Acute Myelomonoblastic Leukemia Research Articles

Acute myelomonoblastic leukemia in children, the particularities of extramedullary infiltration based on a clinical case

Childhood acute myeloidleukemia (AML) represents approximately 5% of childhood malignancies and 15% to 25% of pediatric acute leukemia. The extramedullary manifestation of infiltrating clonal blast populations in a variety of organs and tissues in acute myeloid leukemia (AML) is defined as a distinct entity in the 2016 WHO classification of myeloid neoplasms, myeloid sarcoma The rate of complete remission after induction chemotherapy was lower in patients with extramedullary infiltration, overall survival and event-free survival were not different between patients with and without extramedullary infiltration. Purpose of the study: Presentation of a clinical case of ALM type M4 with the presence of an extramedullary infiltrate in the tissue of the central nervous system in children. Materials and methods: The clinical, paraclinical, imaging data of the patient were studied in parallel with the specialized literature on similar cases. Results: Boy, 5 years old, goes to the doctor with accusations of bilateral palpebral edema, bilateral temporal region edema and bilateral exophthalmos , more pronounced on the left. In the general analysis of the blood: - Hemoglobin - 89 g/l , Leukocytes - 7.2 x 10^9/l; unsegmented neutrophil - 1%; segmented - 18%; lymphocytes - 44%; monocytes - 20%; blast cells - 16%; Platelets - 70 x 10^9/l;VSH - 44 mm/h. During the physical examination: the peripheral lymph nodes are palpable. No signs of central nervous system damage. It is supposed the diagnosis: Acute myeloid leukemia, sarcoma, or neuroblastoma. A medullary puncture: moderately cellular marrow was determined, with blastcells 15.2%. Morphologically, it is more similar to acute myelo-monoblastic leukemia FAB-M4. Computerized Tomography-multiple, hyperdense pathological foci, with localization with inand bilateral extraorbital, associated with exophthalmos. The formation from the sphenoid sinus extends to the nasopharynx , through the pterygopalatine fossa, with narrowing of the lumen and mass effect on the palatine tonsils. Immunophenotyping: CD45-/+ SS low 8% population, CD36+ 6%CD64+ monoblasts 8%, Promonocytes /monocytes – (CD64+/CD14+) 25%.He underwent treatment according to the AML BFM 2004 program with numerous complications, andcranial radiotherapy. At the moment, the child is in morphological remission. Conclusions. The differential diagnosis of hyperdense intracranial masses may include neuroblastoma, meningioma, lymphoma, metastases, or sarcomas. Correct and early diagnosis and initiation of specific treatment are essential to increase the survival rate in cases of acute leukemia in children.

Диагностика острых лейкозов

Over the past 10 years, the dynamics of the incidence of hemoblastosis has been noticeable, as well as an increase in mortality rate in patients with hemoblastosis. The basis of the practical research was the cases of leukemia diagnostics carried out from 2017 to 2018 on the basis of the Department of Hematology and Chemotherapy, the Department of Laboratory Diagnostics and the Laboratory of Clinical Immunology of Khabarovsk Krai Clinical Hospital No.1. During 2018, 53 cases of acute leukemia (primary diagnosed cases) were detected, which is 10.4 % more compared to 2017. The share of AML (acute myeloid leukemia) is 53 %, ALL (acute lymphoblastic leukemia) – 26 %, undifferentiated leukemia – 11 %, AMML (acute myelomonoblastic leukemia) – 8 %, APL (acute promyelocytic leukemia) – 2 %. In the diagnosis of acute leukemia, a comprehensive study is needed, including a complete blood count, cytological examination of the bone marrow, cytochemical examinations and immunophenotyping.

ИССЛЕДОВАНИЕ СРЕДНЕГО ВОЗРАСТА ВОЗНИКНОВЕНИЯ ГЕННЫХ МУТАЦИЙ ПРИ ОСТРОМ МИЕЛОМОНОБЛАСТНОМ ЛЕЙКОЗЕ

Aim: to determine the average age of occurrence of gene mutations in acute myelomonoblastic leukemia (AMML). Materials and methods. Bone marrow and peripheral blood samples from 40 patients (average age 50 years, including 13 aged 15 to 45 years, 15 aged 45-60 years, 12 aged over 60 years) with newly detected AMML were examined. Detection of chromosomal abnormalities was performed using standard cytogenetic and real-time polymerase chain reaction methods. Point mutations were screened in 8 genes: FLT3 (n=35), NPM1 (n=25), TP53 (n=24), C-KIT (n=23), NRAS (n=19), WT1 (n=18), DNMT3A (n=13), and KRAS (n=4) by direct automatic sequencing method. Results. The majority of patients (56.3%) had a normal karyotype, 15.6% had aneuploid karyotype, and 28.1% had other structural and quantitative chromosome abnormalities. 35.0% of patients had point mutations in the studied genes at the time of diagnosis of OMML. The highest mutation rates were found for the DNMT3A (30.8%), NPM1 (20.0%), and FLT3 (20.0%) genes. The frequency of double mutants was 15.2%. The average age of detection of mutations in the c-KIT and NPM1 genes corresponded to young adults (33.5±2.9 and 44.2±11.4, respectively), for 3 genes — to middle age (DNMT3A — 49.3±18.4; WT1 — 51.0; FLT3 — 54.0±12.3), for the TP53 gene — to the elderly (n=1, 63 years). The average age of double mutants was 42.2±13.7 years due to NPM1 and c-KIT co-mutations.

Особенности формирования онкогематологических заболеваний в отдаленные сроки после перенесенной острой лучевой болезни

Purpose: To clarify the frequency, nosological forms, the timing of development and the features of the clinical course of developed oncohematological diseases on the basis of a retrospective analysis of the results of long-term follow-up of patients who underwent acute radiation syndrome (ARS).
 Material and methods: An analysis of clinical histories from archives of A.I. Burnasyan Federal Medical Biophysical Center of 157 patients who underwent ARS of varying severity, and some scientific publications. Various oncohematological diseases developed in the long-term period in 8 patients with ARS I–III severity: in 5 patients – myelodysplastic syndromes (MDS), in 2 – chronic myeloid leukemia (CML) and in 1 – acute myelomonoblastic leukemia (OMML).
 Results: The excess absolute risk of developing MDS and leukemia in the group is 7.2×10–4 man-years/Gy. All patients underwent relatively uniform irradiation. MDS developed in 5 patients who underwent ARS as a result of a single acute gamma-beta- and gamma-neutron irradiation at doses of 1.2–5.0 Gy. Nosological forms of MDS: with unilinear dysplasia, with multilinear dysplasia (2 cases), with ringed sideroblasts, with excess blasts. The latency period lasted from 3 to 31 years. Age at the time of irradiation was 28–55 years. CML, Ph-positive form, was detected in 2 patients. Doses of gamma-beta-radiation were 2.0 and 4.3 Gy. Age of patients at the time of irradiation was 22 and 25 years. Diseases developed 3 and 15 years after the undergone ARS and were characterized by a long period of inactive phase (10 and 7 years), which resulted in a blast crisis. OMML in the patient, who suffered during the Chernobyl accident and since 1990 was observed in the URCRM, developed 11.8 years after irradiation at a dose of 3.0 Gy. An analysis of available clinical data makes it possible to question the diagnosis of acute leukemia, and to suppose that chronic myelomonocytic leukemia developed in this patient.
 Conclusion: The obtained data indicate that chronic leukemia forms are characteristic for radiation leukemia, often with a long preceding cytopenic stage (MDS). An essential factor in the realization of the leukemogenic effect is the uniformity of the whole body exposure undoubtedly. In addition, it can’t be ruled out that the carriage of hepatitis B and C viruses also played a role in the formation of MDS.

LINEAGE SWITCH LEUKEMIA LIMFOBLASTIK AKUT MENJADI LEUKEMIA MIELOMONOSITIK AKUT PADA PEREMPUAN USIA 26 TAHUN (Lineage Switch From Acute Lymphoblastic Leukemia To Acute Myelomonocytic Leukemia at A 26 Years Old Woman)

A lineage switch from Acute Lymphoblastic Leukemia (ALL) to Acute Myeloid Leukemia (AML) is very rare. It was estimated between6− 9% of cases that occurred, especially lineage switch from ALL to Acute Myelomonoblastic Leukemia (AMMOL). The reviewers reporta case of a 26 years old women with the first clinical presentation were fever and double visions and diagnosed as B-Acute lymphoblasticleukemia ALL with CD13 and CD33 expression aberrations, based on Bone Marrow Aspiration (BMA) and immunoprephenotyping inHongkong Hospital. After induction therapy, in the second month, BMA was done and found 10% blast, so it couldn't be assessed ascomplete remission. After two (2) months, she comes back to Indonesia to follow continuing the treatment. She was suffered from severeheadache and blurred vision. The blast cell morphology of BMA showed myeloblast 25% and monoblast 60%, consistent with the diagnosisof AMMOL. Moreover, both findings were quite specific for each common cell ALL and acute myelomonocytic leukemia. These findingssupport that this case is completely different leukemic clones occurred at each leukemic expression. Exogenic factor such as chemotherapyand endogenic factor due to chromosomal abnormalities is supposed to be the cause of this lineage switch during the treatment.

Iron Overload in Two Children after Allogeneic Hematopoietic SCT with Concomitant HFE p.s65cgene Mutation

Acute Myelomonoblastic Leukaemia (ANLL M4) and Aplastic Anemia (AA) are rare childhood diseases. Treatment of ANLL involves chemotherapy and radiotherapy, while immunosuppressive therapy is used in the treatment of AA. In selected cases, both disorders can be treated by performing a Hematopoietic Stem Cell Transplantation (HSCT). In addition, supportive medical care which includes antibiotics, antifungal drugs, packed red cells and platelets, is usually essential due to adverse effects caused by the therapy. Herein, we present a 15- year- old boy with ANLL M4 and a 17- year- old girl suffering from Severe Aplastic Anemia (SAA) for 3 and 4 years respectively, in whom iron overload was noted after they had undergone allogeneic HSCT (allo HSCT). On further diagnosis, co-existence of S65C HFE gene carriage was identified in both of them.

Efusi Perikard Hemoragik pada Penderita Leukimia Mielo-Monoblastik Akut

A case of a 23 year-old man with haemorrhagic pericardial effusion has been reported. The man came to the hospital due to chest pain, shortness of breath and fever for 5 days. A pericardial effusion was suggested by observing ECG and chest X-ray, later it was proved by echocardiography. Pericardiocentesis was performed, and 650 cc of haemorrhagic fluid was taken out; his condition improved dramatically. Acute leukemia has been suggested as the cause, due to high level of White Blood Count. Diagnosis of Acute Myelomonoblastic Leukemia (AML) was confirmed by peripheral blood stain and bone marrow aspiration examination. From patient’s history, physical examination, and other tests, no other diseases could suspected as the cause of this hemorrhagic pericardial effusion. Chemotherapy of daunorubicin and cytosine-arabinoside was planned for the treatment, but the patient rejected. He was discharged in relatively good condition although the prognosis is still bad.

Clinical Case of Acute Myeloblastic Leukemia with t(8;21)(q22;q22) in a Patient with Klinefelter’s Syndrome

Klinefelter's syndrome is characterized by abnormal karyotype 47, XXY and a phenotype associated with hypogonadism and gynecomastia. Often the disease can be diagnosed accidentally, when carrying out cytogenetic analysis in cases of a malignant blood disease. We present the clinical case of a patient diagnosed with acute myelomonoblastic leukemia-M4 Eo (AML- M4), where by means of classic cytogenetics a karyotype was found corresponding to Klinefelter's syndrome. Three induction courses of polychemotherapy wermade, which led to remission of the disease, documented both flowcytometrically and cytogenetically.

Isolated Recurrence of Intracranial Granulocytic Sarcoma Mimicking a Falx Meningioma in Acute Myeloblastic Leukemia

Intracranial granulocytic sarcomas are rare tumors, which are composed of immature granulocytic cells. Although it has been well known that these tumors are associated with acute myeloblastic leukemia (AML), they have been almost always related to bone marrow relapse. However, isolated recurrence of granulocytic sarcoma following complete remission from prior AML is extremely rare, especially in the central nervous system. A 44-year-old male presented with isolated recurrence of granulocytic sarcoma mimicking a falx meningioma two years after complete remission by allogenic peripheral blood stem cell transfusion (PBSCT) in the acute myelomonoblastic leukemia (FAB, M4). Because of depressed mental state and mass effect, total surgical resection was performed. Pathological findings were compatible with the granulocytic sarcoma. There was no evidence of leukemic relapse in the peripheral blood. We suggest that this phenomenon can be explained by the hypothesis that a certain barrier effect such as blood brain barrier might lead to the proliferation of intracranial leukemic cells which metastasized before PBSCT.

Long-term propylthiouracil use and acute myeloid leukemia: A case report and review of the literature

Dear Editor, We report a 31-year-old female who had been administered propylthiouracil for 15 years and shortly after delivery developed acute myeloid leukemia with complex karyotype, including a rare t(2;21) translocation. We discuss here the potential mechanisms by which this drug could have contributed to leukemia and review the literature for propylthiouracil-related hematological disorders. Acute Myeloid Leukemia (AML) has very few welldefined chemical triggers. Chronic drug use has been associated with increased AML risk, but no definitive evidence is available yet. Many drugs have in vitro leukemogenicity, and for some of them, literature exists reporting causal association with AML in patients. Thionamide-type thyroid peroxidase inhibitors are commonly used to treat primary hyperthyroidism. Despite the fact that methimazole (MMI) is the drug of choice, many patients develop side effects such as hepatitis, cholestatic jaundice, splenomegaly, and lupus-like syndrome, in addition to mild and common side effects like granulocytopenia, pruritus, urticaria, and maculopapular or papular eruption [1], so that they are then shifted to the older drug of this class, 6-n-propylthiouracil (PTU), originally used as a measure of taste genetics. In addition, in comparison with MMI, PTU has a shorter duration of action and has significantly less transfer across the placenta and into breast milk, making PTU the preferred antithyroid agent for pregnant women. PTU can induce antigranulocyte cytoplasm antibodies [2, 3], as well as antinuclear antibodies [4]. Since its approval by the Food and Drug Administration in 1947, PTU has been associated with many hematological adverse events [5], including granulocytopenia, agranulocytosis [6], and eosinophilia [7]. Thionamides resemble the methyltetrazole-thiol leaving group of certain cephalosporin antibiotics, and both thionamides and cephalosporins have been found to inhibit the vitamin-K-dependent gamma-carboxylation of glutamic acid in vitro [8]: actually, PTU has been associated with hypoprothrombinemia [9], disseminated intravascular coagulation [10], and acute thrombocytopenic purpura [11]. Most importantly, PTU has been associated with bone marrow aplasia [12, 13] and AML [14, 15]. AML itself is favored by immunosuppression. We report here on a patient who had been on PTU for 15 years and who developed AML shortly after delivery. A previously healthy, 31-year-old female was admitted at our division because of sudden onset of ecchymoses and a complete blood count showing leukocytosis and thrombocytopenia. A peripheral blood smear suggestive for AML was confirmed by bone marrow aspiration and trephine biopsies. Immunohistochemistry and immunophenotyping showed acute myelomonoblastic leukemia (FAB M4). Cytogenetics on bone marrow leukocytes showed a complex karyotype with two abnormal clones, one with t(2;21) and another with both t(3;16) and del8p. At past medical history, she reported only having been diagnosed with primary hyperthyroidism at age 16, which was initially treated with MMI. Because of drug intolerance, she was then shifted to PTU 25 mg daily po, a drug that she took for 15 years before AML diagnosis. At that time, she had just been pregnant, having an uncomplicated delivery 4 months before the onset of AML. Ann Hematol (2008) 87:233–235 DOI 10.1007/s00277-007-0369-4

Therapy‐related acute myeloid leukemia in a child with Noonan syndrome and clonal duplication of the germline PTPN11 mutation

A 4-year-old girl with Noonan syndrome (NS) and constitutive PTPN11 mutation presented with stage 4 neuroblastoma and was treated by intensive chemotherapy. During the treatment, cytogenetic analysis revealed the development of a hyperdiploid clone with duplication of the germline PTPN11 mutation in a morphologically normal bone marrow. A few months later, the patient developed acute myelomonoblastic leukemia with an additional clonal deletion of 7q. Although, we cannot conclude whether there is an association between NS and neuroblastoma, this case suggests that duplication of germline PTPN11 mutations, potentially induced by chemotherapy, contributes to leukemogenesis in patients with NS.

Rearrangement of the MLL gene in acute myeloblastic leukemia: report of two rare translocations

Band 11q23 is known to be involved in translocations and insertions with a variety of partner chromosomes. They lead to MLL rearrangement, resulting in a fusion with numerous genes. We report here 2 male adults in whom a diagnosis of acute myelomonoblastic leukemia (FAB M4) and acute monoblastic leukemia (FAB M5) was made. Conventional cytogenetic techniques showed a 45,XY,t(1;11)(p32;q23),-7 karyotype in the first case and a 46,XY, t(11;17)(q23;q21) in the second case. Fluorescent in situ hybridization (FISH) with a specific MLL probe showed the gene to be disrupted, the 3′ region being translocated on the derivative chromosomes 1 and 17, respectively. Fourteen and 24 patients, including ours, with acute myeloblastic leukemia associated with a t(1;11)(p32;q23) and a t(11;17)(q23;q21), respectively have been reported in the literature. Several patients with the latter translocation have also been identified to have acute lymphoblastic leukemia (ALL). Although both translocations are preferentially associated with monocytic differentiation, the t(11;17)(q23;q21) is more common in adults and has been reported in many patients with ALL, compared to the t(1;11)(p32;q23).

Recent Advances in the Treatment of Infant Acute Myeloid Leukemia

Infant acute myeloid leukemia (AML) of less than 12 months old is generally characterized by a high incidence of acute monoblastic or myelomonoblastic leukemia with hyperleukocytosis and extramedullary involvement. Most of the leukemic cells have 11q23 translocations, which lead to the MLL gene rearrangements. The MLL gene rearrangements occur at a high frequency in monoblastic subtype, hyperleukocytosis or young age in infant AML. Compared with acute lymphoblastic leukemia, however, it remains unknown whether prenatal origin exists in the pathogenesis of infant AML. Recently, the treatment outcome of infant AML has been clarified by two study groups, which confirmed the effect of intensive chemotherapy including repeated cycles of cytarabine and anthracyclines for infant AML. Presence of the MLL gene rearrangements, gender, age and white blood cell count showed no influence on the outcome of infant AML. The allogeneic hematopoietic stem cell transplantation (HSCT) remains the treatment of choice for infant AML when a matched related donor is available. Monitoring of minimal residual disease by real-time PCR is a useful technique to predict the outcome or efficacy of the treatment in infant AML. Although intensive chemotherapy and/or allogeneic HSCT have cured most AML infants, some still relapse and ultimately die. A need remains for future development by exploiting the unusual biologic properties of leukemic progenitor cells expressing the abnormal MLL gene product.

Secondary Leukemia Associated With a Conventional Dose of Etoposide: Review of Serial Germ Cell Tumor Protocols

Case reports have suggested that treatment with high-dose etoposide can result in development of a unique secondary leukemia. This study was designed to estimate the risk of developing leukemia for patients receiving conventional doses of etoposide along with cisplatin and bleomycin. We reviewed the records at Indiana University of all untreated patients entering clinical trials using etoposide at conventional doses (cumulative dose, 2000 mg/m2 or less) for germ cell cancer between 1982 and 1991. The records of all patients who received a chemotherapy regimen containing etoposide, ifosfamide, or cisplatin after failing to respond to primary chemotherapy were also reviewed. Between 1982 and 1991, 538 patients entered serial clinical trials with planned cumulative etoposide doses of 1500-2000 mg/m2 in combination with cisplatin plus either ifosfamide or bleomycin. Of these 538 patients, 348 received an etoposide combination as initial chemotherapy and 190 received etoposide as part of salvage treatment. To date, 315 patients are alive, with median follow-up of 4.9 years, and 337 patients have had follow-up beyond 2 years. Two patients (0.37%) developed leukemia. One developed acute undifferentiated leukemia with a t(4;11) (q21;q23) cytogenetic abnormality 2.0 years after starting etoposide-based therapy, and one developed acute myelomonoblastic leukemia with no chromosome abnormalities 2.3 years after beginning chemotherapy. During this period, several hundred patients were treated with etoposide-based chemotherapy and did not enter clinical trials. Three of these patients are known to have developed hematologic abnormalities, including one patient with acute monoblastic leukemia with a t(11;19)(q13;p13) abnormality. Secondary leukemia after treatment with a conventional dose of etoposide does occur, but the low incidence does not alter the risk-to-benefit ratio of etoposide-based chemotherapy in germ cell cancer. The reports of leukemia associated with high doses of etoposide emphasize the need for diligent follow-up of patients and make careful risk-to-benefit analysis imperative.

Relationship Between Acute Myelomonoblastic Leukemia and Infection Due to Human Immunodeficiency Virus

Infection due to the human immunodeficiency virus (HIV) has been complicated by the development of acute nonlymphocytic leukemia in five patients whose cases have previously been reported; other manifestations, including preleukemia, myelofibrosis, and myeloid hyperplasia, have also been reported in patients infected with HIV. We report the sixth case of an HIV-infected patient who developed acute myelomonocytic leukemia; HIV infection was documented by tests for serum antibodies (enzyme-linked immunosorbent assay and western blotting), by a markedly elevated p24 antigen level in plasma, and by cultures of CSF and peripheral blood that were positive for HIV. Furthermore, myelomonoblasts that were cultured without the addition of growth factors displayed evidence of HIV replication through the presence of p24 antigen and reverse transcriptase activity, both of which lasted for 4 weeks in the supernatant fluid of the cell cultures. This case report provides the first data indicating that HIV may infect myelomonoblasts in vivo and represents the sixth reported case of an association between HIV infection and pure acute nonlymphocytic leukemia.

Recurrent acute myelomonoblastic leukaemia presenting as a red eye

A 68-year-old man was first diagnosed as having acute myelomonoblastic leukaemia on March 17, 1983. After two remissions with treatment, he suffered a further relapse, which caused him to present with a red eye, visual failure, and oedema of the right optic nerve head. Examination of cerebrospinal fluid that was obtained on lumbar puncture demonstrated an acute central nervous system relapse. Computed tomographic scanning led to the diagnosis of leukaemic infiltration of the optic nerve. Systemic and intrathecal treatment by appropriate chemotherapy and by orbital radiotherapy led to resolution of the clinical problem.

Preleukemia and urticaria pigmentosa followed by acute myelomonoblastic leukemia

Preleukemia and urticaria pigmentosa followed by acute myelomonoblastic leukemia

Preleukemia and Urticaria Pigmentosa Followed by Acute Myelomonoblastic Leukemia

A preleukemic syndrome, mast cell hyperplasia in the bone marrow, and urticaria pigmentosa simultaneously developed in a 76-year-old woman. A year later, the patient died of acute myelomonoblastic leukemia. These associations provide evidence favoring the origin of the tissue mast cell from a bone marrow stem cell.

"Pan-myeloid" reagent: the monoclonal antibody MCS-2 in the routine immunodiagnostic service of leukemia phenotyping.

This retrospective analysis describes the reactivity of several monoclonal antibodies (MoAbs) which detect myelomonocytic antigens of the cells of 182 leukemias. These leukemias were assigned to definite subtypes of lymphocytic and myelo(mono)-cytic leukemias on the basis of standard leukemia phenotyping using morphological, cytochemical, isoenzymatic and mainly immunological criteria. The MoAb MCS-2 was negative in all cases of lymphocytic leukemia, whereas two of the three other commonly used "myeloid MoAbs" MCS-1, OKM-1 and 1/12/13 showed positivity in B-chronic lymphocytic leukemia (B-CLL), B-lymphoma (MCS-1), T-acute lymphoblastic leukemia (T-ALL) and Sézary syndrome (OKM-1). MCS-2 was positive in all samples of acute myelomonoblastic leukemia (AMMoL), chronic myelocytic leukemia (CML) and CML-myeloid blast crisis, which was not the case for MCS-1, OKM-1, or 1/12/13. In 14 cases (11 acute myeloblastic leukemia (AML), 3 CML-myeloid blast crisis) where MCS-2 was positive and one or all of the three other MoAbs were negative, the cells were mainly Ia-positive and peroxidase-negative. MCS-2 is a diagnostically important MoAb in the routine leukemia phenotyping of myelomonocytic leukemias. After having tested a large number of normal and malignant specimens, we would like to term MCS-2 a "pan-myeloid MoAb" reacting with the myelomonocytic cell lineage from the earliest myeloblast to granulocytes and monocytes.

Isolation and characterization of glycosphingolipids from human leukocytes a unique glycosphingolipid pattern in a case of acute myelomonoblastic leukemia

Neutral glycosphingolipids and gangliosides were isolated from the malignant cells of a patient with acute myelomonoblastic leukemia. Structural analyses were performed by gas-liquid chromatography and by high-performance liquid chromatography combined with enzymatic hydrolysis of glycosphingolipids using glycosidases. We found that, in contrast to normal leukocytes and chronic leukemia cells which have only a single tetraosylceramide species, these acute myelomonoblastic leukemia cells have approximately equal amounts of both globo- and neolactotetraosylceramide. This is the first population of human leukocytes in which we found two families of neutral glycosphingolipids to be present. The ganglioside fraction was composed of appreciable quantities of both NeuAc α2 → 3Gal β1 → 4Glc β1 → 1Cer (GM3, hematoside) and NeuAc α2 → 3Gal β1 → 4GlcNAc β1 → 3Gal β1 → 4Glc β1 → 1Cer (sialoparagloboside). These cells did not have the ‘leukocyte-specific’ N-acetylneuraminosyllactotriaosylceramide found in normal human lymphocytes and neutrophils. These results are discussed in relation to normal leukocyte differentiation and acute leukemia. The present study also illustrates the usefulness of combining enzymatic degradation with high-performance liquid chromatography for glycosphingolipid structural determination.