rates of SOS [14-40%] in patients who underwent HCT within 3 months of receiving gemtuzumab or who received concurrent chemotherapy with potentially hepatotoxic agents).
  • Maradei SC, Maiolino A, de Azevedo AM, Colares M, Bouzas LF, Nucci M. Serum ferritin as risk factor for sinusoidal obstruction syndrome of the liver in patients undergoing hematopoietic stem cell transplantation. Blood 2009; 114: 1270-5. [PubMed: 19401560]
    (Among 427 patients undergoing HCT, 88 [21%] developed SOS of whom 57 [65%] died; risk factors being allogenic HCT [33%], receipt of imatinib [52%], busulfan [39%], and ferritin above 2000 ng/mL [34%]; only one patient received gemtuzumab).
  • Zwaan CM, Reinhardt D, Zimmerman M, Hasle H, Stary J, Stark B, Dworzak M, et al.; International BFM Study Group on Paediatric AML. Salvage treatment for children with refractory first or second relapse of acute myeloid leukaemia with gemtuzumab ozogamicin: results of a phase II study. Br J Haematol 2010; 148: 768-76. [PubMed: 19995399]
    (Among 30 children with refractory or relapsing AML treated with gemtuzumab ozogamicin, "treatment was generally well tolerated", only 19 [63%] had ALT or AST elevations which were ≥5 times ULN in 2 [7%], and none developed SOS).
  • Chevallier P, Prebet T, Turlure P, Hunault M, Vigouroux S, Harousseau JL, Blaise D, et al. Prior treatment with gemtuzumab ozogamicin and the risk of veno-occlusive disease after allogeneic haematopoietic stem cell transplantation. Bone Marrow Transplant 2010; 45: 165-70. [PubMed: 19584826]
    (Among 44 adults with AML treated with allogenic HCT and gemtuzumab ozogamicin, 3 [7%] developed SOS).
  • Löwenberg B, Beck J, Graux C, van Putten W, Schouten HC, Verdonck LF, Ferrant A, et al.; Dutch-Belgian Hemato-Oncology Cooperative Group (HOVON); German Austrian AML Study Group (AMLSG); Swiss Group for Clinical Cancer Research Collaborative Group (SAKK). Gemtuzumab ozogamicin as postremission treatment in AML at 60 years of age or more: results of a multicenter phase 3 study. Blood 2010; 115: 2586-91. [PubMed: 20103782]
    (Randomized trial of gemtuzumab ozogamicin vs placebo in patients with AML after remission, found overall survival was not improved by the monoclonal conjugate [17% vs 16% at 5 years] and 17% had moderate-to-severe hepatic side effects, one patient dying of SOS during the first course of therapy).
  • Reuben A, Koch DG, Lee WM; Acute Liver Failure Study Group. Drug-induced acute liver failure: results of a U.S. multicenter, prospective study. Hepatology 2010; 52: 2065-76. [PMC free article: PMC3992250] [PubMed: 20949552]
    (Among 1198 patients with acute liver failure enrolled in a US prospective study between 1998 and 2007, 133 were attributed to drug induced liver injury, including 2 attributed to antineoplastic agents, 1 due to melphalan and 1 to gemtuzumab ozogamicin).
  • Maniecki MB, Hasle H, Bendix K, Møller HJ. Is hepatotoxicity in patients treated with gemtuzumab ozogamicin due to specific targeting of hepatocytes? Leuk Res 2011; 35: e84-6. [PubMed: 21329979]
    (Immunohistochemical staining of liver tissue showed that both hepatocytes and macrophages [Kupffer cells] express CD33).
  • Malfuson JV, Konopacki J, Thepenier C, Eddou H, Foissaud V, de Revel T. Fractionated doses of gemtuzumab ozogamicin combined with 3 + 7 induction chemotherapy as salvage treatment for young patients with acute myeloid leukemia in first relapse. Ann Hematol 2012; 91: 1871-7. [PubMed: 22820971]
    (Among 14 patients with relapsed AML treated with fractionated doses of gemtuzumab ozogamicin [days 1, 4 and 7: 3 mg/m2 ], 11 had a response and underwent HCT, of whom 4 subsequently developed nonfatal SOS, all resolving with conservative management).
  • Castaigne S, Pautas C, Terré C, Raffoux E, Bordessoule D, Bastie JN, Legrand O, et al.; Acute Leukemia French Association. Effect of gemtuzumab ozogamicin on survival of adult patients with de-novo acute myeloid leukaemia (ALFA-0701): a randomised, open-label, phase 3 study. Lancet 2012; 379 (9825): 1508-16. [PubMed: 22482940]
    (Among 280 patients with previously untreated AML given standard chemotherapy with or without gemtuzumab ozogamicin, grade 3 hepatic adverse events occurred in 6% of standard vs 13% of gemtuzumab treated subjects and SOS occurred in 3 subjects, being fatal in 2).
  • Iacobucci I, Lonetti A, Candoni A, Sazzini M, Papayannidis C, Formica S, Ottaviani E, et al. Profiling of drug-metabolizing enzymes/transporters in CD33+ acute myeloid leukemia patients treated with gemtuzumab-ozogamicin and fludarabine, cytarabine and idarubicin. Pharmacogenomics J 2013; 13: 335-41. [PubMed: 22584460]
    (Analysis of 1931 single nucleotide variants in 225 drug metabolizing enzyme or transporter genes in 95 patients with AML undergoing chemotherapy with gemtuzumab ozogamicin combined with other agents identified several variants associated with a higher or lower risk of hepatotoxicity).
  • Amadori S, Suciu S, Stasi R, Salih HR, Selleslag D, Muus P, De Fabritiis P, et al. Sequential combination of gemtuzumab ozogamicin and standard chemotherapy in older patients with newly diagnosed acute myeloid leukemia: results of a randomized phase III trial by the EORTC and GIMEMA consortium (AML-17). J Clin Oncol 2013; 31: 4424-30. [PubMed: 24127442]
    (Among 472 patients with AML, addition of a course of gemtuzumab ozogamicin before standard chemotherapy resulted in no improvement in overall response rates, but was associated with higher early mortality some of which was due to SOS).
  • Kharfan-Dabaja MA, Hamadani M, Reljic T, Pyngolil R, Komrokji RS, Lancet JE, Fernandez HF, et al. Gemtuzumab ozogamicin for treatment of newly diagnosed acute myeloid leukaemia: a systematic review and meta-analysis. Br J Haemato 2013; 163: 315-25. [PubMed: 24033280]
    (Systematic review and metaanalysis of 7 controlled trials of gemtuzumab ozogamicin in 3942 patients found no increase in overall survival and a higher rate of early mortality [relative risk, RR =1.6] and SOS [RR=7.7]).
  • Tallman MS, McDonald GB, DeLeve LD, Baer MR, Cook MN, Graepel GJ, Kollmer C. Incidence of sinusoidal obstruction syndrome following Mylotarg(gemtuzumab ozogamicin): a prospective observational study of 482 patients in routine clinical practice. Int J Hematol 2013; 97: 456-64. [PubMed: 23460018]
    (Among 482 patients with AML treated with gemtuzumab ozogamicin in multiple clinical practices, 44 [9%] developed SOS of whom 13 [3%] died of resultant multiorgan failure).
  • de Witte T, Suciu S, Meert L, Halkes C, Selleslag D, Bron D, Amadori S, et al. Idarubicin and cytarabine in combination with gemtuzumab ozogamicin (IAGO) for untreated patients with high-risk MDS or AML evolved from MDS: a phase II study from the EORTC and GIMEMA Leukemia Groups (protocol 06013). Ann Hematol 2015; 94: 981-9. [PMC free article: PMC4604495] [PubMed: 26410352]
    (Among 30 patients with high risk myelodysplastic syndromes or AML treated with idarubicin, cytarabine and gemtuzumab ozogamicin [one dose, 5 mg/m2 ], ALT elevations above 5 times ULN arose in 16 [53%] and one patient had nonfatal SOS).
  • Koren-Michowitz M, Maayan H, Apel A, Shem-Tov N, Yerushalmi R, Volchek Y, Avigdor A, et al. Salvage therapy with ARA-C and gemtuzumab ozogamicin in AML patients relapsing after stem cell transplantation. Ann Hematol 2015; 94: 375-8. [PubMed: 25307457]
    (Among 16 patients with AML who relapsed after HCT and were treated with cytarabine and gemtuzumab ozogamicin, serum enzyme elevations occurred in 80% and were above 5 times ULN in 27%, with mild SOS occurring in 3 subjects after repeat HCT).
  • Chalasani N, Bonkovsky HL, Fontana R, Lee W, Stolz A, Talwalkar J, Reddy KR, et al.; United States Drug Induced Liver Injury Network. Features and outcomes of 899 patients with drug-induced liver injury: The DILIN Prospective Study. Gastroenterology 2015; 148: 1340-52.e7. PubMed Citation (Among 899 cases of drug induced liver injury enrolled in a US prospective study between 2004 and 2013, 49 [5.5%] were attributed to antineoplastic agents, but none were linked to use of gemtuzumab ozogamicin).
  • Battipaglia G, Labopin M, Candoni A, Fanin R, El Cheikh J, Blaise D, Michallet M, et al. Risk of sinusoidal obstruction syndrome in allogeneic stem cell transplantation after prior gemtuzumab ozogamicin treatment: a retrospective study from the Acute Leukemia Working Party of the EBMT. Bone Marrow Transplant 2017; 52: 592-9. [PubMed: 28092357]
    (Among 146 adults with AML who received gemtuzumab ozogamicin and underwent HCT, 11 [8%] developed SOS which was fatal in 3 [2%]).


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