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1. Chelghoum Y, Danaïla C, Belhabri A, Charrin C, Le QH, Michallet M, Fiere D, Thomas X: Influence of cigarette smoking on the presentation and course of acute myeloid leukemia. Ann Oncol; 2002 Oct;13(10):1621-7
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  • [Title] Influence of cigarette smoking on the presentation and course of acute myeloid leukemia.
  • BACKGROUND: It is known that cigarette smoking is associated with an approximately 50% increase in leukemia risk.
  • In order to detect a possible influence of cigarette smoking on initial characteristics at the time of presentation and on the course of the disease, we conducted a retrospective study in 643 patients with newly diagnosed acute myeloid leukemia.
  • RESULTS: Cigarette smoking was significantly related to male gender (P <0.0001), professional occupancy (P = 0.002), presence of organomegaly (P = 0.01), and lower peripheral blood and bone marrow leukemic cell involvement (P = 0.007 and P = 0.0001, respectively).
  • Leukemia of French-American-British (FAB) M1 subtype was more frequent in non-smokers (P = 0.005).
  • However, a higher rate of severe pulmonary infection was observed in smokers during induction chemotherapy (P = 0.02).
  • Other characteristics associated with poor prognosis included mainly older age, unfavorable karyotype, secondary acute myeloid leukemia (AML) and elevated World Health Organization (WHO) performance status.
  • CONCLUSIONS: Cigarette smoking has a deleterious effect on survival in AML by shortening complete remission duration and subsequent survival.


2. Mashita T, Shimoda T, Yoshioka H, Takahashi Y, Mitsuda M: A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy. J Vet Med Sci; 2006 Jan;68(1):97-101
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  • [Title] A cat with acute myeloblastic leukemia without maturation (M1) treated with combination chemotherapy.
  • Acute myeloblastic leukemia without maturation (M1) was diagnosed according to the FAB classification.
  • Chemotherapy was initiated with cyclophosphamide, vincristine, prednisolone, and cytosine arabinoside.

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  • (PMID = 16462128.001).
  • [ISSN] 0916-7250
  • [Journal-full-title] The Journal of veterinary medical science
  • [ISO-abbreviation] J. Vet. Med. Sci.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; EC 1.11.1.7 / Peroxidase
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3. Srivastava MD, Ambrus JL: Effect of 1,25(OH)2 Vitamin D3 analogs on differentiation induction and cytokine modulation in blasts from acute myeloid leukemia patients. Leuk Lymphoma; 2004 Oct;45(10):2119-26
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  • [Title] Effect of 1,25(OH)2 Vitamin D3 analogs on differentiation induction and cytokine modulation in blasts from acute myeloid leukemia patients.
  • In acute myeloid leukemia (AML), cell proliferation and differentiation are uncoupled, causing a maturation block.
  • Induction of terminal differentiation is a potential therapeutic strategy.
  • We investigated 1alpha, 25(OH)2 Vitamin D3 and 5 of its more potent analogs with reduced calcium resorbing activity for differentiation of blast cells from AML (FAB M1) patients, compared to TPA.
  • Vitamin D3 and its analogs can induce differentiation of primary cells from AML patients in vitro, but may need to be combined with other agents for terminal differentiation of blasts and effective therapy in vivo.
  • [MeSH-major] Calcitriol / analogs & derivatives. Cell Differentiation / drug effects. Cytokines / antagonists & inhibitors. Granulocyte Precursor Cells / drug effects. Leukemia, Myeloid, Acute / pathology
  • [MeSH-minor] Acute Disease. Cell Adhesion. Cells, Cultured. Dose-Response Relationship, Drug. Humans. Interleukin-6 / antagonists & inhibitors. Interleukin-8 / antagonists & inhibitors. Structure-Activity Relationship


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4. Ressel A, Trümper L, Bäsecke J: [Occlusion of the femoral arteries in de novo AML]. Med Klin (Munich); 2007 May 15;102(5):388-92
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  • [Title] [Occlusion of the femoral arteries in de novo AML].
  • [Transliterated title] Femoralarterienverschluss bei De-novo-AML.
  • BACKGROUND: Leukemic emboli in acute (AML) and chronic myelocytic leukemia (CML) are associated with hyperleukocytosis (>100,000/microl leukocytes) and most frequently detected at autopsy.
  • CASE REPORT: A 53-year-old woman was admitted with hyperleukocytosis and acute pain in her right leg.
  • An occlusion of the right femoral arteries as the presenting symptom of a de novo AML (FAB M1/WHO: AML without maturation) with hyperleukocytosis was diagnosed.
  • CONCLUSION: Leukemic emboli of large vessels are uncommon in leukemia with hyperleukocytosis.
  • Leukemic emboli mainly occur in AML and CML in blast crisis and are rare in acute (ALL) and chronic lymphocytic leukemia (CLL).
  • Therapeutic options, apart from the immediate start of chemotherapy, are leukapheresis and embolectomy.
  • [MeSH-major] Arterial Occlusive Diseases / etiology. Femoral Artery. Leukemia, Myeloid, Acute / diagnosis. Neoplastic Cells, Circulating
  • [MeSH-minor] Angiography. Blood Coagulation Tests. Diagnosis, Differential. Female. Granulocyte Precursor Cells / pathology. Humans. Leukocyte Count. Leukocytosis / diagnosis. Leukocytosis / pathology. Middle Aged

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  • (PMID = 17497090.001).
  • [ISSN] 0723-5003
  • [Journal-full-title] Medizinische Klinik (Munich, Germany : 1983)
  • [ISO-abbreviation] Med. Klin. (Munich)
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
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5. Takahashi T, Maruyama Y, Satoh Y, Yoshimoto M, Tsujisaki M: Complex t(8;14;21)(q22;q13;q22), a variant of t(8;21), with t(15;21)(q15;p11) in a patient with acute myelogenous leukemia (M1). Cancer Genet Cytogenet; 2004 Dec;155(2):152-3
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  • [Title] Complex t(8;14;21)(q22;q13;q22), a variant of t(8;21), with t(15;21)(q15;p11) in a patient with acute myelogenous leukemia (M1).
  • [MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Genetic Variation. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / prevention & control. Translocation, Genetic
  • [MeSH-minor] Antimetabolites, Antineoplastic / therapeutic use. Core Binding Factor Alpha 2 Subunit. Cytarabine / therapeutic use. Drug Therapy, Combination. Female. Humans. Idarubicin / therapeutic use. Karyotyping. Leukocytes, Mononuclear / chemistry. Middle Aged. Oncogene Proteins, Fusion / genetics. RNA, Messenger / genetics. Reverse Transcriptase Polymerase Chain Reaction. Secondary Prevention. Transcription Factors / genetics

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  • (PMID = 15571802.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Antimetabolites, Antineoplastic; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 0 / Transcription Factors; 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin
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6. McGrattan P, Alexander HD, Humphreys MW, Kettle PJ: Tetrasomy 13 as the sole cytogenetic abnormality in acute myeloid leukemia M1 without maturation. Cancer Genet Cytogenet; 2002 Jun;135(2):192-5
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  • [Title] Tetrasomy 13 as the sole cytogenetic abnormality in acute myeloid leukemia M1 without maturation.
  • We report a case of acute myeloid leukemia (AML) M1 showing a 48,XY,+13,+13 karyotype.
  • Treatment was according to the Medical Research Council AML14 trial protocol with two courses of DAT chemotherapy.
  • Tetrasomy 13 as the sole cytogenetic abnormality has not been reported previously in M1 AML and has only been reported in three other AML cases, all with an immature phenotype and poor outcome.
  • [MeSH-major] Aneuploidy. Chromosomes, Human, Pair 13. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Drug Resistance, Neoplasm. Fatal Outcome. Granulocyte Colony-Stimulating Factor / administration & dosage. Humans. Male. Middle Aged. Thioguanine / administration & dosage. Vidarabine / administration & dosage. Vidarabine / analogs & derivatives

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  • (PMID = 12127406.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 143011-72-7 / Granulocyte Colony-Stimulating Factor; FA2DM6879K / Vidarabine; FTK8U1GZNX / Thioguanine; ZS7284E0ZP / Daunorubicin; DAT protocol 1; FLAG protocol
  • [Number-of-references] 10
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7. Herry A, Douet-Guilbert N, Guéganic N, Morel F, Le Bris MJ, Berthou C, De Braekeleer M: Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association. Ann Hematol; 2006 Apr;85(4):244-9
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  • [Title] Del(5q) and MLL amplification in homogeneously staining region in acute myeloblastic leukemia: a recurrent cytogenetic association.
  • We report here a 71 year-old female presenting with acute myeloblastic leukemia (FAB-M1) after treatment of essential thrombocythemia with Vercyte.
  • Twenty-one cases, including ours, of myelodysplastic syndromes and acute myelogenous leukemia with MLL amplification present in hsr or dmin were found in the literature.
  • Most of these patients shared some characteristics: they were old, they had de novo acute myeloid leukemia (AML) with a complex karyotype and a short survival, 90% of them having also a del(5q).
  • Therefore, the simultaneous presence of MLL amplification and del(5q) appears to be a nonrandom association that could be the signature of AML in elderly patients with a poor prognosis.
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 7 / genetics. Gene Amplification. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics
  • [MeSH-minor] 6-Mercaptopurine / therapeutic use. Aged. Cytogenetic Analysis. Fatal Outcome. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence / methods. Karyotyping. Pipobroman / therapeutic use. Prognosis. Sensitivity and Specificity. Thrombocytosis / diagnosis. Thrombocytosis / drug therapy

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  • (PMID = 16425025.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 6Q99RDT97R / Pipobroman; E7WED276I5 / 6-Mercaptopurine; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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8. Dimicoli S, Fohlen-Walter A, Mansuy L, Buisine J, Grégoire MJ, Lecompte T, Bordigoni P, Jonveaux P, Lesesve JF: [Acute myeloblastic leukemia without maturation (AML-M1) with basophilic elements and associated with translocation t(6;9)]. Ann Biol Clin (Paris); 2003 May-Jun;61(3):352-7
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  • [Title] [Acute myeloblastic leukemia without maturation (AML-M1) with basophilic elements and associated with translocation t(6;9)].
  • [Transliterated title] Leucémie aiguë myéloblastique sans maturation (LAM1) avec éléments basophiles associée à la translocation t(6;9).
  • The clinical, hematological, and cytogenetic data from a 4 year-old child with acute myeloid (AML-M1) and basophilia is reported.
  • This abnormality is rare and associated with myelodysplastic syndromes or with subtypes of acute myeloid leukemia (M1, M2, M4, M7), usually with preceding or underlying myelodysplasia.
  • The prognosis is poor, without response to chemotherapy regimen alone.
  • Allogeneic bone marrow transplantation appears likely to be a more appropriate treatment.
  • [MeSH-major] Basophils. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

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  • (PMID = 12805015.001).
  • [ISSN] 0003-3898
  • [Journal-full-title] Annales de biologie clinique
  • [ISO-abbreviation] Ann. Biol. Clin. (Paris)
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Hemoglobins
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9. Jelić-Puskarić B, Ostojić-Kolonić S, Planinc-Peraica A, Obad-Kovacević D, Kardum-Skelin I, Jaksić B: Myeloid sarcoma involving the breast. Coll Antropol; 2010 Jun;34(2):641-4
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  • [Title] Myeloid sarcoma involving the breast.
  • Myeloid sarcoma is a tumor mass with extramedullary growth pattern, composed of myeloblasts or immature myeloid cells.
  • The development of myeloid sarcoma may precede or concur with acute or chronic myeloid leukemia (AML or CML) or other myeloproliferative diseases or myelodysplastic syndromes (MDS).
  • Isolated myeloid sarcoma of the breast is very rare.
  • Based on the morphology, cytochemical characteristics and immature cell immunophenotype, it was considered a case of acute myeloid leukemia without maturation.
  • In spite of intensive chemotherapy, the patient died within a year of diagnosis.
  • In cases of isolated breast myeloid sarcoma, the diagnosis can be missed if the possibility of myeloid sarcoma is not remembered on differential diagnosis of a breast neoplasm.
  • [MeSH-major] Breast Neoplasms / pathology. Sarcoma, Myeloid / pathology
  • [MeSH-minor] Adult. Anemia / etiology. Anemia / pathology. Biopsy, Fine-Needle. Bone Marrow / pathology. Fatal Outcome. Female. Humans. Leukemia, Myeloid, Acute / pathology. Leukocytosis / etiology. Leukocytosis / pathology. Recurrence. Thrombocytopenia / etiology. Thrombocytopenia / pathology


10. Øyan AM, Bø TH, Jonassen I, Gjertsen BT, Bruserud Ø, Kalland KH: cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation. Int J Oncol; 2006 May;28(5):1065-80
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  • [Title] cDNA microarray analysis of non-selected cases of acute myeloid leukemia demonstrates distinct clustering independent of cytogenetic aberrations and consistent with morphological signs of differentiation.
  • Acute myeloid leukemia (AML) is a heterogeneous disease with respect to biology and clinical course.
  • Until now the basis for prognostic evaluation and therapeutic decision has been the karyotype, genetic FLT3 abnormalities and the initial chemotherapy response.
  • In an attempt to address this question, we performed cDNA microarray analysis on peripheral blood samples of 25 patients with newly diagnosed AML with high blast counts.
  • Leave-one-out crossvalidation (LOOCV) showed with high accuracy that gene expression classifiers could predict if leukaemia samples belonged to the FAB AML-M1 or to the FAB AML-M2 groups.
  • Except for an accumulation of samples classified as FAB M1 and M2 in cluster 3, there was no evident relationship between the clusters and the FAB classification.
  • Each subgroup displayed clearly distinguished gene expression patterns validated using real-time quantitative PCR analysis.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics. Oligonucleotide Array Sequence Analysis


11. Skladanowski A, Bozko P, Sabisz M, Larsen AK: Dual inhibition of PI3K/Akt signaling and the DNA damage checkpoint in p53-deficient cells with strong survival signaling: implications for cancer therapy. Cell Cycle; 2007 Sep 15;6(18):2268-75
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  • [Title] Dual inhibition of PI3K/Akt signaling and the DNA damage checkpoint in p53-deficient cells with strong survival signaling: implications for cancer therapy.
  • Natural (intrinsic) resistance of many tumor types to DNA damaging agents is closely associated with their capacity to undergo robust cell cycle arrest in G(2)/M.
  • G(2) arrest is regulated by the DNA damage checkpoint and by survival signaling, with a potential role of PI3K/Akt in checkpoint function.
  • We compared the influence of UCN-01, which affects both the DNA damage checkpoint and PI3K/Akt-mediated survival signaling, with the PI3K inhibitors wortmannin and LY294002 in p53-deficient M1 acute myeloid leukemia cells treated with the DNA damaging agent cisplatin.
  • Unexpectedly, dual inhibition of both survival and checkpoint signaling by UCN-01, also increased the cytotoxicity of cisplatin, but to a lesser degree than wortmannin or LY294002.
  • Our results elucidate a novel function for PI3K/Akt as a survival factor during DNA damage-induced G(2) arrest and could have important pharmacological consequences for the application of response modulators in p53-deficient tumors with strong survival signaling.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Damage / physiology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Signal Transduction / physiology. Tumor Suppressor Protein p53 / deficiency
  • [MeSH-minor] Animals. Cell Cycle / drug effects. Cell Cycle / physiology. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / genetics. Cell Survival / physiology. Mice. Neoplasms / drug therapy. Neoplasms / enzymology

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  • (PMID = 17890906.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Tumor Suppressor Protein p53; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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12. Reisch N, Roehnisch T, Sadeghi M, Greiner L, Regenbogen C, Rieger J, Emmerich B, Oduncu F: AML M1 presenting with recurrent acute large arterial vessel thromboembolism. Leuk Res; 2007 Jun;31(6):869-71
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  • [Title] AML M1 presenting with recurrent acute large arterial vessel thromboembolism.
  • Acute leukemia may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.
  • Disordered hemostasis is characteristic for acute promyelocytic leukemia (APL, FAB M3).
  • We report a case of severe recurrent acute arterial thromboembolism at presentation in AML FAB M1.
  • Most likely, the ischemic events in our patient resulted from leukemia as the thrombus material included many leukemic blasts.
  • Despite leg amputation just a couple of hours before and extremely high infectious risk of the patient, chemotherapy was administered.
  • The clinical course of cessation of the ischemic events and a fast reduction of the blasts in the peripheral blood smear after chemotherapeutic treatment of the patient outlines the importance and life saving role of early chemotherapy even under adverse circumstances.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Thromboembolism / etiology
  • [MeSH-minor] Adult. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery. Leukemia, Promyelocytic, Acute / complications

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  • (PMID = 17011031.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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13. Lesesve JF, Dugué F, Grégoire MJ, Witz F, Dror Y: Shwachman-Diamond syndrome with late-onset neutropenia and fatal acute myeloid leukaemia without maturation: a case report. Eur J Haematol; 2003 Nov;71(5):393-5
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  • [Title] Shwachman-Diamond syndrome with late-onset neutropenia and fatal acute myeloid leukaemia without maturation: a case report.
  • We report on a male patient affected by Shwachman Diamond syndrome (SDS) who presented an unusual delayed neutropenia and then developed a poorly differentiated acute myeloid leukaemia (M0-AML) with trilineage myelodysplasia in adulthood.
  • The patient was treated with conventional chemotherapy but never reached complete remission of leukaemia and died 18 months after diagnosis.
  • SDS is an inherited bone marrow failure syndrome with a high propensity to leukaemic transformation.
  • [MeSH-major] Exocrine Pancreatic Insufficiency / complications. Leukemia, Myeloid / etiology. Neutropenia / etiology
  • [MeSH-minor] Acute Disease. Cell Differentiation. Child. Fatal Outcome. Genetic Predisposition to Disease. Humans. Male. Pancytopenia / etiology. Sepsis / etiology. Syndrome

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  • (PMID = 14667205.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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14. Monteleone PM, Steele DA, King AK, Konefal S, Kelleher JF: Bilateral breast relapse in acute myelogenous leukemia. J Pediatr Hematol Oncol; 2001 Feb;23(2):126-9
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  • [Title] Bilateral breast relapse in acute myelogenous leukemia.
  • We present the case of an 11.5-year-old girl with M1 acute myelogenous leukemia (AML) who had isolated extramedullary relapse develop in both breasts 12 months after diagnosis and 7 months off chemotherapy.
  • She received further chemotherapy, focal radiation therapy, then underwent a matched, unrelated bone marrow transplant and continues in remission 37 months later.
  • Review of the literature revealed 10 cases in other children younger than 21-years-old with AML and breast involvement.
  • Breast involvement in AML is rare in children.
  • However, regular breast examinations should be performed as part of routine follow-up in all girls with AML.
  • [MeSH-major] Breast / pathology. Leukemia, Myeloid, Acute / pathology. Vidarabine / analogs & derivatives
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biopsy. Bone Marrow Transplantation. Child. Combined Modality Therapy. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Etoposide / administration & dosage. Female. Graft vs Host Disease / etiology. Humans. Idarubicin / administration & dosage. Immunologic Factors / therapeutic use. Interleukin-2 / therapeutic use. Leukemic Infiltration. Radiotherapy, High-Energy. Recurrence. Salvage Therapy. Thioguanine / administration & dosage. Transplantation Conditioning

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  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • Hazardous Substances Data Bank. CYTARABINE .
  • Hazardous Substances Data Bank. THIOGUANINE .
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. FLUDARABINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. VIDARABINE .
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  • (PMID = 11216705.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunologic Factors; 0 / Interleukin-2; 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; FA2DM6879K / Vidarabine; FTK8U1GZNX / Thioguanine; P2K93U8740 / fludarabine; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
  • [Number-of-references] 23
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