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1. Lee SY, Kim M, Lim J, Kim Y, Han K, Kim SY, Kim HJ, Park IY: [A case of therapy-related acute myeloid leukemia associated with inv(16)]. Korean J Lab Med; 2007 Feb;27(1):19-21
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  • [Title] [A case of therapy-related acute myeloid leukemia associated with inv(16)].
  • The inv(16)(p13q22) is found in de novo AML and is closely associated with the FAB subtype M4eo.
  • The inv(16) is rarely reported in therapy-related AML (t-AML) patients.
  • Herein, we report a case of t-AML with inv(16) after combination chemotherapy using antimitotic agent and alkylating agent (cis-platin-paclitaxel) for ovarian serous cystadenocarcinoma.
  • [MeSH-major] Antimitotic Agents / adverse effects. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosome Inversion. Chromosomes, Human, Pair 16 / genetics. Leukemia, Myeloid, Acute / chemically induced

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  • (PMID = 18094545.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Antimitotic Agents; 0 / Taxoids; Q20Q21Q62J / Cisplatin; TP protocol
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2. Byrd JC, Ruppert AS, Mrózek K, Carroll AJ, Edwards CG, Arthur DC, Pettenati MJ, Stamberg J, Koduru PR, Moore JO, Mayer RJ, Davey FR, Larson RA, Bloomfield CD: Repetitive cycles of high-dose cytarabine benefit patients with acute myeloid leukemia and inv(16)(p13q22) or t(16;16)(p13;q22): results from CALGB 8461. J Clin Oncol; 2004 Mar 15;22(6):1087-94
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  • [Title] Repetitive cycles of high-dose cytarabine benefit patients with acute myeloid leukemia and inv(16)(p13q22) or t(16;16)(p13;q22): results from CALGB 8461.
  • PURPOSE: To study the impact of repetitive (three to four courses) versus a single course of high-dose cytarabine (HDAC) consolidation therapy on outcome of patients with acute myeloid leukemia (AML) and inv(16)(p13q22) or t(16;16)(p13;q22).
  • PATIENTS AND METHODS: We examined the cumulative incidence of relapse (CIR), relapse-free survival (RFS), and overall survival (OS) for 48 adults younger than 60 years with inv(16)/t(16;16) who had attained a complete remission on one of four consecutive clinical trials and were assigned to receive HDAC consolidation therapy.
  • CONCLUSION: We conclude that, in AML patients with inv(16)/t(16;16), repetitive HDAC therapy decreases the likelihood of relapse compared with consolidation regimens including less HDAC.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Chromosome Inversion. Chromosomes, Human, Pair 16. Cytarabine / administration & dosage. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Analysis of Variance. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Proportional Hazards Models. Recurrence. Survival Analysis. United States

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  • (PMID = 15020610.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA31946; United States / NCI NIH HHS / CA / CA77658
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 04079A1RDZ / Cytarabine
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3. Kumagawa M, Suzuki K, Nagano M, Takamatsu Y, Suzumiya J, Tamura K: [High dose ara-C therapy induced bradycardia in an acute myeloid leukemia patient with inv (16)(p13q22)]. Rinsho Ketsueki; 2003 Jun;44(6):404-6
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  • [Title] [High dose ara-C therapy induced bradycardia in an acute myeloid leukemia patient with inv (16)(p13q22)].
  • A 20-year-old Japanese woman was diagnosed as having acute myeloid leukemia with inv(16)(p13 q22).
  • She achieved complete remission (CR) after treatment with a standard dose of cytarabine(ara-C) and idarubicin.
  • [MeSH-major] Bradycardia / chemically induced. Cytarabine / adverse effects. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Inversion. Chromosomes, Human, Pair 16 / genetics. Etoposide / administration & dosage. Female. Humans. Idarubicin / administration & dosage. Remission Induction

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  • (PMID = 12884821.001).
  • [ISSN] 0485-1439
  • [Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology
  • [ISO-abbreviation] Rinsho Ketsueki
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 6PLQ3CP4P3 / Etoposide; ZRP63D75JW / Idarubicin
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4. Giusiano S, Formisano-Tréziny C, Benziane A, Maroc N, Picard C, Hermitte F, Taranger-Charpin C, Gabert J: Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis. Int J Lab Hematol; 2010 Aug 1;32(4):398-409
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  • [Title] Development of a biochip-based assay integrated in a global strategy for identification of fusion transcripts in acute myeloid leukemia: a work flow for acute myeloid leukemia diagnosis.
  • Three major types of rearrangements are involved in acute myeloid leukemias (AML): t(8;21)(q22;q22), inv(16)(p13q22), and 11q23/MLL abnormalities.
  • Today, the challenge is to propose an individual follow-up for each patient even for those with a rare fusion event.
  • Using cell lines, we developed and validated a biochip-based assay called the AMLFusionChip that identifies every FT of AML1-ETO, CBFbeta-MYH11 as well as MLL-AF9, MLL-ENL, MLL-AF6, and MLL-AF10.
  • This AMLFusionChip strategy fits into the concept of personalized medicine for the largest number of patients.
  • [MeSH-major] Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction / methods

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  • (PMID = 19930410.001).
  • [ISSN] 1751-553X
  • [Journal-full-title] International journal of laboratory hematology
  • [ISO-abbreviation] Int J Lab Hematol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / RNA, Messenger; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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5. Owatari S, Otsuka M, Uozumi K, Takeshita T, Hanada S: Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma. Int J Hematol; 2007 Jan;85(1):32-5
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  • [Title] Two cases of secondary acute myeloid leukemia accompanying adult T-cell leukemia/lymphoma.
  • We identified 2 cases of secondary acute myeloid leukemia (AML) following adult T-cell leukemia/lymphoma (ATL) in patients who had previously received chemotherapy.
  • Both cases were thought to represent therapy-related AML because the patients had previously received combination chemotherapy including epipodophyllotoxin, anthracycline, and alkylating agents for the ATL.
  • The cases were diagnosed as AML M4 with eosinophilia and AML M2, with the chromosomal abnormalities inv(16)(p13q22) and t(8;21)(q22;q22), respectively.
  • In our hospital, only these 2 cases of secondary AML accompanying ATL were identified among 90 cases of acute- or lymphoma-type ATL diagnosed from October 1999 to July 2006.
  • The frequency of coexisting AML and ATL is lower than that reported for acute leukemia coexisting with other lymphoid malignancies.
  • The low frequency of secondary leukemia with ATL may be associated with the short survival times of ATL patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia-Lymphoma, Adult T-Cell / complications. Neoplasms, Second Primary / chemically induced
  • [MeSH-minor] Acute Disease. Alkylating Agents / therapeutic use. Anthracyclines / therapeutic use. Chromosome Aberrations. Female. Humans. Leukemia, Myeloid, Acute / chemically induced. Leukemia, Myelomonocytic, Acute / chemically induced. Male. Middle Aged. Podophyllotoxin / therapeutic use

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  • (PMID = 17261499.001).
  • [ISSN] 0925-5710
  • [Journal-full-title] International journal of hematology
  • [ISO-abbreviation] Int. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Anthracyclines; L36H50F353 / Podophyllotoxin
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6. Andreeva SV, Drozdova VD, Kavardakova NV: [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia]. Tsitol Genet; 2010 May-Jun;44(3):41-52
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  • [Title] [Phenomenon of the evolution of clonal chromosomal abnormalities in childhood acute myeloid leukemia].
  • Analysis of chromosomal abnormalities in bone marrow cells in 116 children with diagnosis of acute myeloid leukemia (AML) was performed.
  • The high frequency of evolution was established at t(15;17)(q22;q22) and the absence at inv(16)(p13q22).
  • Identity of abnormal chromosome structure at diagnosis and relapse of disease can be an evidence of the influence of chemical agent on establishment of some types of evolution of chromosome abnormalities in leukemic cells in AML in children.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 20608159.001).
  • [ISSN] 0564-3783
  • [Journal-full-title] T︠S︡itologii︠a︡ i genetika
  • [ISO-abbreviation] Tsitol. Genet.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Ukraine
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7. Kundu M, Liu PP: Function of the inv(16) fusion gene CBFB-MYH11. Curr Opin Hematol; 2001 Jul;8(4):201-5
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  • [Title] Function of the inv(16) fusion gene CBFB-MYH11.
  • Inv(16)(p13q22) is associated with acute myeloid leukemia subtype M4Eo, which is characterized by the presence of myelomonocytic blasts and atypical eosinophils.
  • This chromosomal rearrangement results in the fusion of CBFB and MYH11 genes.
  • Mouse models indicate that the fusion gene, Cbfb-MYH11, inhibits differentiation of hematopoietic cells.
  • Although expression of Cbfb-MYH11 is not sufficient for leukemogenesis, a combination of Cbfb-MYH11 and additional mutations can lead specifically to the development of myeloid leukemia.
  • In vitro studies indicate that expression of CBFB-MYH11 leads to sequestration of CBFalpha2 in the cytoplasm.
  • It also has been shown to inhibit CBF-mediated transactivation, slow cell cycle progression, delay the apoptotic response to DNA damaging agents, and protect CBFalpha2 from degradation.
  • [MeSH-major] Leukemia, Myelomonocytic, Acute / etiology. Oncogene Proteins, Fusion / physiology
  • [MeSH-minor] Animals. Chromosome Inversion. Core Binding Factor alpha Subunits. Core Binding Factor beta Subunit. DNA-Binding Proteins / physiology. Hematopoiesis. Mice. Transcription Factor AP-2. Transcription Factors / physiology

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  • (PMID = 11561156.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Cbfb protein, mouse; 0 / Core Binding Factor alpha Subunits; 0 / Core Binding Factor beta Subunit; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factor AP-2; 0 / Transcription Factors; 0 / core binding factor alpha
  • [Number-of-references] 48
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8. Linassier C, Barin C, Calais G, Letortorec S, Brémond JL, Delain M, Petit A, Georget MT, Cartron G, Raban N, Benboubker L, Leloup R, Binet C, Lamagnère JP, Colombat P: Early secondary acute myelogenous leukemia in breast cancer patients after treatment with mitoxantrone, cyclophosphamide, fluorouracil and radiation therapy. Ann Oncol; 2000 Oct;11(10):1289-94
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  • [Title] Early secondary acute myelogenous leukemia in breast cancer patients after treatment with mitoxantrone, cyclophosphamide, fluorouracil and radiation therapy.
  • BACKGROUND: The topoisomerase II-targeted drugs, epipodophyllotoxins and anthracyclines, have been shown to induce therapy-related AML (t-AML) characterized by a short latency period after chemotherapy, the absence of prior myelodysplastic syndrome and stereotyped chromosome aberrations.
  • PATIENTS AND METHODS: We retrospectively analyzed patients referred to our hospital for AML with a past history of polychemotherapy for breast cancer, including mitoxantrone, either as adjuvant (8 patients)/neoadjuvant (1 patient) therapy or for metastatic disease (1 patient).
  • t-AML developed 13-36 months (median 16) after beginning chemotherapy for breast cancer, and 4-28 months (median 10.5) after ending treatment.
  • As described in t-AML following treatment with epipodophyllotoxins or anthracyclines, we found a majority of FAB M4, M5 and M3 phenotypes (7 of 10), and characteristic karyotype abnormalities that also can be found in de novo AML: breakpoint on chromosome 11q23 (3 patients), inv(16)(p13q22) (2 patients), t(15;17)(q22;q11) (1 patient), t(8;21)(q22;q22) (1 patient) and del(20q)(q11) (1 patient).
  • CONCLUSIONS: The combination of mitoxantrone with cyclophosphamide, fluorouracil, and radiation therapy can induce t-AML, as with other topoisomerase II-targeted drugs.


9. Manfredi R, Sabbatani S, Chiodo F: Advanced acute myelogenous leukaemia (AML) during HAART-treated HIV disease, manifesting initially as a thyroid mass. Scand J Infect Dis; 2005;37(10):781-3
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  • [Title] Advanced acute myelogenous leukaemia (AML) during HAART-treated HIV disease, manifesting initially as a thyroid mass.
  • A rare case report of acute myelogenous 46 XY, inv(16)(p13q22) leukaemia occurring in a patient with his HIV infection controlled by highly active antiretroviral therapy is reported, in the context of a review of the available literature evidences.
  • Although at its initial presentation the haematological disease had a very advanced (M5) stage expressing a predominant monocytic phenotype, two 1-week cytotoxic chemotherapy cycles carried out with cytarabin-daunorubicin, achieved complete remission (as assessed by combined diagnostic imaging, and repeated bone marrow studies).
  • A such favourable clinical response to acute, advanced myelogenous leukaemia with an insidious recognition is considered infrequent, especially in the setting of HIV disease.
  • [MeSH-major] Antiretroviral Therapy, Highly Active. HIV Infections / complications. HIV Infections / drug therapy. Leukemia, Myeloid, Acute / pathology

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  • (PMID = 16191903.001).
  • [ISSN] 0036-5548
  • [Journal-full-title] Scandinavian journal of infectious diseases
  • [ISO-abbreviation] Scand. J. Infect. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Sweden
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