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1. Figueroa ME, Skrabanek L, Li Y, Jiemjit A, Fandy TE, Paietta E, Fernandez H, Tallman MS, Greally JM, Carraway H, Licht JD, Gore SD, Melnick A: MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation. Blood; 2009 Oct 15;114(16):3448-58
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  • [Title] MDS and secondary AML display unique patterns and abundance of aberrant DNA methylation.
  • Increasing evidence shows aberrant hypermethylation of genes occurring in and potentially contributing to pathogenesis of myeloid malignancies.
  • To determine the extent of promoter hypermethylation in such tumors, we compared the distribution of DNA methylation of 14 000 promoters in MDS and secondary acute myeloid leukemia (AML) patients enrolled in a phase 1 trial of 5-azacytidine and the histone deacetylase inhibitor entinostat against de novo AML patients and normal CD34(+) bone marrow cells.
  • The MDS and secondary AML patients displayed more extensive aberrant DNA methylation involving thousands of genes than did the normal CD34(+) bone marrow cells or de novo AML blasts.
  • Aberrant methylation in MDS and secondary AML tended to affect particular chromosomal regions, occurred more frequently in Alu-poor genes, and included prominent involvement of genes involved in the WNT and MAPK signaling pathways.
  • [MeSH-major] Azacitidine / administration & dosage. DNA Methylation / drug effects. DNA, Neoplasm / metabolism. Enzyme Inhibitors / administration & dosage. Leukemia, Myeloid, Acute. Myelodysplastic Syndromes. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / metabolism

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  • (PMID = 19652201.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00101179
  • [Grant] United States / NCI NIH HHS / CA / R21 CA110507; United States / NCI NIH HHS / CA / U10 CA021115; United States / NCI NIH HHS / CA / U54 CA143876-01; United States / NCI NIH HHS / CA / K24 CA111717; United States / NCI NIH HHS / CA / R01 CA125635; United States / NCI NIH HHS / CA / U01 CA070095; United States / NCI NIH HHS / CA / U54 CA143876; United States / NICHD NIH HHS / HD / R01 HD044078; United States / NCI NIH HHS / CA / CA21115; United States / NCI NIH HHS / CA / U24 CA114737; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CA / U01CA70095
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Wnt Proteins; EC 3.5.1.98 / Histone Deacetylases; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2765680
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2. Rizzieri DA, O'Brien JA, Broadwater G, Decastro CM, Dev P, Diehl L, Beaven A, Lagoo A, Gockerman JP, Chao NJ, Moore JO: Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia. Cancer; 2009 Jul 1;115(13):2922-9
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  • [Title] Outcomes of patients who undergo aggressive induction therapy for secondary acute myeloid leukemia.
  • BACKGROUND: Response and survival in 96 patients with secondary acute myeloid leukemia (sAML) who received aggressive induction chemotherapy was reviewed.
  • Patients with AML after previous chemotherapy or radiation therapy had a higher morphologic remission rate compared with those arising from myelodysplastic syndrome or myeloproliferative disease (82% vs 62%; P = .027).
  • In this population of patients who received aggressive chemotherapy, Charlson comorbidity index or a higher number of factors recognized as high risk in leukemia patients did not affect the chance of OS, DFS, and EFS, although having more recognized leukemia risk factors was related to a lower chance of surviving 1 year.
  • [MeSH-major] Leukemia, Myeloid, Acute / drug therapy. Neoplasms, Second Primary / drug therapy

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  • (PMID = 19452542.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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3. Ducastelle S, Adès L, Gardin C, Dombret H, Prébet T, Deconinck E, Rio B, Thomas X, Debotton S, Guerci A, Gratecos N, Stamatoullas A, Fegueux N, Dreyfus F, Fenaux P, Wattel E: Long-term follow-up of autologous stem cell transplantation after intensive chemotherapy in patients with myelodysplastic syndrome or secondary acute myeloid leukemia. Haematologica; 2006 Mar;91(3):373-6
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  • [Title] Long-term follow-up of autologous stem cell transplantation after intensive chemotherapy in patients with myelodysplastic syndrome or secondary acute myeloid leukemia.
  • We report on the outcomes of 53 patients with myelodysplastic syndromes (MDS) or acute myeloid leukemia secondary to MDS, autografted in first complete remission.
  • [MeSH-major] Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / surgery. Stem Cell Transplantation


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4. Willems L, Suarez F, Messas E, Baubion N, Decaudin D, Fourquet A, Ghez D, Delarue R, Hermine O, Buzyn A, Varet B, Rubio MT: [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer]. Bull Cancer; 2010 Feb;97(2):245-54
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  • [Title] [High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer].
  • Secondary acute myeloid leukaemia (AML) occurring after breast cancer is a rare long-term complication of the chemo- and/or radiation therapy required to treat breast cancer.
  • The usually recognized curative option of these secondary AML includes courses of anthracycline-based chemotherapy followed by haematopoietic stem cell transplantation (HSCT).
  • Cardiac dysfunction during AML treatment of these patients previously treated with anthracyclines for breast cancer has not been reported to date.
  • We evaluated the evolution of cardiac function in seven patients treated with anthracyclines and/or autologous or allogeneic bone marrow transplantation for secondary AML occurring after breast cancer.
  • All of the patients who received a cumulative anthracycline dose above the cardiac toxicity threshold developed cardiac symptoms during AML chemotherapy courses.
  • Thus, the risk of severe cardiac dysfunction after treatment of secondary AML following breast cancer must be taken in account as part of the therapeutic strategy of those patients.
  • As discussed here, an accurate evaluation of risk factors, the use of sensitive detection tests and of cardioprotective drugs as well as that of non-cardiotoxic chemotherapy might decrease the occurrence and severity of this life-threatening complication.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Myeloid / therapy. Neoplasms, Second Primary / therapy
  • [MeSH-minor] Acute Disease. Adult. Chemotherapy, Adjuvant / adverse effects. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Daunorubicin / administration & dosage. Daunorubicin / adverse effects. Epirubicin / administration & dosage. Epirubicin / adverse effects. Female. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Heart Diseases / chemically induced. Heart Diseases / drug therapy. Heart Diseases / physiopathology. Humans. Middle Aged. Remission Induction. Stroke Volume / drug effects. Stroke Volume / physiology

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  • (PMID = 19819776.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil; ZS7284E0ZP / Daunorubicin; FEC protocol
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5. Kuptsova-Clarkson N, Ambrosone CB, Weiss J, Baer MR, Sucheston LE, Zirpoli G, Kopecky KJ, Ford L, Blanco J, Wetzler M, Moysich KB: XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia. Int J Mol Epidemiol Genet; 2010;1(4):278-94
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  • [Title] XPD DNA nucleotide excision repair gene polymorphisms associated with DNA repair deficiency predict better treatment outcomes in secondary acute myeloid leukemia.
  • We evaluated these polymorphisms and XPD haplotypes in adult de novo (n=214) and secondary (n=79) acute myeloid leukemia (AML) patients treated with cytarabine and anthracycline chemotherapy.
  • Differential responses were observed in secondary, but not de novo, AML.
  • Among secondary AML patients, the odds of achieving complete remission (CR) were higher for the XPD 312Asn/Asn (OR= 11.23; 95% CI, 2.23-56.63) and XPD 751Gln/Gln (OR= 7.07; 95% CI, 1.42-35.18) genotypes.
  • If validated, these findings could support stratification of chemotherapy in secondary AML.

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  • (PMID = 21394217.001).
  • [ISSN] 1948-1756
  • [Journal-full-title] International journal of molecular epidemiology and genetics
  • [ISO-abbreviation] Int J Mol Epidemiol Genet
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353; United States / NCI NIH HHS / CA / CA108353-01; United States / NCI NIH HHS / CA / R03 CA108353-02; United States / NCI NIH HHS / CA / R03 CA108353-01
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS247623; NLM/ PMC3049908
  • [Keywords] NOTNLM ; Acute Myeloid Leukemia (AML) / DNA repair gene polymorphisms / pharmacogenetics/pharmacogenomics / secondary AML
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6. Hallemeier CL, Girgis MD, Blum WG, Brown RA, Khoury HJ, Devine SM, Vij R, Lin HS, DiPersio JF, Adkins DR: Long-term remissions in patients with myelodysplastic syndrome and secondary acute myelogenous leukemia undergoing allogeneic transplantation following a reduced intensity conditioning regimen of 550 cGy total body irradiation and cyclophosphamide. Biol Blood Marrow Transplant; 2006 Jul;12(7):749-57
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  • [Title] Long-term remissions in patients with myelodysplastic syndrome and secondary acute myelogenous leukemia undergoing allogeneic transplantation following a reduced intensity conditioning regimen of 550 cGy total body irradiation and cyclophosphamide.
  • We analyzed outcomes of patients with myelodysplastic syndrome (MDS) or secondary acute myelogenous leukemia (sAML) that were treated at our institution with a reduced intensity conditioning (RIC) regimen of 550-cGy total body irradiation and cyclophosphamide followed by related donor (RD) or unrelated donor (URD) transplantation.
  • [MeSH-major] Bone Marrow Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy. Neoplasms, Second Primary / therapy. Peripheral Blood Stem Cell Transplantation / methods. Transplantation Conditioning / methods


7. Preudhomme C, Renneville A, Bourdon V, Philippe N, Roche-Lestienne C, Boissel N, Dhedin N, André JM, Cornillet-Lefebvre P, Baruchel A, Mozziconacci MJ, Sobol H: High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder. Blood; 2009 May 28;113(22):5583-7
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  • [Title] High frequency of RUNX1 biallelic alteration in acute myeloid leukemia secondary to familial platelet disorder.
  • Familial platelet disorder (FPD), a rare autosomal dominant disorder characterized by quantitative and qualitative platelet abnormalities, is considered as a model of genetic predisposition to acute myeloid leukemia (AML).
  • So far, monoallelic RUNX1 germline mutations have been found in 19 of 20 families with reported FPD, and the analysis of blast cells from only 5 patients at acute leukemia (AL) stage has shown no additional RUNX1 abnormality.
  • In addition to the germline RUNX1 mutation, we identified a second RUNX1 alteration in 6 AML cases (acquired point mutations in 4 cases and duplication of the altered RUNX1 allele associated with acquired trisomy 21 in 2 other cases).
  • Although haploinsufficiency of RUNX1 causes FPD, our findings suggest that a second genetic event involving RUNX1 is often associated with progression to AML.
  • [MeSH-major] Blood Platelet Disorders / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics


8. Ostgård LS, Kjeldsen E, Holm MS, Brown Pde N, Pedersen BB, Bendix K, Johansen P, Kristensen JS, Nørgaard JM: Reasons for treating secondary AML as de novo AML. Eur J Haematol; 2010 Sep;85(3):217-26
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  • [Title] Reasons for treating secondary AML as de novo AML.
  • In a Danish bi-regional registry-based study, we conducted an analysis of the incidence and clinical importance of secondary acute myeloid leukaemia (AML).
  • In a total of 630 cases of AML, we found 157 (25%) cases of secondary AML.
  • The secondary leukaemia arose from MDS (myelodysplastic syndrome) in 77 cases (49%), CMPD (chronic myeloproliferative disorder) in 43 cases (27%) and was therapy-related AML (t-AML) in 37 cases (24%).
  • Median age at diagnosis of AML was 69 yr in secondary cases when compared to 66 yr in de novo cases (P = 0.006).
  • In univariate analyses, secondary AML was associated with an inferior complete remission (CR) rate (P = 0.008) and poorer overall survival (OS, P = 0.003) whereas in complete remitters, disease-free survival (DFS) of secondary cases was equal to that of de novo cases.
  • Interestingly, in all further analyses of CR-rates, OS and DFS, when correcting for the influence of age, cytogenetic abnormalities, performance status and leucocyte count (WBC), presence of secondary AML completely lost prognostic significance.
  • We conclude that the presence of secondary AML does not per se convey an unfavourable prognosis and that patients with secondary AML should be offered the chance of benefiting from treatment according to current frontline AML protocols.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Myelodysplastic Syndromes / complications


9. 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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10. Koh Y, Kim I, Bae JY, Song EY, Kim HK, Yoon SS, Lee DS, Park SS, Park MH, Park S, Kim BK: Prognosis of secondary acute myeloid leukemia is affected by the type of the preceding hematologic disorders and the presence of trisomy 8. Jpn J Clin Oncol; 2010 Nov;40(11):1037-45
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  • [Title] Prognosis of secondary acute myeloid leukemia is affected by the type of the preceding hematologic disorders and the presence of trisomy 8.
  • BACKGROUND: Differences in the clinical course of secondary acute myeloid leukemia according to the type of the preceding disorders are not defined.
  • We compared the outcomes of therapy-related acute myeloid leukemia, acute myeloid leukemia following myelodysplastic syndrome and acute myeloiod leukemia following myeloproliferative neoplasm.
  • We also intended to find prognostic factors in secondary acute myeloid leukemia overall.
  • RESULTS: Ninety-five secondary acute myeloid leukemia patients (median age of 56.4 years) were analyzed.
  • Twenty-six, 57 and 12 patients had therapy-related leukemia, leukemia following myelodysplastic syndrome and myeloproliferative neoplasm, respectively.
  • Compared to therapy-related leukemia (P = 0.027) and leukemia following myelodysplastic syndrome (P = 0.050), leukemia following myeloproliferative neoplasm had shorter overall survival.
  • In secondary leukemia, presence of trisomy 8 had a prognostic impact (P = 0.003) along with cytogenetic risk group (P = 0.016).
  • CONCLUSIONS: Prognosis of secondary acute myeloid leukemia was different according to the type of the preceding disorders with the worst prognosis in leukemia following myeloprolfierative neoplasm.
  • Along with cytogenetic risk grouping, trisomy 8 had a poor prognostic impact in secondary acute myeloid leukemia.
  • [MeSH-major] Chromosomes, Human, Pair 8 / genetics. Leukemia, Myeloid, Acute / etiology. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Trisomy

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  • (PMID = 20587614.001).
  • [ISSN] 1465-3621
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; ZRP63D75JW / Idarubicin; ZS7284E0ZP / Daunorubicin
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11. Gombos DS, Hungerford J, Abramson DH, Kingston J, Chantada G, Dunkel IJ, Antoneli CB, Greenwald M, Haik BG, Leal CA, Medina-Sanson A, Schefler AC, Veerakul G, Wieland R, Bornfeld N, Wilson MW, Yu CB: Secondary acute myelogenous leukemia in patients with retinoblastoma: is chemotherapy a factor? Ophthalmology; 2007 Jul;114(7):1378-83
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  • [Title] Secondary acute myelogenous leukemia in patients with retinoblastoma: is chemotherapy a factor?
  • PURPOSE: To describe a series of patients with secondary acute myelogenous leukemia (sAML) and retinoblastoma (RB).
  • MAIN OUTCOME MEASURES: History of RB and development of sAML, management of RB (surgery, radiotherapy, chemotherapy), age at diagnosis of RB and leukemia, French-American-British (FAB) subtype, and current status of patient (alive or dead).
  • Mean latent period from RB to AML diagnosis was 9.8 years (median, 42 months).
  • Ten children died of their leukemia.
  • CONCLUSIONS: Acute myelogenous leukemia is a rare secondary malignancy among retinoblastoma patients, many of whom were treated with primary or adjuvant chemotherapy.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Enzyme Inhibitors / adverse effects. Leukemia, Myeloid, Acute / chemically induced. Neoplasms, Second Primary / chemically induced. Podophyllotoxin / adverse effects. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy. Topoisomerase II Inhibitors


12. Park TS, Choi JR, Yoon SH, Song J, Kim J, Kim SJ, Kwon O, Min YH: Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript. Cancer Genet Cytogenet; 2008 Dec;187(2):61-73
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  • [Title] Acute promyelocytic leukemia relapsing as secondary acute myelogenous leukemia with translocation t(3;21)(q26;q22) and RUNX1-MDS1-EVI1 fusion transcript.
  • Acute promyelocytic leukemia (APL) is a subtype of acute myelogenous leukemia (AML) that is characterized by peculiar clinical and biologic features, including severe hemorrhagic diathesis, specific recurrent chromosomal aberration, and distinct morphologic features with predominant pathologic promyelocytes.
  • A reciprocal translocation involving chromosomes 15 and 17, t(15;17)(q22;q21), is a characteristic feature of APL that represents approximately 5-8% of AML.
  • In contrast to other AML subtypes, APL is particularly sensitive to treatment with all trans-retinoic acid (ATRA) combined with chemotherapy, converting this once fatal leukemia to a highly curable disease.
  • Nonetheless, therapy-related myelodysplastic syndrome-acute myelogenous leukemia (t-MDS/AML) has been reported as a rare complication of chemotherapy in APL.
  • Of 30 APL cases described as t-MDS/AML in the literature, only 1 case relapsed as acute leukemia with t(3;21)(q26;q22).
  • Here we describe a rare case of APL relapsing as secondary AML with t(3;21)(q26;q22) and clinically characterize this patient using the RUNX1 (previously AML1)-MDS1-EVI1 fusion transcript (with follow-up for 55 months), and review the relevant literature.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Promyelocytic, Acute / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 19027486.001).
  • [ISSN] 1873-4456
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / RUNX1 protein, human; 0 / Transcription Factors; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 5688UTC01R / Tretinoin
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13. Suzuki K, Ohishi K, Sekine T, Masuya M, Katayama N: Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone. Int J Hematol; 2007 May;85(4):344-9
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  • [Title] Selective blast cell reduction in elderly patients with acute myeloid leukemia secondary to myelodysplastic syndrome treated with methylprednisolone.
  • The management of elderly patients with acute myeloid leukemia (AML) and a poor performance status is challenging.
  • An 89-year-old man with AML secondary to myelodysplastic syndrome (MDS) and a poor performance status (4) underwent treatment with methylprednisolone (mPSL) (125 mg/body), which resulted in a remarkable reduction of blast cells in the peripheral blood.
  • On the basis of this experience, we gave the same mPSL dose to other elderly patients with MDS/AML (n=5) or AML-M4 (n=1) who had a poor performance status (3 or higher) and appeared unable to tolerate standard cytotoxic chemotherapies.
  • Selective and significant blast cell reduction was observed in 4 of the 5 patients with MDS/AML, whereas no effects were seen in the AML patient.
  • Although our experience is limited, these findings may provide a clue to understanding the mechanisms regulating the survival of blast cells of MDS/AML and indicate that mPSL may provide a benefit to a subset of these patients.
  • [MeSH-major] Blast Crisis / drug therapy. Blast Crisis / etiology. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Methylprednisolone / administration & dosage. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy


14. Khattab TM, Jastaniah WA, Felimban SK, Elemam N, Abdullah K, Ahmed B: How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia. J Clin Oncol; 2009 May 20;27(15_suppl):10048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] How could improvement in the management of T-cell acute lymphoblastic leukemia be achieved? Experience of Princess Nourah Oncology Center, National Guard Hospital, Jeddah, Saudi Arabia.
  • : 10048 Background: T-cell acute lymphoblastic leukemia (T-ALL) is representing 10-15% of pediatric ALL.
  • Overall survival 27/52 (52%) and 25 pts. died (48%); 15 secondary to disease recurrence (9 on UKALL, 4 BFM, 2 CCG 1961); 4 during induction, 1 fulminant hepatic failure, 1 tumor lysis syndrome, and 4 due to toxicities (mucormycosis, staphylococcal toxic shock syndrome, CMV pneumonia, pseudomonas sepsis).
  • Mean length of survivors 4 year (range 4-140 month) and mean length for non-survivors 1 year (range 0.1-40 months).

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  • (PMID = 27962474.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Bello CM, Yu D, Zhu W, Wetzstein GA, Lancet JE: Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors. J Clin Oncol; 2009 May 20;27(15_suppl):7088

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes following induction chemotherapy in patients with AML arising from MDS: Analysis of prognostic factors.
  • : 7088 Background: Secondary acute myeloid leukemia (sAML) arising from myelodysplasia (MDS) or a myeloproliferative neoplasm (MPN) has a poor prognosis.
  • METHODS: Retrospective chart review of patients with untreated AML from MDS/MPN treated with standard induction therapy from January 2004 to September 2008.
  • Multivariable analysis indicated that the same three factors were significantly negatively associated with CR/CRp as well as OS: PR cytogenetics, prior treatment with DM/L, and long transformation to AML on log scale.
  • Only 32% of the group that received prior treatment with a DM/L achieved CR/CRp compared to 78% in non DM/L-treated patients (OR = 0.13, 95% CI: 0.04-0.42).
  • The median OS for those treated with a DM/L was 3.7 mo compared to 10.5 mo for non DM/L-treated patients (p < 0.0001).
  • CONCLUSIONS: Prior MDS treatment with a DM/L, PR cytogenetics and long transformation to AML are independent negative prognostic factors for response and OS in patients with sAML following induction therapy, suggesting that such patients may be better served by novel approaches, and that stratification for these risk factors should be considered in future clinical trials.

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  • (PMID = 27961482.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Villano JL, Letarte N, Yu JM, Shakir AR, Bressler L: Hematologic adverse events associated with temozolomide (TMZ). J Clin Oncol; 2009 May 20;27(15_suppl):2053

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : 2053 Background: Secondary acute myeloid leukemia (AML) is reported to occur in 3%-10% of patients treated with alkylating agents for Hodgkin's lymphoma, non-Hodgkin's lymphoma, ovarian cancer, breast cancer, and multiple myeloma.
  • The incidence of secondary AML is greatest at 5-10 years after treatment, and AML often follows myelodysplastic syndrome (MDS).
  • Among these patients, we identified 140 cases that we labeled as major hematologic adverse events: agranulocytosis (8 cases), aplasia (42), aplastic anemia (52), leukemia (26), MDS (6), and lymphoma (6).
  • Risk of leukemia/MDS from our review may also be significant, but length of follow-up is insufficient and the real risk is likely still unknown.

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  • (PMID = 27964671.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Maris MB, Ravandi F, Stuart R, Stone R, Cripe L, Cooper M, Strickland S, Turturro F, Stock W, Berman C: A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML). J Clin Oncol; 2009 May 20;27(15_suppl):7048

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A phase II study of voreloxin as single agent therapy for elderly patients (pts) with newly diagnosed acute myeloid leukemia (AML).
  • Interim results of REVEAL-1, a phase II study of single agent voreloxin in newly diagnosed elderly AML pts, are reported.
  • Eligibility: newly diagnosed AML (de novo or secondary AML), pts age ≥ 60 and ≥ 1 additional adverse risk factor (age ≥ 70, secondary AML, intermediate or unfavorable cytogenetics, or PS 2).
  • Voreloxin PK were similar to those in an earlier single agent phase I study in relapsed/refractory AML.
  • CONCLUSIONS: In REVEAL-1, voreloxin demonstrates clinical activity with 2 dosing schedules in previously untreated elderly (age ≥ 60) patients with AML who are unlikely to benefit from standard chemotherapy.

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  • (PMID = 27961427.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Kröger N, Shimoni A, Zabelina T, Schieder H, Panse J, Ayuk F, Wolschke C, Renges H, Dahlke J, Atanackovic D, Nagler A, Zander A: Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS). Bone Marrow Transplant; 2006 Feb;37(4):339-44
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  • [Title] Reduced-toxicity conditioning with treosulfan, fludarabine and ATG as preparative regimen for allogeneic stem cell transplantation (alloSCT) in elderly patients with secondary acute myeloid leukemia (sAML) or myelodysplastic syndrome (MDS).
  • We investigated a dose-reduced conditioning regimen consisting of treosulfan and fludarabine followed by allogeneic stem cell transplantation (SCT) in 26 patients with secondary AML or MDS.
  • Acute graft-versus-host disease (GvHD) grade II-IV was seen in 23% and severe grade III GvHD in 12% of the patients.
  • No patients experienced grade IV acute GvHD.
  • [MeSH-major] Antilymphocyte Serum / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Busulfan / analogs & derivatives. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / therapy. Transplantation Conditioning / methods. Vidarabine / analogs & derivatives
  • [MeSH-minor] Acute Disease. Adult. Aged. Disease-Free Survival. Female. Graft vs Host Disease / drug therapy. Graft vs Host Disease / prevention & control. HLA Antigens / analysis. Humans. Male. Middle Aged. Prospective Studies. Recurrence. Siblings. Survival Rate. Transplantation, Homologous. Treatment Outcome


19. Czibere A, Prall WC, Zerbini LF, Grall F, Craigie EC, Ulrich SD, Giagounidis AA, Haas R, Libermann TA, Aivado M: The nonsteroidal anti-inflammatory drug Exisulind selectively induces apoptosis via JNK in secondary acute myeloid leukemia after myelodysplastic syndrome. Cell Cycle; 2005 Jun;4(6):812-7
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  • [Title] The nonsteroidal anti-inflammatory drug Exisulind selectively induces apoptosis via JNK in secondary acute myeloid leukemia after myelodysplastic syndrome.
  • Treatment of patients suffering from myelodysplastic syndromes and secondary acute myeloid leukemia after MDS is often unsuccessful.
  • Exisulind is another potentially pro-apoptotic agent, and therefore, we investigated its influence on proliferation, differentiation, cell cycle and apoptosis in two sAML/MDS cell lines, one de-novo AML cell line and healthy CD34+ bone marrow cells.
  • Exisulind had no effect on de-novo AML or normal CD34+ cells.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Apoptosis / drug effects. JNK Mitogen-Activated Protein Kinases / metabolism. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Sulindac / analogs & derivatives


20. Nemoto N, Suzukawa K, Shimizu S, Shinagawa A, Takei N, Taki T, Hayashi Y, Kojima H, Kawakami Y, Nagasawa T: Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23). Genes Chromosomes Cancer; 2007 Sep;46(9):813-9
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  • [Title] Identification of a novel fusion gene MLL-MAML2 in secondary acute myelogenous leukemia and myelodysplastic syndrome with inv(11)(q21q23).
  • We have identified a novel fusion partner of MLL, namely the mastermind like 2 (MAML2 gene), in secondary acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) with inv(11)(q21q23).
  • RT-PCR and sequencing revealed that exon 7 of MLL was fused to exon 2 of MAML2 in the AML and MDS cells.
  • MLL-MAML2 in secondary AML/MDS and MECT1-MAML2 in mucoepithelioid carcinoma, benign Wartin's tumor, and clear cell hidradenoma consist of the same COOH-terminal part of MAML2.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Nuclear Proteins / genetics. Oncogene Proteins, Fusion / genetics. Transcription Factors / genetics


21. Al-Ali HK, Brand R, van Biezen A, Finke J, Boogaerts M, Fauser AA, Egeler M, Cahn JY, Arnold R, Biersack H, Niederwieser D, de Witte T: A retrospective comparison of autologous and unrelated donor hematopoietic cell transplantation in myelodysplastic syndrome and secondary acute myeloid leukemia: a report on behalf of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT). Leukemia; 2007 Sep;21(9):1945-51
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  • [Title] A retrospective comparison of autologous and unrelated donor hematopoietic cell transplantation in myelodysplastic syndrome and secondary acute myeloid leukemia: a report on behalf of the Chronic Leukemia Working Party of the European Group for Blood and Marrow Transplantation (EBMT).
  • Hematopoietic cell transplantation (HCT) is an effective treatment for myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML).
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / mortality. Leukemia, Myeloid / mortality. Leukemia, Myeloid / therapy. Myelodysplastic Syndromes / mortality. Myelodysplastic Syndromes / therapy
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Age Distribution. Aged. Disease-Free Survival. Female. Humans. Incidence. Male. Middle Aged. Recurrence. Retrospective Studies. Survival Analysis. Tissue Donors. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome


22. Szotkowski T, Muzik J, Voglova J, Koza V, Maaloufova J, Kozak T, Jarosova M, Michalova K, Zak P, Steinerova K, Vydra J, Lanska M, Katrincsakova B, Sicova K, Pavlik T, Dusek L, Indrak K: Prognostic factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic. Neoplasma; 2010;57(6):578-89
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  • [Title] Prognostic factors and treatment outcome in 1,516 adult patients with de novo and secondary acute myeloid leukemia in 1999-2009 in 5 hematology intensive care centers in the Czech Republic.
  • Acute myeloid leukemia (AML) is a severe condition with a high mortality.
  • The study represents a detailed analysis of the role of these factors and treatment outcomes based on a long-term follow-up of patients treated in 5 hematology intensive care centers in the Czech Republic.The studied group comprised 1,188 patients with de novo AML and 328 patients with secondary AML.
  • Curatively treated patients achieved fewer complete remissions and relapsed more often than those with de novo AML.
  • Patients with secondary AML had lower rates of allogeneic transplantation as part of consolidation therapy and a significantly shorter median overall survival.
  • However, the treatment outcome of de novo AML patients is not satisfactory, the only exception being those with acute promyelocytic leukemia.
  • [MeSH-major] Leukemia, Myeloid, Acute / mortality. Neoplasms, Second Primary / mortality


23. Römermann D, Hasemeier B, Metzig K, Schlegelberger B, Länger F, Kreipe H, Lehmann U: [Methylation status of LINE-1 sequences in patients with MDS or secondary AML]. Verh Dtsch Ges Pathol; 2007;91:338-42
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  • [Title] [Methylation status of LINE-1 sequences in patients with MDS or secondary AML].
  • [Transliterated title] Methylierungszustand von LINE-1-Sequenzen bei Patienten mit MDS oder sekundärer AML.
  • [MeSH-minor] Humans. Leukemia, Myeloid, Acute / genetics

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  • (PMID = 18314632.001).
  • [ISSN] 0070-4113
  • [Journal-full-title] Verhandlungen der Deutschen Gesellschaft für Pathologie
  • [ISO-abbreviation] Verh Dtsch Ges Pathol
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
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24. Winter SS, Holdsworth MT, Devidas M, Raisch DW, Chauvenet A, Ravindranath Y, Ducore JM, Amylon MD: Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296. Pediatr Blood Cancer; 2006 Feb;46(2):179-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antimetabolite-based therapy in childhood T-cell acute lymphoblastic leukemia: a report of POG study 9296.
  • PURPOSE: A previous Pediatric Oncology Group (POG) study showed high incidence of secondary acute myelogenous leukemia (AML) in children treated for T-cell acute lymphoblastic leukemia (T-ALL) or higher-stage lymphoblastic lymphoma.
  • To prevent secondary neoplasms, induce prolonged asparagine depletion, and maintain high event-free survival (EFS) in children with newly diagnosed T-ALL or higher-stage non-Hodgkins lymphoma (NHL), we designed this pilot study to determine feasibility and safety of substituting methotrexate/mercaptopurine for teniposide/cytarabine and PEG-asparaginase for native asparaginase.
  • No patients treated entirely on this study developed secondary neoplasms.
  • One patient taken off study for asparaginase toxicity was treated with multiagent therapy that contained teniposide, and died from secondary myelodysplasia (sMDS)/AML.
  • EFS was not compromised and secondary neoplasms were decreased.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Adolescent. Anthracyclines / administration & dosage. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Asparaginase / administration & dosage. Asparaginase / adverse effects. Child. Child, Preschool. Disease-Free Survival. Drug Hypersensitivity / etiology. Female. Follow-Up Studies. Humans. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / mortality. Male. Pilot Projects. Remission Induction. Sepsis / etiology. Sepsis / mortality

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  • (PMID = 16007607.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 U10 CA5312; United States / NCI NIH HHS / CA / CA29139
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; EC 3.5.1.1 / Asparaginase
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25. Infante-Rivard C, Vermunt JK, Weinberg CR: Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia. Am J Epidemiol; 2007 Jun 1;165(11):1248-54
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  • [Title] Excess transmission of the NAD(P)H:quinone oxidoreductase 1 (NQO1) C609T polymorphism in families of children with acute lymphoblastic leukemia.
  • Topoisomerase II is a DNA-processing enzyme, and secondary acute myeloid leukemia has been associated with exposure to drugs that inhibit its action.
  • Hence, prenatal exposure to chemicals that inhibit topoisomerase II could plausibly contribute to the incidence of childhood leukemia.
  • To assess its role in the etiology of childhood acute lymphoblastic leukemia, the authors studied transmission of the variant T allele in the families (parents and grandparents) of 657 affected children in Québec, Canada (1980-2000).
  • [MeSH-major] Family Health. Inheritance Patterns. NAD(P)H Dehydrogenase (Quinone) / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 17332311.001).
  • [ISSN] 0002-9262
  • [Journal-full-title] American journal of epidemiology
  • [ISO-abbreviation] Am. J. Epidemiol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z01 ES045005-11
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; J64922108F / Benzene
  • [Other-IDs] NLM/ NIHMS33454; NLM/ PMC2080583
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26. Rodriguez V, Erlandson L, Arndt CA, Wiseman GA, Anderson PM: Low toxicity and efficacy of (153)samarium-EDTMP and melphalan as a conditioning regimen for secondary acute myelogenous leukemia. Pediatr Transplant; 2005 Feb;9(1):122-6
Hazardous Substances Data Bank. Samarium, Elemental .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low toxicity and efficacy of (153)samarium-EDTMP and melphalan as a conditioning regimen for secondary acute myelogenous leukemia.
  • We report the case of a 15-yr-old girl who developed secondary acute myelogenous leukemia (AML) 4 yr after completion of therapy for metastatic Ewing sarcoma (primary right acetabulum with metastatic disease to the lungs).
  • [MeSH-major] Leukemia, Myeloid, Acute / therapy. Melphalan. Organometallic Compounds / therapeutic use. Organophosphorus Compounds / therapeutic use. Radioisotopes. Samarium. Transplantation Conditioning / methods

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  • (PMID = 15667625.001).
  • [ISSN] 1397-3142
  • [Journal-full-title] Pediatric transplantation
  • [ISO-abbreviation] Pediatr Transplant
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Organometallic Compounds; 0 / Organophosphorus Compounds; 0 / Radioisotopes; 122575-21-7 / samarium ethylenediaminetetramethylenephosphonate; 42OD65L39F / Samarium; Q41OR9510P / Melphalan
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27. Lim Z, Brand R, Martino R, van Biezen A, Finke J, Bacigalupo A, Beelen D, Devergie A, Alessandrino E, Willemze R, Ruutu T, Boogaerts M, Falda M, Jouet JP, Niederwieser D, Kroger N, Mufti GJ, De Witte TM: Allogeneic hematopoietic stem-cell transplantation for patients 50 years or older with myelodysplastic syndromes or secondary acute myeloid leukemia. J Clin Oncol; 2010 Jan 20;28(3):405-11
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  • [Title] Allogeneic hematopoietic stem-cell transplantation for patients 50 years or older with myelodysplastic syndromes or secondary acute myeloid leukemia.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy


28. Burmeister T, Meyer C, Thiel G, Reinhardt R, Thiel E, Marschalek R: A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32). Blood Cells Mol Dis; 2008 Sep-Oct;41(2):210-4
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  • [Title] A MLL-KIAA0284 fusion gene in a patient with secondary acute myeloid leukemia and t(11;14)(q23;q32).
  • MLL aberrations are found in approximately 10% of acute leukemias.
  • We describe here the case of a patient who developed secondary acute myeloid leukemia five years after the patient had received adjuvant radiochemotherapy because of breast cancer.
  • The expression of KIAA0284 in various tissues and hematologic diseases was investigated by real time quantitative PCR and turned out to be very low in all lymphatic and myeloid diseases investigated.
  • [MeSH-major] Leukemia, Myeloid, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Neoplasms, Second Primary / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

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  • (PMID = 18640063.001).
  • [ISSN] 1096-0961
  • [Journal-full-title] Blood cells, molecules & diseases
  • [ISO-abbreviation] Blood Cells Mol. Dis.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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29. Allen SL, Kolitz JE, Lundberg AS, Bennett JM, Capizzi RL, Budman DR: Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia. Leuk Res; 2010 Apr;34(4):487-91
Hazardous Substances Data Bank. CYTARABINE .

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  • [Title] Phase I trials of amonafide as monotherapy and in combination with cytarabine in patients with poor-risk acute myeloid leukemia.
  • Amonafide-l-malate (amonafide) is a unique DNA intercalator that maintains activity in the presence of MDR mechanisms, a frequent cause of treatment-failure in secondary AML.
  • 43 patients with relapsed/refractory or secondary AML or CML blast crisis were enrolled into two phase I dose-escalation studies investigating amonafide as monotherapy or in combination with cytarabine.
  • Between both trials responses occurred in 9/20 patients with secondary AML.
  • Both trials demonstrated an acceptable safety profile and significant antileukemic activity in patients with poor-risk AML, especially those with secondary AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / administration & dosage. Leukemia, Myeloid, Acute / drug therapy. Naphthalimides / administration & dosage

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  • [Copyright] Copyright (c) 2009 Elsevier Ltd. All rights reserved.
  • (PMID = 19748672.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Naphthalimides; 04079A1RDZ / Cytarabine; 1Q8D39N37L / amonafide
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30. Rihani R, Bazzeh F, Faqih N, Sultan I: Secondary hematopoietic malignancies in survivors of childhood cancer: an analysis of 111 cases from the Surveillance, Epidemiology, and End Result-9 registry. Cancer; 2010 Sep 15;116(18):4385-94
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  • [Title] Secondary hematopoietic malignancies in survivors of childhood cancer: an analysis of 111 cases from the Surveillance, Epidemiology, and End Result-9 registry.
  • BACKGROUND: Studying secondary hematological malignancies in a large cohort of patients can help predict risks and trends associated with current therapies.
  • METHODS: The authors analyzed data from the Surveillance, Epidemiology, and End Resultsecondary 9 (SEER-9) database on patients with a primary malignancy (diagnosed before the age of 20 years) between 1973 and 2005 who developed a secondary hematological malignancy.
  • Primary cancer and histological subtype, incidence, risk factors, outcomes, and changes in risk patterns of secondary hematological malignancies were analyzed for 1973 to 1985, 1986 to 1995, and 1996 to 2005.
  • RESULTS: Of 34,867 patients with a histology-confirmed primary malignancy, 111 developed secondary hematological malignancies (median, 44 months).
  • The main histological subtype of secondary hematological malignancy was acute myeloid leukemia (AML) (49%), which had the shortest median latency time and the worst 5-year survival (18% ± 5.3%; P = .044).
  • Secondary Hodgkin lymphoma had the best 5-year survival (83% ± 15%).
  • The 5-year overall survival for patients with secondary hematological malignancies was 31% ± 4.7%.
  • The risk of secondary AML steadily increased from 1986 to 2005, whereas SIRs for acute lymphoblastic leukemia did not change over time.
  • Non-Hodgkin lymphoma, the second most common secondary hematological malignancy, occurred at a median of 112 months, and its risk steadily increased over time periods.
  • CONCLUSIONS: Childhood cancer survivors are at increased risk of developing secondary hematological malignancies, particularly secondary AML.
  • This risk has continued to rise even in recent years, emphasizing the need to study other factors contributing to secondary hematological malignancies and closely monitor these patients.

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  • [Copyright] © 2010 American Cancer Society.
  • (PMID = 20549819.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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31. de Witte T, Hagemeijer A, Suciu S, Belhabri A, Delforge M, Kobbe G, Selleslag D, Schouten HC, Ferrant A, Biersack H, Amadori S, Muus P, Jansen JH, Hellström-Lindberg E, Kovacsovics T, Wijermans P, Ossenkoppele G, Gratwohl A, Marie JP, Willemze R: Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial. Haematologica; 2010 Oct;95(10):1754-61
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

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  • [Title] Value of allogeneic versus autologous stem cell transplantation and chemotherapy in patients with myelodysplastic syndromes and secondary acute myeloid leukemia. Final results of a prospective randomized European Intergroup Trial.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / methods. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / therapy

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  • (PMID = 20494931.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00002926
  • [Grant] United States / NCI NIH HHS / CA / 5U10 CA11488-32; United States / NCI NIH HHS / CA / 5U10 CA11488-27; United States / NCI NIH HHS / CA / 5U10 CA11488-38; United States / NCI NIH HHS / CA / 5U10 CA11488-28; United States / NCI NIH HHS / CA / 5U10 CA11488-35; United States / NCI NIH HHS / CA / 5U10 CA11488-31; United States / NCI NIH HHS / CA / 5U10 CA11488-26; United States / NCI NIH HHS / CA / 5U10 CA11488-37; United States / NCI NIH HHS / CA / U10 CA011488; United States / NCI NIH HHS / CA / 5U10 CA11488-29; United States / NCI NIH HHS / CA / 5U10 CA11488-36; United States / NCI NIH HHS / CA / 5U10 CA11488-33; United States / NCI NIH HHS / CA / 5U10 CA11488-34; United States / NCI NIH HHS / CA / 5U10 CA11488-30
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2948102
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32. Weintraub M, Revel-Vilk S, Charit M, Aker M, Pe'er J: Secondary acute myeloid leukemia after etoposide therapy for retinoblastoma. J Pediatr Hematol Oncol; 2007 Sep;29(9):646-8
Hazardous Substances Data Bank. ETOPOSIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute myeloid leukemia after etoposide therapy for retinoblastoma.
  • Most chemotherapy regimens used in retinoblastoma include etoposide, an epipodophyllotoxin associated with a risk of secondary myeloid leukemia.
  • The use of etoposide in patients with a cancer predisposition syndrome such as retinoblastoma is potentially harmful, however, reports of secondary acute myeloid leukemia in patients treated with etoposide for retinoblastoma are rare.
  • We report a case of a patient who developed secondary acute myeloid leukemia after etoposide treatment for retinoblastoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Etoposide / adverse effects. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / diagnosis. Retinal Neoplasms / drug therapy. Retinoblastoma / drug therapy
  • [MeSH-minor] Acute Disease. Female. Humans. Infant. Treatment Outcome

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  • [ErratumIn] J Pediatr Hematol Oncol. 2007 Oct;29(10):728. Pèer, Jacob [corrected to Pe'er, Jacob]
  • (PMID = 17805043.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide
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33. Monreal MB, Pardo ML, Pavlovsky MA, Fernandez I, Corrado CS, Giere I, Sapia S, Pavlovsky S: Increased immature hematopoietic progenitor cells CD34+/CD38dim in myelodysplasia. Cytometry B Clin Cytom; 2006 Mar;70(2):63-70
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  • METHODS: We analyzed the expression of CD38 and HLA-DR on CD34+ cells by flow cytometry in 36 patients with MDS, as well as in healthy donors (n = 12) and patients with other hematological disorders: non-Hodgkin lymphomas and multiple myeloma, both in complete remission (CR) (n = 32); acute lymphoblastic leukemia in CR (n = 17); de novo acute myeloblastic leukemia (AML) at diagnosis (n = 22) and in CR (n = 37); and AML secondary to MDS at diagnosis (n = 19).
  • RESULTS: Compared to normal BM, the fraction of immature HPC, characterized as CD34+bright, intermediate FSC/SSC, and CD38dim, was significantly increased in high risk MDS and secondary AML, but not in low risk MDS, (P < or = 0.001, P = 0.03, and P = 0.7).
  • De novo AML showed decreased immature HPC.
  • Increased immature HPC in high risk MDS and secondary AML may reflect blocked differentiation of CD34+ cells in these diseases.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Disease Progression. Female. Flow Cytometry. HLA-DR Antigens / immunology. Humans. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Lymphoma, Non-Hodgkin / diagnosis. Lymphoma, Non-Hodgkin / immunology. Male. Middle Aged. Multiple Myeloma / diagnosis. Multiple Myeloma / immunology. Observer Variation. Phenotype. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Prognosis. Reproducibility of Results. Risk Factors

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  • [Copyright] Copyright 2005 International Society for Analytical Cytology.
  • (PMID = 16470534.001).
  • [ISSN] 1552-4949
  • [Journal-full-title] Cytometry. Part B, Clinical cytometry
  • [ISO-abbreviation] Cytometry B Clin Cytom
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / HLA-DR Antigens; EC 3.2.2.5 / Antigens, CD38
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34. Szotkowski T, Rohon P, Zapletalova L, Sicova K, Hubacek J, Indrak K: Secondary acute myeloid leukemia - a single center experience. Neoplasma; 2010;57(2):170-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute myeloid leukemia - a single center experience.
  • Secondary acute myeloid leukemia (sAML) may arise from the previous clonal disorder of hematopoiesis, usually from myelodysplastic syndrome (MDS) or from chronic myeloproliferative neoplasia (cMPN) or after exposure to a leukemogenic agent (previous chemotherapy or radiotherapy, some immunosuppressive drugs or environmental leukemogenic agents).
  • Secondary origin of AML is associated with unfavorable prognosis and it is not considered to be conventionally curable (with the exception of secondary acute promyelocytic leukemia).
  • Over that period of time, a total 574 patients with AML were diagnosed.
  • Of those, 430 patients were diagnosed as having primary AML; in 86 patients, sAML transformed from myelodysplastic syndrome and 58 patients were followed or treated for various malignancies or were treated with potentially leukemogenic agents because of non-malignant disorders.
  • Patients with secondary AML are older and less commonly treated with curative intention than those with primary AML.
  • With the exception of secondary acute promyelocytic leukemia, the prognosis of which does not differ from very good prognosis of the primary forms, secondary AML is not considered a conventionally curable disease.
  • [MeSH-major] Leukemia, Myeloid, Acute / etiology. Myelodysplastic Syndromes / complications. Myeloproliferative Disorders / complications. Neoplasm Recurrence, Local / etiology. Neoplasms, Second Primary / etiology


35. Mansour MR, Duke V, Foroni L, Patel B, Allen CG, Ancliff PJ, Gale RE, Linch DC: Notch-1 mutations are secondary events in some patients with T-cell acute lymphoblastic leukemia. Clin Cancer Res; 2007 Dec 01;13(23):6964-9
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  • [Title] Notch-1 mutations are secondary events in some patients with T-cell acute lymphoblastic leukemia.
  • PURPOSE: Activating Notch-1 mutations are frequent in T-cell acute lymphoblastic leukemia (T-ALL), occurring in >50% of patients.
  • In murine models of T-ALL, Notch-1 activation can both directly initiate leukemia and cooperate secondarily to other primary events.
  • Whether acquisition of Notch-1 mutations is an early initiating event or a secondary event in the pathogenesis of human T-ALL is unclear.
  • Seven of these were low-level mutations (quantified at < or =10%), despite high blast counts, suggesting that they were acquired as a secondary event in a subclone.
  • One relapsed with a secondary T-cell leukemia and different Notch mutation.
  • CONCLUSIONS: These results suggest that Notch-1 mutations can sometimes be acquired as secondary events in leukemogenesis and must be used cautiously as solitary minimal residual disease markers.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation. Receptor, Notch1 / genetics

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  • (PMID = 18056171.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500389
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NOTCH1 protein, human; 0 / Receptor, Notch1
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36. Mihailov G, Ganeva P, Vassileva N, Guenova M, Balacenko G, Toshkov S, Hodjadjik D: Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report. J BUON; 2007 Jul-Sep;12(3):403-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary acute myeloid leukemia early after therapy for Hodgkin's disease--a case report.
  • A case of acute myeloid leukemia (AML) after successful therapy for Hodgkin's disease (HD) is reported.
  • Seven months after the CR was obtained the patient developed AML.
  • Knowing that the prognosis of patients with secondary AML (sAML) after primary HD is poor we decided to perform autologous peripheral stem cells' transplantation.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / surgery. Neoplasms, Second Primary / diagnosis. Neoplasms, Second Primary / surgery

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  • (PMID = 17918297.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Greece
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37. Tavernier E, Le QH, de Botton S, Dhédin N, Bulabois CE, Reman O, Vey N, Lhéritier V, Dombret H, Thomas X: Secondary or concomitant neoplasms among adults diagnosed with acute lymphoblastic leukemia and treated according to the LALA-87 and LALA-94 trials. Cancer; 2007 Dec 15;110(12):2747-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Secondary or concomitant neoplasms among adults diagnosed with acute lymphoblastic leukemia and treated according to the LALA-87 and LALA-94 trials.
  • BACKGROUND: Second malignant neoplasms are a serious complication after successful treatment of childhood acute lymphoblastic leukemia (ALL).
  • RESULTS: By February 2005 secondary or concomitant neoplasms were documented in 23 patients, including 9 acute myeloid leukemias (AML) or myelodysplasias (MDS), 4 non-Hodgkin lymphomas (NHL), 5 skin tumors, and 5 other solid tumors (1 lung cancer, 1 tongue carcinoma, 1 thymoma, 1 condrosarcoma, 1 histiocytosis).
  • The overall cumulative risk of secondary neoplasms was 2.1% at 5 years, 4.9% at 10 years, and 9.4% at 15 years.
  • The development of secondary neoplasm was not associated with the use of any specific cytotoxic agent.
  • However, the median OS in patients developing AML/MDS was 5.7 months.
  • The risk of secondary or concomitant neoplasm appeared higher than that of childhood ALL previously reported in the literature.
  • [MeSH-major] Neoplasms, Second Primary / etiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


38. Varet B, Ifrah N: [Criteria for suspecting a myelodysplastic syndrome]. Rev Prat; 2010 Dec 20;60(10):1404-7
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  • The myelodysplastic syndromes are a group of heterogeneous acquired and clonal disorders that are characterized by the intramedullar, abnormal death of myeloid progenitors leading to peripheral variable cytopenias.
  • It is predictive for the risk of transformation in secondary acute myeloid leukemia.

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  • (PMID = 21425539.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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39. Stifter G, Heiss S, Gastl G, Tzankov A, Stauder R: Over-expression of tumor necrosis factor-alpha in bone marrow biopsies from patients with myelodysplastic syndromes: relationship to anemia and prognosis. Eur J Haematol; 2005 Dec;75(6):485-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Enhanced bone marrow (BM) angiogenesis is regarded as an essential cofactor in the progression of MDS to acute myelogenous leukemia (AML) and microvessel formation may be induced by TNF-alpha as well.
  • METHODS: TNF-alpha expression and BM vessels were immunohistochemically analyzed on 89 paraffin-embedded BM biopsies from patients with MDS and secondary AML, including 12 control samples.
  • MVD was increased in MDS and secondary AML and correlated with marrow cellularity and expression of TNF-alpha, but was not of prognostic significance.
  • CONCLUSIONS: TNF-alpha expression and MVD are elevated in MDS and secondary AML.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Erythroid Precursor Cells / metabolism. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myelodysplastic Syndromes / metabolism. Tumor Necrosis Factor-alpha / biosynthesis


40. Chen YC, Sheen JM, Huang LT, Wu KS, Hsiao CC: Disseminated tuberculous myositis in a child with acute myelogenous leukemia. Pediatr Neonatol; 2009 Apr;50(2):74-7
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  • [Title] Disseminated tuberculous myositis in a child with acute myelogenous leukemia.
  • We present a case of disseminated tuberculous myositis in a girl with secondary acute myelogenous Leukemia following successful chemotherapy for undifferentiated sarcoma of the maxillary sinus.
  • [MeSH-major] Leukemia, Myeloid, Acute / complications. Myositis / complications. Tuberculosis / complications


41. Larson RA: Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia? Best Pract Res Clin Haematol; 2007 Mar;20(1):29-37
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is secondary leukemia an independent poor prognostic factor in acute myeloid leukemia?
  • Secondary leukemia is a poorly defined term that often refers to the development of acute myeloid leukemia (AML) following the history of a previous disease, such as a myelodysplastic syndrome or a chronic myeloproliferative disorder.
  • Secondary leukemia can also be a consequence of treatment with chemotherapy, including alkylating agents and topoisomerase II inhibitors, and/or radiotherapy, or due to exposure to environmental carcinogens.
  • Outcomes for this large and variable group of patients with secondary AML have been poor compared to people who develop AML de novo.
  • The question arises whether a diagnosis of secondary leukemia per se indicates a poor prognosis or whether their bad outcomes result from an association with certain morphologic and biologic characteristics.
  • Morphologic dysplasia in de novo AML is related to unfavorable cytogenetics, but has no independent prognostic relevance under the conditions of intensive chemotherapy.
  • While there is no significant correlation between cytogenetic risk groups and dysplasia, cytogenetic features do have an impact on outcome among both de novo and secondary AML patients.
  • In various subgroups of secondary AML, the spectrum of cytogenetic abnormalities is similar to de novo AML, but the frequency of abnormalities associated with unfavorable and intermediate risk cytogenetics, such as a complex karyotype, trisomy 8, monosomy 7, and others, is higher in secondary AML.
  • The survival of patients with therapy-related myeloid leukemia (t-AML) is generally shorter than for those with de novo AML within the same cytogenetic risk group.
  • Across the population of t-AML, however, survival varies according to cytogenetic risk group, with longer survival in patients with favorable-risk karyotypes.
  • The term secondary AML is too broad and imprecise to be of importance and should not be used.
  • These AML patients should be enrolled on front-line chemotherapy trials and should be stratified by pretreatment disease status and exposure history, if necessary.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / genetics
  • [MeSH-minor] Acute Disease. Humans. Myelodysplastic Syndromes. Myeloproliferative Disorders. Neoplasms, Second Primary / drug therapy. Neoplasms, Second Primary / genetics. Prognosis. Survival Analysis

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  • (PMID = 17336252.001).
  • [ISSN] 1521-6926
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 23
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42. Bacher U, Haferlach T, Schoch C: Gain of 9p due to an unbalanced rearrangement der(9;18): a recurrent clonal abnormality in chronic myeloproliferative disorders. Cancer Genet Cytogenet; 2005 Jul 15;160(2):179-83
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  • Three cases were diagnosed as polycythemia vera; one case presented with secondary acute myeloid leukemia following idiopathic osteomyelofibrosis.

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  • (PMID = 15993276.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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43. Schoen C, Unzicker C, Stuhler G, Elias J, Einsele H, Grigoleit GU, Abele-Horn M, Mielke S: Life-threatening infection caused by daptomycin-resistant Corynebacterium jeikeium in a neutropenic patient. J Clin Microbiol; 2009 Jul;47(7):2328-31
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  • Here we report, for the first time, the isolation of a highly daptomycin-resistant strain of Corynebacterium jeikeium causing a life-threatening infection in a neutropenic patient undergoing cord blood transplantation for secondary acute myeloid leukemia.
  • [MeSH-minor] Cord Blood Stem Cell Transplantation / adverse effects. Humans. Leukemia, Myeloid, Acute / complications. Male. Microbial Sensitivity Tests. Middle Aged

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  • (PMID = 19420177.001).
  • [ISSN] 1098-660X
  • [Journal-full-title] Journal of clinical microbiology
  • [ISO-abbreviation] J. Clin. Microbiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; NWQ5N31VKK / Daptomycin
  • [Other-IDs] NLM/ PMC2708472
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44. Borthakur G, Lin E, Jain N, Estey EE, Cortes JE, O'Brien S, Faderl S, Ravandi F, Pierce S, Kantarjian H: Survival is poorer in patients with secondary core-binding factor acute myelogenous leukemia compared with de novo core-binding factor leukemia. Cancer; 2009 Jul 15;115(14):3217-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survival is poorer in patients with secondary core-binding factor acute myelogenous leukemia compared with de novo core-binding factor leukemia.
  • BACKGROUND: Therapy related secondary acute myelogenous leukemia (AML) was commonly associated with prior exposure to alkylating agents or topoisomerase inhibitor.
  • The long-term outcome of such patients with secondary AML was found to be worse than that of patients with de novo AML.
  • Earlier reports suggested similar outcomes for patients with de novo and secondary AML associated with core-binding factor (CBF) abnormalities.
  • METHODS: A total of 188 patients with CBF AML were analyzed.
  • The frequency of secondary CBF AML was 9%.
  • RESULTS: Patients with secondary CBF AML were found to have significantly worse overall (OS) and event-free survival (EFS) compared with patients with de novo CBF AML.
  • Secondary CBF AML status appeared to have only marginal significance in multivariate analysis.
  • CONCLUSIONS: Matched analysis (by age, Eastern Cooperative Oncology Group performance status, and additional cytogenetic abnormality) indicated worse OS and EFS in patients with secondary CBF AML.
  • [MeSH-major] Core Binding Factors / metabolism. Leukemia, Myeloid, Acute / mortality. Neoplasms, Second Primary / mortality

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  • (PMID = 19441109.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factors; 04079A1RDZ / Cytarabine
  • [Other-IDs] NLM/ NIHMS629439; NLM/ PMC4184418
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45. Hijiya N, Hudson MM, Lensing S, Zacher M, Onciu M, Behm FG, Razzouk BI, Ribeiro RC, Rubnitz JE, Sandlund JT, Rivera GK, Evans WE, Relling MV, Pui CH: Cumulative incidence of secondary neoplasms as a first event after childhood acute lymphoblastic leukemia. JAMA; 2007 Mar 21;297(11):1207-15
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  • [Title] Cumulative incidence of secondary neoplasms as a first event after childhood acute lymphoblastic leukemia.
  • CONTEXT: Little is known about the incidence of secondary neoplasms after 15 to 20 years in children and adolescents who were treated for acute lymphoblastic leukemia.
  • OBJECTIVES: To investigate the cumulative incidence of secondary neoplasms in pediatric patients treated for acute lymphoblastic leukemia over 30 years and to characterize late-occurring tumors.
  • DESIGN, SETTING, AND PATIENTS: Retrospective study of 2169 patients with acute lymphoblastic leukemia treated between 1962 and 1998 at St Jude Children's Research Hospital, Memphis, Tenn, who achieved complete remission and had a median follow-up time of 18.7 years (range, 2.4-41.3 years).
  • MAIN OUTCOME MEASURES: Cumulative incidences of secondary neoplasms in first remission and standard incidence ratios of observed rates compared with rates of cancer development in the general US population.
  • RESULTS: Secondary neoplasms developed as the first event in 123 patients and comprised 46 myeloid malignancies, 3 lymphomas, 14 basal cell carcinomas, 16 other carcinomas, 6 sarcomas, 16 meningiomas, and 22 other brain tumors.
  • The cumulative incidence of secondary neoplasm was 4.17% (SE, 0.46%) at 15 years and increased substantially after 20 years, reaching 10.85% (SE, 1.27%) at 30 years.
  • The cumulative incidence of each tumor type at 30 years was 2.19% (SE, 0.32%) for myeloid malignancy, 0.17% (SE, 0.10%) for lymphoma, 3.00% (SE, 0.59%) for brain tumor, 4.91% (SE, 1.04%) for carcinoma, and 0.57% (SE, 0.37%) for sarcoma.
  • CONCLUSIONS: The cumulative incidence of secondary neoplasms increases steadily over 30 years after treatment of acute lymphoblastic leukemia.
  • Although the majority of the late-occurring secondary neoplasms are low-grade tumors, the increase in incidence of more aggressive malignant neoplasms is significantly higher than expected in the general population.
  • These results suggest that lifelong follow-up of acute lymphoblastic leukemia survivors is needed to ascertain the full impact of treatment and other leukemia-related factors on secondary neoplasm development.

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  • (PMID = 17374815.001).
  • [ISSN] 1538-3598
  • [Journal-full-title] JAMA
  • [ISO-abbreviation] JAMA
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / CA-36401; United States / NCI NIH HHS / CA / CA-51001; United States / NCI NIH HHS / CA / CA-60419; United States / NCI NIH HHS / CA / CA-71907; United States / NCI NIH HHS / CA / CA-78224; United States / NIGMS NIH HHS / GM / GM-61393
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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46. Park MJ, Park YH, Ahn HJ, Choi W, Paik KH, Kim JM, Chang YH, Ryoo BY, Yang SH: Secondary hematological malignancies after breast cancer chemotherapy. Leuk Lymphoma; 2005 Aug;46(8):1183-8
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  • [Title] Secondary hematological malignancies after breast cancer chemotherapy.
  • According to several reports, the 10 year incidence of secondary acute myelogenous leukemia (AML) or myelodysplastic syndrome (MDS) after systemic chemotherapy is approximately 1.5%.
  • We detected 2 cases of secondary AML and 1 case of MDS, 19, 52 and 12 months, respectively, after systemic chemotherapy for breast cancer.
  • Published data on the occurrence of secondary hematological malignancies other than AML or MDS in this setting are scarce.
  • We encountered diffuse large B-cell lymphoma, angioimmunoblastic lymphoma and mantle cell lymphoma as secondary hematological malignancies after systemic chemotherapy for breast cancer.


47. Podgornik H, Debeljak M, Zontar D, Cernelc P, Prestor VV, Jazbec J: RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia. Cancer Genet Cytogenet; 2007 Oct 1;178(1):77-81
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  • [Title] RUNX1 amplification in lineage conversion of childhood B-cell acute lymphoblastic leukemia to acute myelogenous leukemia.
  • Amplification of RUNX1 (alias AML1) is a recurrent karyotypic abnormality in childhood acute lymphoblastic leukemia (ALL) that is generally associated with a poor outcome.
  • It does not occur with other primary chromosomal abnormalities in acute ALL.
  • AML1 amplification in acute myelogenous leukemia (AML) is a rare secondary event described mainly in therapy-related cases.
  • AML1 amplification was found in a 13-year-old patient with AML M4/M5 leukemia that occurred 5 years after she had been diagnosed with common B-cell ALL.
  • Conventional cytogenetic, fluorescent in situ hybridization (FISH), and polymerase chain reaction methods revealed no other chromosomal change expected to occur in a disease that we assumed to be a secondary leukemia.
  • [MeSH-major] Core Binding Factor Alpha 2 Subunit / genetics. Gene Expression Regulation, Neoplastic. Leukemia, B-Cell / genetics. Leukemia, B-Cell / pathology. Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology


48. Ariffin H, Muthukkumaran T, Stanslas J, Sabariah AR, Veerasekaran N, Lin HP: Secondary B-cell acute lymphoblastic leukemia following Wilms' tumor: clinical and in vitro chemosensitivity studies. Leuk Lymphoma; 2005 Aug;46(8):1233-7
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  • [Title] Secondary B-cell acute lymphoblastic leukemia following Wilms' tumor: clinical and in vitro chemosensitivity studies.
  • We report the clinical features and in vitro chemosensitivity assay findings of a 13-year-old girl who developed secondary B-cell acute lymphoblastic leukemia (ALL) 7 years after a diagnosis of Wilms' tumor.

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  • (PMID = 16085568.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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49. Sonneck K, Mannhalter C, Krauth MT, Sperr WR, Schwarzinger I, Fonatsch C, Haas O, Geissler K, Valent P: An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase. Eur J Haematol; 2005 Jul;75(1):73-7
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  • [Title] An unusual case of myelodysplastic syndrome with prolonged clonal stability, indolent clinical course over a decade, and spontaneous regression of AML in the terminal phase.
  • An unusual case of secondary acute myeloid leukemia (AML) with indolent clinical course is described.
  • In 2001, transformation to secondary AML with an increase in bone marrow blasts (>20%) and thrombocytopenia, was found.
  • However, the bone marrow still showed AML with >20% blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / physiopathology. Myelodysplastic Syndromes / complications

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  • [Copyright] (c) Blackwell Munksgaard 2005.
  • (PMID = 15946315.001).
  • [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
  • [Chemical-registry-number] 0 / Receptors, Androgen
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50. Davidsson J, Paulsson K, Lindgren D, Lilljebjörn H, Chaplin T, Forestier E, Andersen MK, Nordgren A, Rosenquist R, Fioretos T, Young BD, Johansson B: Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations. Leukemia; 2010 May;24(5):924-31
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  • [Title] Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations.
  • Although childhood high hyperdiploid acute lymphoblastic leukemia is associated with a favorable outcome, 20% of patients still relapse.
  • This ancestral clone was characterized by numerical changes only, with structural changes and RTK-RAS mutations being secondary to the high hyperdiploid pattern.
  • [MeSH-major] Chromosome Deletion. Diploidy. Genes, ras / genetics. Mutation / genetics. Neoplasm Recurrence, Local / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics


51. Tabone MD, Leverger G: [Outcome of children cured of acute lymphoblastic leukemia]. Bull Acad Natl Med; 2009 Oct;193(7):1519-28
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  • [Title] [Outcome of children cured of acute lymphoblastic leukemia].
  • More than 80% of children with acute lymphoblastic leukemia can now be cured.
  • Cognitive function, school performance and socialization are usually normal in non irradiated patients.
  • Secondary neoplasms are rare, but some are related to previous treatments.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma. Survivors

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  • (PMID = 20669633.001).
  • [ISSN] 0001-4079
  • [Journal-full-title] Bulletin de l'Académie nationale de médecine
  • [ISO-abbreviation] Bull. Acad. Natl. Med.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 32
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52. Bateman CM, Colman SM, Chaplin T, Young BD, Eden TO, Bhakta M, Gratias EJ, van Wering ER, Cazzaniga G, Harrison CJ, Hain R, Ancliff P, Ford AM, Kearney L, Greaves M: Acquisition of genome-wide copy number alterations in monozygotic twins with acute lymphoblastic leukemia. Blood; 2010 Apr 29;115(17):3553-8
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  • [Title] Acquisition of genome-wide copy number alterations in monozygotic twins with acute lymphoblastic leukemia.
  • Chimeric fusion genes are highly prevalent in childhood acute lymphoblastic leukemia (ALL) and are mostly prenatal, early genetic events in the evolutionary trajectory of this cancer.
  • Recurrent CNAs are probably "driver" events contributing critically to clonal diversification and selection, but at diagnosis, their developmental timing is "buried" in the leukemia's covert natural history.
  • These data place all "driver" CNAs secondary to the prenatal gene fusion event and most probably postnatal in the sequential, molecular pathogenesis of ALL.
  • [MeSH-major] Gene Dosage. Genome-Wide Association Study. Polymorphism, Single Nucleotide. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Twins, Monozygotic

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  • [CommentIn] Blood. 2010 Apr 29;115(17):3424-5 [20430963.001]
  • (PMID = 20061556.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Twin Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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53. Barresi V, Palumbo GA, Musso N, Consoli C, Capizzi C, Meli CR, Romano A, Di Raimondo F, Condorelli DF: Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML. Leuk Res; 2010 Nov;34(11):1539-42
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  • [Title] Clonal selection of 11q CN-LOH and CBL gene mutation in a serially studied patient during MDS progression to AML.
  • By conventional metaphase and SNP array cytogenetics we serially studied a patient affected by high-risk myelodysplastic syndrome (MDS), documenting the conversion from partial trisomy 8q to trisomy 8 and partial tetrasomy 8q during progression to acute myeloid leukemia (AML).
  • Moreover, the serial application of high resolution genomic array analysis at different disease stages allowed the description of cryptic abnormalities and the demonstration of their enrichment in the AML phase.
  • In particular the detection and quantification of a copy-neutral loss of heterozygosity region located in chromosome 11q guided the search for point mutations in the CBL gene, thus allowing the escription of the novel missense mutation K382E and the demonstration of its selection during progression to secondary AML.
  • [MeSH-major] Chromosomes, Human, Pair 11. Leukemia, Myeloid, Acute / genetics. Loss of Heterozygosity. Myelodysplastic Syndromes / genetics. Proto-Oncogene Proteins c-cbl / genetics

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 20674974.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] EC 6.3.2.- / CBL protein, human; EC 6.3.2.- / Proto-Oncogene Proteins c-cbl
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54. Then Bergh F, Niklas A, Strauss A, von Ahsen N, Niederwieser D, Schwarz J, Wagner A, Al-Ali HK: Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis. Acta Haematol; 2006;116(3):207-10
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  • [Title] Rapid progression of Myelodysplastic syndrome to acute myeloid leukemia on sequential azathioprine, IFN-beta and copolymer-1 in a patient with multiple sclerosis.
  • Within several months, unusually rapid for this subtype, MDS progressed to secondary acute myeloid leukemia.
  • [MeSH-major] Azathioprine / adverse effects. Interferon-beta / adverse effects. Leukemia, Myeloid / chemically induced. Multiple Sclerosis / complications. Multiple Sclerosis / drug therapy. Myelodysplastic Syndromes / complications. Peptides / adverse effects
  • [MeSH-minor] Acute Disease. Disease Progression. Fatal Outcome. Female. Glatiramer Acetate. Humans. Middle Aged


55. Delhommeau F, Dupont S, Della Valle V, James C, Trannoy S, Massé A, Kosmider O, Le Couedic JP, Robert F, Alberdi A, Lécluse Y, Plo I, Dreyfus FJ, Marzac C, Casadevall N, Lacombe C, Romana SP, Dessen P, Soulier J, Viguié F, Fontenay M, Vainchenker W, Bernard OA: Mutation in TET2 in myeloid cancers. N Engl J Med; 2009 May 28;360(22):2289-301
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  • [Title] Mutation in TET2 in myeloid cancers.
  • BACKGROUND: The myelodysplastic syndromes and myeloproliferative disorders are associated with deregulated production of myeloid cells.
  • METHODS: We conducted a combination of molecular, cytogenetic, comparative-genomic-hybridization, and single-nucleotide-polymorphism analyses to identify a candidate tumor-suppressor gene common to patients with myelodysplastic syndromes, myeloproliferative disorders, and acute myeloid leukemia (AML).
  • RESULTS: We initially identified deletions or mutations in TET2 in three patients with myelodysplastic syndromes, in three of five patients with myeloproliferative disorders, in two patients with primary AML, and in one patient with secondary AML.
  • We selected the six patients with myelodysplastic syndromes or AML because they carried acquired rearrangements on chromosome 4q24; we selected the five patients with myeloproliferative disorders because they carried a dominant clone in hematopoietic progenitor cells that was positive for the V617F mutation in the Janus kinase 2 (JAK2) gene.
  • TET2 defects were observed in 15 of 81 patients with myelodysplastic syndromes (19%), in 24 of 198 patients with myeloproliferative disorders (12%) (with or without the JAK2 V617F mutation), in 5 of 21 patients with secondary AML (24%), and in 2 of 9 patients with chronic myelomonocytic leukemia (22%).
  • CONCLUSIONS: Somatic mutations in TET2 occur in about 15% of patients with various myeloid cancers.
  • [MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation. Myelodysplastic Syndromes / genetics. Myeloproliferative Disorders / genetics. Proto-Oncogene Proteins / genetics


56. Preiss BS, Bergmann OJ, Friis LS, Sørensen AG, Frederiksen M, Gadeberg OV, Mourits-Andersen T, Oestergaard B, Kerndrup GB, AML Study Group of Southern Denmark: Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML. Cancer Genet Cytogenet; 2010 Oct 15;202(2):108-22
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  • [Title] Cytogenetic findings in adult secondary acute myeloid leukemia (AML): frequency of favorable and adverse chromosomal aberrations do not differ from adult de novo AML.
  • During a 15-year period, 161 adult patients were diagnosed with secondary acute myeloid leukemia (s-AML) in the region of Southern Denmark.
  • In 73 patients, the AML diagnosis was preceded by myelodysplastic syndrome (MDS-AML), in 31 patients by an antecedent hematologic disease, and in 57 patients by treatment with chemotherapy and/or irradiation (t-AML).
  • MDS-AML correlated to a normal karyotype (P < 0.001).
  • t-AML correlated to abnormal clones with numerical and structural aberrations (P = 0.03), five or more unrelated aberrations (P = 0.03), marker chromosomes (P = 0.006), abnormal mitoses only (P = 0.01), female sex (P < 0.001), and -7 (P = 0.006).
  • The frequencies of aberrations in s-AML patients were compared with an age-matched group of de novo AML patients diagnosed in the same area and period.
  • In this comparison, s-AML only correlated to -7 (P = 0.02).
  • In 42 patients, we found that MDS patients with an abnormal karyotype were more likely to show cytogenetic evolution during progression to AML than MDS patients with a normal karyotype (P = 0.01).
  • We conclude that population-based cytogenetic studies of adult s-AML and age- and sex-matched de novo AML show comparable distributions of chromosome abnormalities.
  • [MeSH-major] Chromosome Aberrations. Cytogenetic Analysis. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics


57. Szotkowski T, Jarosova M, Faber E, Hubacek J, Hlusi A, Papajik T, Pikalova Z, Kucerova L, Holzerova M, Budikova M, Buriankova E, Plachy R, Potomkova J, Klusova N, Szotkowska R, Indrak K: Precursor T-lymphoblastic lymphoma as a secondary malignancy in a young patient after successful treatment of acute promyelocytic leukemia. Onkologie; 2009 Sep;32(8-9):513-5
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  • [Title] Precursor T-lymphoblastic lymphoma as a secondary malignancy in a young patient after successful treatment of acute promyelocytic leukemia.
  • BACKGROUND: Acute promyelocytic leukemia (APL) is a relatively rare subtype of acute myeloid leukemia.
  • It has become the best curable subtype of acute leukemias in adults due to the inclusion of all-trans-retinoic acid (ATRA) in the treatment.
  • However, chemotherapy administration is inevitably related to many complications, including the risk of secondary malignancies.
  • T-lymphoblastic lymphoma (T-LBL) is an infrequent disease that belongs to the group of highly aggressive lymphomas.
  • CONCLUSION: Several cases of secondary acute lymphoblastic leukemias in 'cured' APL patients have been described, but probably no patient with secondary precursor T-LBL.
  • Secondary malignancy has become one of the topics discussed (not only) in APL patients.
  • [MeSH-major] Leukemia, Promyelocytic, Acute / complications. Leukemia, Promyelocytic, Acute / therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / etiology


58. Tam CS, Seymour JF, Prince HM, Kenealy M, Wolf M, Januszewicz EH, Westerman D: Treatment-related myelodysplasia following fludarabine combination chemotherapy. Haematologica; 2006 Nov;91(11):1546-50
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  • Although myelodysplasia (MDS) and secondary acute myeloid leukemia (sAML) are rare following fludarabine monotherapy, the risk of these diseases may potentially be increased when fludarabine is combined with cyclophosphamide or mitoxantrone due to synergistic effects on the inhibition of DNA repair.

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  • (PMID = 17082012.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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59. Karp JE, Smith BD, Gojo I, Lancet JE, Greer J, Klein M, Morris L, Levis MJ, Gore SD, Wright JJ, Garrett-Mayer E: Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features. Clin Cancer Res; 2008 May 15;14(10):3077-82
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  • [Title] Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features.
  • PURPOSE: Acute myelogenous leukemia (AML) does not have a high cure rate, particularly in patients with poor-risk features.
  • Tipifarnib is an oral farnesyltransferase inhibitor with activity in AML.
  • We conducted a phase II trial of maintenance tipifarnib monotherapy for 48 adults with poor-risk AML in first CR.
  • Comparison of CR durations for 25 patients who received two-cycle timed sequential therapy followed by tipifarnib maintenance with 23 historically similar patients who did not receive tipifarnib showed that tipifarnib was associated with DFS prolongation for patients with secondary AML and adverse cytogenetics.
  • CONCLUSIONS: This study suggests that some patients with poor-risk AML, including patients with secondary AML and adverse cytogenetics, may benefit from tipifarnib maintenance therapy.

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  • (PMID = 18483374.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 69854; United States / NCI NIH HHS / CA / U01 CA069854-07; United States / NCI NIH HHS / CA / U01 CA069854; United States / NCI NIH HHS / CA / U01 CA70095; United States / NCI NIH HHS / CA / U01 CA070095
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinolones; 192185-72-1 / tipifarnib
  • [Other-IDs] NLM/ NIHMS281726; NLM/ PMC3074480
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60. Paulsson K, Forestier E, Lilljebjörn H, Heldrup J, Behrendtz M, Young BD, Johansson B: Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia. Proc Natl Acad Sci U S A; 2010 Dec 14;107(50):21719-24
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  • [Title] Genetic landscape of high hyperdiploid childhood acute lymphoblastic leukemia.
  • High hyperdiploid acute lymphoblastic leukemia (ALL) is one of the most common malignancies in children.
  • Here we provide a comprehensive characterization of the genetic landscape of high hyperdiploid childhood ALL, including the heterogeneous pattern of secondary genetic events.
  • [MeSH-major] Chromosome Aberrations. Diploidy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


61. Sandlund JT, Pui CH, Zhou Y, Behm FG, Onciu M, Razzouk BI, Hijiya N, Campana D, Hudson MM, Ribeiro RC: Effective treatment of advanced-stage childhood lymphoblastic lymphoma without prophylactic cranial irradiation: results of St Jude NHL13 study. Leukemia; 2009 Jun;23(6):1127-30
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  • [Title] Effective treatment of advanced-stage childhood lymphoblastic lymphoma without prophylactic cranial irradiation: results of St Jude NHL13 study.
  • There has been a steady improvement in cure rates for children with advanced-stage lymphoblastic non-Hodgkin's lymphoma.
  • To further improve cure rates whereas minimizing long-term toxicity, we designed a protocol (NHL13) based on a regimen for childhood T-cell acute lymphoblastic leukemia, which features intensive intrathecal chemotherapy for central -nervous system-directed therapy and excludes prophylactic cranial irradiation.
  • From 1992 to 2002, 41 patients with advanced-stage lymphoblastic lymphoma were enrolled on the protocol.
  • Adverse events included two induction failures, one death from typhlitis during remission, three relapses and one secondary acute myeloid leukemia.
  • The treatment described here produces high cure rates in children with lymphoblastic lymphoma without the use of prophylactic cranial irradiation.

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  • (PMID = 19194463.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; None / None / / P30 CA021765-31; United States / NCI NIH HHS / CA / CA 21765; United States / NCI NIH HHS / CA / P30 CA021765-31
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS161582; NLM/ PMC2843413
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62. D'Andrea AD: Targeting DNA repair pathways in AML. Best Pract Res Clin Haematol; 2010 Dec;23(4):469-73
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  • [Title] Targeting DNA repair pathways in AML.
  • DNA repair inhibitors, such as poly-ADP-ribose polymerase (PARP) inhibitors, may be useful in a small subset of acute myeloid leukemia (AML) patients, especially those who have complex karyotypes or those with secondary AML.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA Repair / drug effects. Enzyme Inhibitors / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / metabolism

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  • [Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.
  • (PMID = 21130409.001).
  • [ISSN] 1532-1924
  • [Journal-full-title] Best practice & research. Clinical haematology
  • [ISO-abbreviation] Best Pract Res Clin Haematol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Enzyme Inhibitors; 0 / Poly(ADP-ribose) Polymerase Inhibitors; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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63. Tretiak NM, Vakul'chuk OM, Kalinina SIu: [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)]. Lik Sprava; 2008 Jan-Feb;(1-2):89-96
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  • [Title] [Induced acute non-lymphoblastic leukemia and prognostic significance of cytogenetic abnormalities: trisomy in chromosome 8, inv(16)(p13q22), and t(8;21)(q22;q22)].
  • 3 patients with secondary acute non-lymphoblastic leucosis have been observed.


64. Xu XQ, Wang JM, Lü SQ, Chen L, Yang JM, Zhang WP, Song XM, Hou J, Ni X, Qiu HY: Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population. Haematologica; 2009 Jul;94(7):919-27
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  • [Title] Clinical and biological characteristics of adult biphenotypic acute leukemia in comparison with that of acute myeloid leukemia and acute lymphoblastic leukemia: a case series of a Chinese population.
  • BACKGROUND: Biphenotypic acute leukemia is a rare disorder that is difficult to diagnose.
  • It displays features of both myeloid and lymphoid lineage.
  • There is still a lack of studies in biphenotypic acute leukemia in a Chinese population.
  • We present here a comprehensive investigation of the clinical and biological characteristics, and outcome of biphenotypic acute leukemia in our hospital in over a seven year period.
  • DESIGN AND METHODS: We retrospectively analyzed 452 adult acute leukemia patients diagnosed according to French-American-British (FAB) classification and biphenotypic acute leukemia diagnosed according to European Group for the Immunological Characterization of Leukemias (EGIL) classification, respectively.
  • Biological characteristics, response to treatment, and outcome were examined in biphenotypic acute leukemia patients and compared with that in acute myeloid leukemia and acute lymphoblastic leukemia patients with complete follow-up profiles diagnosed in the same period.
  • RESULTS: Of 452 acute leukemia patients, 21 cases (4.6%) were diagnosed as biphenotypic acute leukemia.
  • Among them, 14 (66.7%) were B lymphoid and myeloid, 5 (23.8%) were T lymphoid and myeloid, one (4.8%) was T/B lymphoid and one (4.8%) was trilineage differentiation.
  • When compared with acute myeloid leukemia and acute lymphoblastic leukemia, patients with biphenotypic acute leukemia showed significantly higher incidence of CD34 antigen expression, unfavorable karyotypes, and extramedullary infiltration (p<0.05).
  • In this cohort of patients with biphenotypic acute leukemia, t(9;22) was the most common abnormality in chromosome structure.
  • The median disease-free survival and overall survival in biphenotypic acute leukemia patients was five months and ten months, respectively, significantly shorter than those in acute myeloid leukemia and acute lymphoblastic leukemia patients (p<0.05).
  • CONCLUSIONS: The prognosis of biphenotypic acute leukemia patients is poor when compared with de novo acute myeloid leukemia or acute lymphoblastic leukemia.
  • Biphenotypic acute leukemia patients showed a much higher incidence of CD34 antigen expression, complex abnormal karyotype, extramedullary infiltration, relapse, and resistance to therapy after relapse.
  • [MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Myeloid, Acute / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis


65. Bhojwani D, Moskowitz N, Raetz EA, Carroll WL: Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia. Paediatr Drugs; 2007;9(3):149-56
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  • [Title] Potential of gene expression profiling in the management of childhood acute lymphoblastic leukemia.
  • Childhood acute lymphoblastic leukemia (ALL) is a heterogeneous disease.
  • Identification of patients who are predicted to have an unfavorable outcome may allow for early intervention such as intensification of therapy or avoidance of drugs that are associated with specific secondary effects such as therapy-related acute myelogenous leukemia.
  • [MeSH-major] Gene Expression Profiling. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma
  • [MeSH-minor] Child. Diploidy. Drug Resistance, Neoplasm / genetics. Humans. Oligonucleotide Array Sequence Analysis. Oncogene Proteins / genetics. Secondary Prevention

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  • (PMID = 17523695.001).
  • [ISSN] 1174-5878
  • [Journal-full-title] Paediatric drugs
  • [ISO-abbreviation] Paediatr Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA114762
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Oncogene Proteins
  • [Number-of-references] 36
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66. Nakai K, Kanda Y, Fukuhara S, Sakamaki H, Okamoto S, Kodera Y, Tanosaki R, Takahashi S, Matsushima T, Atsuta Y, Hamajima N, Kasai M, Kato S: Value of chemotherapy before allogeneic hematopoietic stem cell transplantation from an HLA-identical sibling donor for myelodysplastic syndrome. Leukemia; 2005 Mar;19(3):396-401
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  • The cumulative incidence of grade II-IV acute GVHD was 33%.
  • OS at 5 years was 57% for patients who underwent allo-SCT as a primary treatment for refractory anemia with excess blasts in transformation (RAEB-t) or secondary acute myeloid leukemia (AML) and 54% for those who underwent allo-SCT in remission after induction chemotherapy (P=0.81).
  • Although only a randomized controlled trial will be able to establish a definite conclusion, these results do not support the administration of induction chemotherapy for patients with RAEB-t or secondary AML before allo-SCT.


67. Pui CH, Campana D, Pei D, Bowman WP, Sandlund JT, Kaste SC, Ribeiro RC, Rubnitz JE, Raimondi SC, Onciu M, Coustan-Smith E, Kun LE, Jeha S, Cheng C, Howard SC, Simmons V, Bayles A, Metzger ML, Boyett JM, Leung W, Handgretinger R, Downing JR, Evans WE, Relling MV: Treating childhood acute lymphoblastic leukemia without cranial irradiation. N Engl J Med; 2009 Jun 25;360(26):2730-41
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  • [Title] Treating childhood acute lymphoblastic leukemia without cranial irradiation.
  • BACKGROUND: Prophylactic cranial irradiation has been a standard treatment in children with acute lymphoblastic leukemia (ALL) who are at high risk for central nervous system (CNS) relapse.
  • CNS leukemia (CNS-3 status) or a traumatic lumbar puncture with blast cells at diagnosis and a high level of minimal residual disease (> or = 1%) after 6 weeks of remission induction were significantly associated with poorer event-free survival.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] 6-Mercaptopurine / administration & dosage. Adolescent. Asparaginase / administration & dosage. Asparaginase / adverse effects. Central Nervous System Neoplasms / drug therapy. Child. Child, Preschool. Combined Modality Therapy. Cranial Irradiation. Cyclophosphamide / administration & dosage. Daunorubicin / administration & dosage. Dexamethasone / administration & dosage. Hematopoietic Stem Cell Transplantation. Humans. Infant. Methotrexate / adverse effects. Remission Induction / methods. Risk Factors. Secondary Prevention. Survival Analysis. Treatment Outcome. Vincristine / administration & dosage

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  • Hazardous Substances Data Bank. DAUNORUBICIN .
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  • [Copyright] 2009 Massachusetts Medical Society
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  • (PMID = 19553647.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00137111
  • [Grant] United States / NIGMS NIH HHS / GM / U01 GM061393; United States / NCI NIH HHS / CA / R01 CA078224; United States / NCI NIH HHS / CA / R37 CA036401; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / R01 CA051001-13; United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA78224; United States / NCI NIH HHS / CA / R01 CA060419; United States / NCI NIH HHS / CA / CA60419; United States / NIGMS NIH HHS / GM / GM61393; United States / NCI NIH HHS / CA / P30 CA021765; United States / NIGMS NIH HHS / GM / U01 GM061393-090007; United States / NCI NIH HHS / CA / R01 CA051001; United States / NCI NIH HHS / CA / R01 CA036401; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / U01 CA060419
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 7S5I7G3JQL / Dexamethasone; 8N3DW7272P / Cyclophosphamide; E7WED276I5 / 6-Mercaptopurine; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
  • [Other-IDs] NLM/ NIHMS118392; NLM/ PMC2754320
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68. Wu S, Fischer L, Gökbuget N, Schwartz S, Burmeister T, Notter M, Hoelzer D, Fuchs H, Blau IW, Hofmann WK, Thiel E: Expression of interleukin 15 in primary adult acute lymphoblastic leukemia. Cancer; 2010 Jan 15;116(2):387-92
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  • [Title] Expression of interleukin 15 in primary adult acute lymphoblastic leukemia.
  • We determined the expression of IL-15 in lymphoblasts and evaluated its potential impact on the outcome in adult acute lymphoblastic leukemia (ALL).
  • These patients were enrolled in the German Multicenter Acute Lymphoblastic Leukemia June 1999 and July 2003 study trials.
  • [MeSH-major] Interleukin-15 / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Disease-Free Survival. Female. Gene Expression. Humans. Immunophenotyping. Karyotyping. Lymphatic Metastasis. Male. Mediastinal Neoplasms / secondary. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19924795.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-15
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69. Valera ET, Brassesco MS, Germeshausen M, Silveira Vda S, Queiroz RG, Roxo P, Scrideli CA, de Menezes UP, Ferriani V, Tone LG: Acute lymphoblastic leukemia following severe congenital neutropenia or de novo ALL? Leuk Res; 2009 Sep;33(9):e139-42
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  • [Title] Acute lymphoblastic leukemia following severe congenital neutropenia or de novo ALL?
  • Acute lymphoblastic leukemia (ALL) presenting with neutropenia alone is very rare.
  • Nevertheless, the genetic background for SCN is heterogeneous and a non-described mutation for SCN followed by a secondary ALL cannot be excluded.
  • [MeSH-major] Neutropenia / congenital. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 19398129.001).
  • [ISSN] 1873-5835
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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70. Moorman AV, Raimondi SC, Pui CH, Baruchel A, Biondi A, Carroll AJ, Forestier E, Gaynon PS, Harbott J, Harms DO, Heerema N, Pieters R, Schrappe M, Silverman LB, Vilmer E, Harrison CJ, Ponte di Legno Working Group: No prognostic effect of additional chromosomal abnormalities in children with acute lymphoblastic leukemia and 11q23 abnormalities. Leukemia; 2005 Apr;19(4):557-63
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  • [Title] No prognostic effect of additional chromosomal abnormalities in children with acute lymphoblastic leukemia and 11q23 abnormalities.
  • This study characterized the additional chromosomal abnormalities (ACA) associated with 11q23 rearrangements in 450 infants and children with acute lymphoblastic leukemia (ALL) and examined the impact of these ACA on survival.
  • Del(11)(q23) abnormalities were heterogeneous and occasionally secondary to t(9;22)(q34;q11.2).
  • This study has conclusively demonstrated that there is no prognostic effect of secondary chromosomal changes in association with 11q23 abnormalities in childhood ALL.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / mortality

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  • (PMID = 15744345.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA21765; United States / NCI NIH HHS / CA / CA36401; United States / NCI NIH HHS / CA / CA51001; United States / NCI NIH HHS / CA / CA60419; United States / NCI NIH HHS / CA / CA78224; United States / NIGMS NIH HHS / GM / GM61393
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
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71. Borgmann A, Zinn C, Hartmann R, Herold R, Kaatsch P, Escherich G, Möricke A, Henze G, von Stackelberg A, ALL-REZ BFM Study Group: Secondary malignant neoplasms after intensive treatment of relapsed acute lymphoblastic leukaemia in childhood. Eur J Cancer; 2008 Jan;44(2):257-68

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  • [Title] Secondary malignant neoplasms after intensive treatment of relapsed acute lymphoblastic leukaemia in childhood.
  • PURPOSE: To investigate the cumulative incidence of and the risk factors for developing second malignant neoplasms (SMN) in children and adolescents following treatment for relapse of acute lymphocytic leukaemia (ALL).
  • METHODS: Patients (1376) up to 18 years of age with first relapse of non-B-cell ALL were treated and achieved a 2nd complete remission (CR).
  • RESULTS: Out of the 1376 patients 21 were diagnosed with SMN including non-lymphoblastic leukaemia/myelodysplastic syndrome (n=6), osteo-/Ewing's-/fibroblastic sarcoma (n=4), B-cell ALL/lymphoma (n=2), thyroid carcinoma (n=2), basal cell carcinoma, adeno carcinoma, squamous cell carcinoma, meningioma, malignant histiocytosis, glioblastoma and anaplastic astrocytoma (n=1 each).
  • The association of SMN to SCT seemed to be a secondary effect at least partially mediated by exposure to high doses of VP16 and CY given for conditioning therapy.
  • [MeSH-major] Neoplasms, Second Primary / epidemiology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Disease-Free Survival. Female. Germany / epidemiology. Humans. Incidence. Infant. Male. Multicenter Studies as Topic. Remission Induction. Risk Factors. Secondary Prevention

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  • (PMID = 17981026.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Mertens R; Imbach P; Pongratz E; Rupprecht T; Henze G; Wickmann L; Otte J; Bode U; Eberl W; Pekrun A; Kirschstein M; Hofmann K; Frank R; Möbius D; Andler W; Niekrens C; Breu H; Suttorp M; Göbel U; Weinmann G; Sauerbrey A; Beck JF; Janka-Schaub G; Welte K; Kulozik A; Tautz C; Graf N; Fink FM; Zintl F; Hermann J; Rupprath G; Dupuis W; Rodehüser M; Schrappe M; Berthold F; Sternschulte W; Körholz D; Schmitt K; Selle B; Gutjahr P; Dürken M; Christiansen H; Rose M; Borkhardt A; Burdach S; Jürgens H; Scheurlen W; Eggers G; Geib R; Dickerhoff R; Bielack S; Rauh W; Niethammer D; Debatin KM; Gadner H; Dohrn B; Schlegel PG; Niggli F
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72. Lemez P, Attarbaschi A, Béné MC, Bertrand Y, Castoldi G, Forestier E, Garand R, Haas OA, Kagialis-Girard S, Ludwig WD, Matutes E, Mejstríková E, Pages MP, Pickl W, Porwit A, Orfao A, Schabath R, Starý J, Strobl H, Talmant P, van't Veer MB, Zemanová Z, European Group for the Immunological Characterization of Leukemias (EGIL): Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases. Eur J Haematol; 2010 Oct;85(4):300-8
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  • [Title] Childhood near-tetraploid acute lymphoblastic leukemia: an EGIL study on 36 cases.
  • OBJECTIVES: Patients with near-tetraploid (karyotype: 81 - 103 chromosomes) acute lymphoblastic leukemia (NT-ALL) constitute about 1% of childhood ALL and data reported on them are limited and controversial.
  • Secondary myelodysplastic syndrome developed in two patients with NT-BCP-ALL.
  • [MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma

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  • [Copyright] © 2010 John Wiley & Sons A/S.
  • (PMID = 20561032.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; EC 2.7.10.2 / Fusion Proteins, bcr-abl
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73. Shivakumar R, Tan W, Wilding GE, Wang ES, Wetzler M: Biologic features and treatment outcome of secondary acute lymphoblastic leukemia--a review of 101 cases. Ann Oncol; 2008 Sep;19(9):1634-8
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  • [Title] Biologic features and treatment outcome of secondary acute lymphoblastic leukemia--a review of 101 cases.
  • BACKGROUND: Secondary acute lymphoblastic leukemia (sALL) is a rare disease and its biologic features are not well characterized.

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  • (PMID = 18467310.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA16056
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2733065
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74. Chiu PP, Jiang H, Dick JE: Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance. Blood; 2010 Dec 9;116(24):5268-79
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  • [Title] Leukemia-initiating cells in human T-lymphoblastic leukemia exhibit glucocorticoid resistance.
  • T-cell acute lymphoblastic leukemia (T-ALL) is associated with a significant risk of disease relapse, but the biological basis for relapse is poorly understood.
  • Long-term proliferation in response to NOTCH1 activating signals in OP9-DL1 coculture system or capacity to initiate leukemia in xenografts by the CD7(+)CD1a(-) subset of primary T-ALL samples was superior to other subsets, refining the identity of T-ALL L-ICs.
  • T-ALL engraftment was improved in nonobese diabetic/severe combined immunodeficiency (NOD/scid)IL2Rγ(null) (NSG) mice compared with NOD/scid with anti-CD122 treatment (NS122), but both showed changes in leukemia immunophenotype.
  • Clonal analysis of xenografts using the TCRG locus revealed the presence of subclones of T-ALL L-ICs, some of which possess a selective growth advantage and correlated with the capacity of CD7(+)CD1a(+) xenograft cells to engraft secondary NSG mice.

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  • (PMID = 20810926.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / Antigens, CD7; 0 / Antineoplastic Agents, Hormonal; 0 / CD1a antigen; 0 / Glucocorticoids; 0 / Notch1 protein, mouse; 0 / Receptor, Notch1; 7S5I7G3JQL / Dexamethasone
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75. Stanulla M, Dynybil C, Bartels DB, Dördelmann M, Löning L, Claviez A, Schrappe M, ALL-BFM study group: The NQO1 C609T polymorphism is associated with risk of secondary malignant neoplasms after treatment for childhood acute lymphoblastic leukemia: a matched-pair analysis from the ALL-BFM study group. Haematologica; 2007 Nov;92(11):1581-2
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  • [Title] The NQO1 C609T polymorphism is associated with risk of secondary malignant neoplasms after treatment for childhood acute lymphoblastic leukemia: a matched-pair analysis from the ALL-BFM study group.
  • In a matched-pair study, we analyzed the association of a phenotypically relevant NQO1 polymorphism (C609T) with risk of secondary malignant neoplasms (SMN) after treatment for childhood acute lymphoblastic leukemia.
  • [MeSH-major] NAD(P)H Dehydrogenase (Quinone) / genetics. Neoplasms, Second Primary / genetics. Polymorphism, Genetic. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • (PMID = 18024413.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 3.5.1.1 / Asparaginase; VB0R961HZT / Prednisone; ZS7284E0ZP / Daunorubicin; PVDA protocol
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76. Skärby TV, Anderson H, Heldrup J, Kanerva JA, Seidel H, Schmiegelow K, Nordic Society of Paediatric Haematology and Oncology (NOPHO): High leucovorin doses during high-dose methotrexate treatment may reduce the cure rate in childhood acute lymphoblastic leukemia. Leukemia; 2006 Nov;20(11):1955-62
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  • [Title] High leucovorin doses during high-dose methotrexate treatment may reduce the cure rate in childhood acute lymphoblastic leukemia.
  • We explored the relationship between time to relapse and different exposure variables (serum methotrexate (S-MTX) 23, 36 and 42 h after start of administration, MTX elimination time and leucovorin (LV) dose) during high-dose MTX (HDM) treatment of 445 children with acute lymphoblastic leukemia.
  • MTX was infused at 5 g/m2 (non-high risk) or 8 g/m2 (high risk) over 24 h, 2-9 times per patient.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Leucovorin / adverse effects. Methotrexate / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Vitamin B Complex / adverse effects
  • [MeSH-minor] Case-Control Studies. Child. Child, Preschool. Disease-Free Survival. Drug Interactions. Female. Humans. Male. Registries. Risk Factors. Secondary Prevention


77. Radhakrishnan A, Sithinamsuwan P, Harvey AS, Flanagan D, Fitt G, Berlangieri S, Jackson GD, Berkovic SF, Scheffer IE: Multifocal epilepsy: the role of palliative resection - intractable frontal and occipital lobe epilepsy secondary to radiotherapy for acute lymphoblastic leukaemia. Epileptic Disord; 2008 Dec;10(4):362-70
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  • [Title] Multifocal epilepsy: the role of palliative resection - intractable frontal and occipital lobe epilepsy secondary to radiotherapy for acute lymphoblastic leukaemia.
  • We report an adolescent with intractable frontal and occipital lobe seizures, secondary to complications of treatment for acute lymphoblastic leukaemia as a young child.
  • Detailed electro-clinical and imaging studies showed multiple, frontal lobe seizures per day with less frequent and non-debilitating, simple, occipital lobe seizures.
  • [MeSH-major] Epilepsies, Partial / etiology. Epilepsies, Partial / surgery. Epilepsy, Frontal Lobe / surgery. Neurosurgical Procedures. Occipital Lobe. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / complications. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy. Radiotherapy / adverse effects

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  • (PMID = 19017581.001).
  • [ISSN] 1294-9361
  • [Journal-full-title] Epileptic disorders : international epilepsy journal with videotape
  • [ISO-abbreviation] Epileptic Disord
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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78. Amare Kadam PS, Raje GC, Pais AP, Banavali S: Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL. Cancer Genet Cytogenet; 2008 Apr 1;182(1):27-32
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  • [Title] Coexistence of ETV6/RUNX1 and MLL aberrations in B-cell precursor acute lymphoblastic leukemia discloses a small subclass of BCP-ALL.
  • Out of 76 pediatric cases of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) positive for ETV6/RUNX1 (previously TEL/AML1) resulting from t(12;21), 7 cases revealed coexistence of ETV6/RUNX1 and MLL aberrations.
  • ETV6/RUNX1 and MLL aberration clone size in these cases was suggestive of ETV6/RUNX1 as an early primary event, originating in the embryonic or infant stage and developing into leukemia by later acquisition of MLL aberration, ETV6 loss, and ETV6/RUNX1 duplication as secondary events.
  • [MeSH-major] Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics

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  • (PMID = 18328947.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
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79. Cox CV, Martin HM, Kearns PR, Virgo P, Evely RS, Blair A: Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia. Blood; 2007 Jan 15;109(2):674-82
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  • [Title] Characterization of a progenitor cell population in childhood T-cell acute lymphoblastic leukemia.
  • A significant proportion of children with T-cell acute lymphoblastic leukemia (T-ALL) continue to fail therapy.
  • These T-ALL cells successfully repopulated secondary and tertiary recipients with equivalent levels of engraftment, demonstrating self-renewal ability.
  • The immunophenotype and genotype of the original leukemia cells were preserved with serial passage in the NOD/SCID mice.
  • [MeSH-major] Leukemia-Lymphoma, Adult T-Cell / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Stem Cells / immunology. Stem Cells / pathology


80. Afzal S, Ethier MC, Dupuis LL, Tang L, Punnett AS, Richardson SE, Allen U, Abla O, Sung L: Risk factors for infection-related outcomes during induction therapy for childhood acute lymphoblastic leukemia. Pediatr Infect Dis J; 2009 Dec;28(12):1064-8
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  • [Title] Risk factors for infection-related outcomes during induction therapy for childhood acute lymphoblastic leukemia.
  • BACKGROUND: The primary objective was to describe microbiologically documented infections during induction therapy for acute lymphoblastic leukemia.
  • The secondary objectives were to describe risk factors for microbiologically documented infections and for patients with a febrile episode, to identify risk factors for recurrence of fever or reinitiation of antibiotics.
  • CONCLUSIONS: About 20% of children with acute lymphoblastic leukemia have a microbiologically documented infection during induction.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Bacterial Infections / complications. Precursor Cell Lymphoblastic Leukemia-Lymphoma / microbiology

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  • (PMID = 19773675.001).
  • [ISSN] 1532-0987
  • [Journal-full-title] The Pediatric infectious disease journal
  • [ISO-abbreviation] Pediatr. Infect. Dis. J.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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81. Hussein K, Bock O, Theophile K, Schulz-Bischof K, Porwit A, Schlue J, Jonigk D, Kreipe H: MPLW515L mutation in acute megakaryoblastic leukaemia. Leukemia; 2009 May;23(5):852-5
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  • [Title] MPLW515L mutation in acute megakaryoblastic leukaemia.
  • A series of primary and secondary acute myeloid leukaemias (AML) with megakaryoblastic phenotype and myelofibrosis unrelated to PMF (n=12) was analysed for the MPL(W515K/L) mutation by pyrosequencing.
  • None of the secondary AML cases evolving from pre-existing PMF showed MPL(W515K/L) (n=4).
  • We conclude that MPL(W515L) occurs in a considerable proportion of acute megakaryoblastic leukaemias with myelofibrosis unrelated to PMF.
  • [MeSH-major] Leukemia, Megakaryoblastic, Acute / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Mutation / genetics. Primary Myelofibrosis / genetics. Receptors, Thrombopoietin / genetics

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  • [CommentIn] Leukemia. 2009 Nov;23(11):2159-60 [19657363.001]
  • (PMID = 19194467.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Thrombopoietin; 143641-95-6 / MPL protein, human; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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82. Récher C, Beyne-Rauzy O, Demur C, Chicanne G, Dos Santos C, Mas VM, Benzaquen D, Laurent G, Huguet F, Payrastre B: Antileukemic activity of rapamycin in acute myeloid leukemia. Blood; 2005 Mar 15;105(6):2527-34
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  • [Title] Antileukemic activity of rapamycin in acute myeloid leukemia.
  • In this study, we show that mTOR inhibition by rapamycin strongly inhibits the growth of the most immature acute myeloid leukemia (AML) cell lines through blockade in G0/G1 phase of the cell cycle.
  • Accordingly, 2 downstream effectors of mTOR, 4E-BP1 and p70S6K, are phosphorylated in a rapamycin-sensitive manner in a series of 23 AML cases.
  • Interestingly, the mTOR inhibitor markedly impairs the clonogenic properties of fresh AML cells while sparing normal hematopoietic progenitors.
  • Moreover, rapamycin induces significant clinical responses in 4 of 9 patients with either refractory/relapsed de novo AML or secondary AML.
  • Overall, our data strongly suggest that mTOR is aberrantly regulated in most AML cells and that rapamycin and analogs, by targeting the clonogenic compartment of the leukemic clone, may be used as new compounds in AML therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. G0 Phase / drug effects. G1 Phase / drug effects. Leukemia, Myeloid, Acute / metabolism. Protein Kinases / metabolism. Sirolimus / pharmacology

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  • (PMID = 15550488.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibiotics, Antineoplastic; 0 / EIF4EBP1 protein, human; 0 / Phosphoproteins; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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83. Yetgin S, Tavil B, Aytac S, Kuskonmaz B, Kanra G: Unexpected protection from infection by two booster hepatitis B virus vaccination in children with acute lymphoblastic leukemia. Leuk Res; 2007 Apr;31(4):493-6
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  • [Title] Unexpected protection from infection by two booster hepatitis B virus vaccination in children with acute lymphoblastic leukemia.
  • The protective power of two booster dose vaccination against hepatitis B virus (HBV) infection has not been previously studied in patients with acute lymphoblastic leukemia (ALL) who remained unresponsive to immunization.
  • Our study results suggest that a high protective role of HBV vaccination was also observed in non-seroconversion ALL patients.
  • [MeSH-major] Hepatitis B / prevention & control. Hepatitis B Vaccines / administration & dosage. Immunization, Secondary. Precursor Cell Lymphoblastic Leukemia-Lymphoma / complications

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  • [ErratumIn] Leuk Res. 2008 Nov;32(11):1791. Karna, Güler [corrected to Kanra, Güler]
  • (PMID = 16930691.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Engerix-B; 0 / GenHevac B Pasteur; 0 / Hepatitis B Antibodies; 0 / Hepatitis B Vaccines; 0 / Vaccines, Synthetic
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84. Horsley SW, Colman S, McKinley M, Bateman CM, Jenney M, Chaplin T, Young BD, Greaves M, Kearney L: Genetic lesions in a preleukemic aplasia phase in a child with acute lymphoblastic leukemia. Genes Chromosomes Cancer; 2008 Apr;47(4):333-40
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  • [Title] Genetic lesions in a preleukemic aplasia phase in a child with acute lymphoblastic leukemia.
  • In a small fraction ( approximately 2%) of cases of childhood acute lymphoblastic leukemia (ALL) clinical presentation of leukemia is preceded, some 2-9 months earlier, by a transient, remitting phase of nonclassical aplastic anemia, usually in connection with infection.
  • These data identify for the first time the leukemic genotype of an aplasia preceding clinical ALL and indicate that multiple secondary genetic abnormalities can contribute to a dominant subclone several months before a diagnosis of ALL.
  • [MeSH-major] Anemia, Aplastic / complications. Anemia, Aplastic / genetics. Core Binding Factor Alpha 2 Subunit / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Preleukemia / genetics

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18181181.001).
  • [ISSN] 1098-2264
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / A6438; United Kingdom / Cancer Research UK / / A6789
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / TEL-AML1 fusion protein
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85. Li Y, Qiu L, Zou D, Zhao Y, Mi Y, Wang J: Additional chromosomal abnormalities and their prognostic significance in adult Philadelphia-positive acute lymphoblastic leukemia: with or without imatinib in chemotherapy. Ann Hematol; 2009 Nov;88(11):1069-77
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  • [Title] Additional chromosomal abnormalities and their prognostic significance in adult Philadelphia-positive acute lymphoblastic leukemia: with or without imatinib in chemotherapy.
  • The study analyzed the characteristics and prognostic significance of additional chromosomal abnormalities in 110 Chinese adults with Philadelphia chromosome-positive (Ph-positive) acute lymphoblastic leukemia (ALL).
  • Secondary aberrations were present in 60.9% of the cases.
  • All chromosomes were involved in secondary aberrations, and chromosomes 9, 7, 21, 18, and 14 were most frequently abnormal.
  • Patients with loss of chromosomes 7, 7p, 9, and 9p had inferior outcome compared to patients with other secondary aberrations and those without secondary aberrations, in both CT and ICT group.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Pyrimidines / therapeutic use. Salvage Therapy

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  • (PMID = 19277658.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 8A1O1M485B / Imatinib Mesylate; 8N3DW7272P / Cyclophosphamide; BZ114NVM5P / Mitoxantrone; E7WED276I5 / 6-Mercaptopurine; EC 2.7.10.2 / Fusion Proteins, bcr-abl; EC 3.5.1.1 / Asparaginase; RSA8KO39WH / Vindesine; VB0R961HZT / Prednisone; YL5FZ2Y5U1 / Methotrexate; ZS7284E0ZP / Daunorubicin
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86. Brakensiek K, Länger F, Schlegelberger B, Kreipe H, Lehmann U: Hypermethylation of the suppressor of cytokine signalling-1 (SOCS-1) in myelodysplastic syndrome. Br J Haematol; 2005 Jul;130(2):209-17
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  • In contrast to acute myeloid leukaemia (AML), comparably little is known about aberrant methylation in myelodysplastic syndrome (MDS), a heterogeneous clonal stem cell disorder with a risk of transformation into secondary AML of up to 30%.
  • Demethylation experiments provided direct evidence that aberrant methylation of SOCS-1 induces transcriptional silencing in myeloid cells.
  • [MeSH-minor] Acute Disease. Cell Differentiation. DNA Methylation. Down-Regulation. Granulocytes / metabolism. Humans. Leukemia, Myeloid / genetics. Leukemia, Myeloid / metabolism. Neoplasm Proteins / metabolism. Polymerase Chain Reaction / methods. Protein-Tyrosine Kinases / metabolism. Signal Transduction. Suppressor of Cytokine Signaling Proteins. Tumor Cells, Cultured

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  • (PMID = 16029449.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / Repressor Proteins; 0 / SOCS1 protein, human; 0 / Suppressor of Cytokine Signaling Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases
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87. Stanulla M, Schaeffeler E, Möricke A, Coulthard SA, Cario G, Schrauder A, Kaatsch P, Dördelmann M, Welte K, Zimmermann M, Reiter A, Eichelbaum M, Riehm H, Schrappe M, Schwab M: Thiopurine methyltransferase genetics is not a major risk factor for secondary malignant neoplasms after treatment of childhood acute lymphoblastic leukemia on Berlin-Frankfurt-Münster protocols. Blood; 2009 Aug 13;114(7):1314-8
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  • [Title] Thiopurine methyltransferase genetics is not a major risk factor for secondary malignant neoplasms after treatment of childhood acute lymphoblastic leukemia on Berlin-Frankfurt-Münster protocols.
  • Treatment for childhood acute lymphoblastic leukemia (ALL) regularly includes the use of thiopurine drugs.
  • Importantly, childhood ALL patients with low TPMT activity have been considered to be at increased risk of developing therapy-associated acute myeloid leukemia and brain tumors.
  • In the present study, we genotyped 105 of 129 patients who developed a secondary malignant neoplasm after ALL treatment on 7 consecutive German Berlin-Frankfurt-Münster trials for all functionally relevant TPMT variants.
  • Frequencies of TPMT variants were similarly distributed in secondary malignant neoplasm patients and the overall ALL patient population of 814 patients.
  • Thus, TPMT does not play a major role in the etiology of secondary malignant neoplasm after treatment for childhood ALL, according to Berlin-Frankfurt-Münster strategies.
  • [MeSH-major] Brain Neoplasms / genetics. Leukemia, Myeloid, Acute / enzymology. Methyltransferases / genetics. Neoplasms, Second Primary / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics


88. Eguchi M, Eguchi-Ishimae M, Knight D, Kearney L, Slany R, Greaves M: MLL chimeric protein activation renders cells vulnerable to chromosomal damage: an explanation for the very short latency of infant leukemia. Genes Chromosomes Cancer; 2006 Aug;45(8):754-60
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  • [Title] MLL chimeric protein activation renders cells vulnerable to chromosomal damage: an explanation for the very short latency of infant leukemia.
  • MLL fusion genes are a predominant feature of acute leukemias in infants and in secondary acute myeloid leukemia (AML) associated with prior chemotherapy with topo-II poisons.
  • [MeSH-major] Chromosome Aberrations. DNA Damage. Leukemia / genetics. Myeloid-Lymphoid Leukemia Protein / metabolism. Oncogene Proteins, Fusion / metabolism

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  • (PMID = 16688745.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / MLL-ENL oncoprotein, human; 0 / Oncogene Proteins, Fusion; 094ZI81Y45 / Tamoxifen; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; 17197F0KYM / afimoxifene
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89. Reiter A, Walz C, Watmore A, Schoch C, Blau I, Schlegelberger B, Berger U, Telford N, Aruliah S, Yin JA, Vanstraelen D, Barker HF, Taylor PC, O'Driscoll A, Benedetti F, Rudolph C, Kolb HJ, Hochhaus A, Hehlmann R, Chase A, Cross NC: The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2. Cancer Res; 2005 Apr 1;65(7):2662-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The t(8;9)(p22;p24) is a recurrent abnormality in chronic and acute leukemia that fuses PCM1 to JAK2.
  • We have identified a t(8;9)(p21-23;p23-24) in seven male patients (mean age 50, range 32-74) with diverse hematologic malignancies and clinical outcomes: atypical chronic myeloid leukemia/chronic eosinophilic leukemia (n = 5), secondary acute myeloid leukemia (n = 1), and pre-B-cell acute lymphoblastic leukemia (n = 1).
  • [MeSH-major] Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 8 / genetics. Chromosomes, Human, Pair 9 / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. Protein-Tyrosine Kinases / genetics. Proto-Oncogene Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Acute Disease. Adult. Aged. Amino Acid Sequence. Autoantigens. Base Sequence. Humans. Janus Kinase 2. Male. Middle Aged. Molecular Sequence Data. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15805263.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Autoantigens; 0 / Cell Cycle Proteins; 0 / Oncogene Proteins, Fusion; 0 / PCM1 protein, human; 0 / PCM1-JAK2 fusion protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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90. Spiegler BJ, Kennedy K, Maze R, Greenberg ML, Weitzman S, Hitzler JK, Nathan PC: Comparison of long-term neurocognitive outcomes in young children with acute lymphoblastic leukemia treated with cranial radiation or high-dose or very high-dose intravenous methotrexate. J Clin Oncol; 2006 Aug 20;24(24):3858-64
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

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  • [Title] Comparison of long-term neurocognitive outcomes in young children with acute lymphoblastic leukemia treated with cranial radiation or high-dose or very high-dose intravenous methotrexate.
  • PURPOSE: Cranial radiation therapy (CRT) is associated with neurocognitive morbidity in survivors of childhood acute lymphoblastic leukemia (ALL).
  • [MeSH-major] Cognition / drug effects. Cognition / radiation effects. Cranial Irradiation / adverse effects. Methotrexate / administration & dosage. Methotrexate / adverse effects. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / radiotherapy
  • [MeSH-minor] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Attention / drug effects. Attention / radiation effects. Brain Neoplasms / prevention & control. Brain Neoplasms / secondary. Child, Preschool. Cohort Studies. Dose Fractionation. Educational Status. Female. Humans. Infant. Infusions, Intravenous. Intelligence Tests. Male. Memory / drug effects. Memory / radiation effects. Retrospective Studies

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  • [CommentIn] J Clin Oncol. 2007 Feb 20;25(6):734-5; author reply 735 [17308283.001]
  • [ErratumIn] J Clin Oncol. 2006 Nov 10;24(32):5181
  • (PMID = 16921038.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; YL5FZ2Y5U1 / Methotrexate
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91. Haining WN, Cardoso AA, Keczkemethy HL, Fleming M, Neuberg D, DeAngelo DJ, Stone RM, Galinsky I, Silverman LB, Sallan SE, Nadler LM, Guinan EC: Failure to define window of time for autologous tumor vaccination in patients with newly diagnosed or relapsed acute lymphoblastic leukemia. Exp Hematol; 2005 Mar;33(3):286-94
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  • [Title] Failure to define window of time for autologous tumor vaccination in patients with newly diagnosed or relapsed acute lymphoblastic leukemia.
  • OBJECTIVES: We and others have shown that B cell precursor acute lymphoblastic leukemia cells (ALL) stimulated with CD40 ligand become efficient antigen-presenting cells (APC) capable of expanding autologous, tumor-specific T cells from patients.
  • [MeSH-major] Cancer Vaccines / therapeutic use. Immunotherapy, Adoptive. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy
  • [MeSH-minor] Adolescent. Adult. Antigen-Presenting Cells / immunology. Antigens, CD40 / immunology. Child. Child, Preschool. Female. Humans. Male. Middle Aged. Secondary Prevention. T-Lymphocytes / immunology. T-Lymphocytes / transplantation. Time Factors

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  • (PMID = 15730852.001).
  • [ISSN] 0301-472X
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / K08HL72750; United States / NCI NIH HHS / CA / P01CA68484
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD40; 0 / Cancer Vaccines
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92. Klepin HD, Balducci L: Acute myelogenous leukemia in older adults. Oncologist; 2009 Mar;14(3):222-32
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute myelogenous leukemia in older adults.
  • The incidence of acute myelogenous leukemia (AML) increases with age.
  • Older AML patients, generally defined by age > or = 60 years, have worse treatment outcomes than younger patients.
  • Older patients are more likely to present with unfavorable cytogenetic abnormalities, multidrug resistance phenotypes, and secondary AML.
  • Investigations of hypomethylating agents and signal transduction inhibitors hold promise for the treatment of AML patients.
  • [MeSH-major] Geriatrics / methods. Leukemia, Myeloid, Acute / pathology. Leukemia, Myeloid, Acute / therapy

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  • (PMID = 19282349.001).
  • [ISSN] 1549-490X
  • [Journal-full-title] The oncologist
  • [ISO-abbreviation] Oncologist
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 72
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93. Seedhouse CH, Grundy M, White P, Li Y, Fisher J, Yakunina D, Moorman AV, Hoy T, Russell N, Burnett A, Pallis M, National Cancer Research Network: Sequential influences of leukemia-specific and genetic factors on p-glycoprotein expression in blasts from 817 patients entered into the National Cancer Research Network acute myeloid leukemia 14 and 15 trials. Clin Cancer Res; 2007 Dec 1;13(23):7059-66
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sequential influences of leukemia-specific and genetic factors on p-glycoprotein expression in blasts from 817 patients entered into the National Cancer Research Network acute myeloid leukemia 14 and 15 trials.
  • PURPOSE: P-glycoprotein (Pgp) is a major prognostic factor for chemotherapy failure in acute myeloid leukemia (AML).
  • This study compared the influence of genetic and leukemia-specific factors on Pgp.
  • RESULTS: Age, low WBC count, high bcl-2, secondary AML and myelodysplastic syndrome, and adverse cytogenetics all correlated strongly with high Pgp (MRK16) protein expression.
  • Moreover, leukemia-specific factors, such as low WBC count and poor risk cytogenetics, have a much greater effect than genetic polymorphisms on Pgp expression in AML blasts.
  • [MeSH-major] Leukemia, Myeloid, Acute / metabolism. Leukemia, Myeloid, Acute / pathology. P-Glycoprotein / biosynthesis

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  • (PMID = 18056183.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Proto-Oncogene Proteins c-bcl-2
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94. Natelson EA: Benzene-induced acute myeloid leukemia: a clinician's perspective. Am J Hematol; 2007 Sep;82(9):826-30
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  • [Title] Benzene-induced acute myeloid leukemia: a clinician's perspective.
  • Benzene-induced acute myeloid leukemia (AML) is considered a secondary form of AML, based both in theory and on limited cohort observations.
  • Its latency, cytogenetic aberrations, and clinical features are thought similar to, or identical with, AML resulting from the use of modern day cytotoxic agents for chemotherapy and immunotherapy.
  • Although distinction between secondary AML and the far more common de novo AML is difficult to establish with certainty in any given case, latency from toxic therapeutic and environmental exposure and certain clinical and pathological features generally separate these two entities.
  • AML is the only human neoplasm proven to be potentially caused by benzene, which actually is an obsolete form of chemotherapy.
  • A review of benzene-induced AML suggests that, in developed countries, this entity should no longer merit serious consideration among workers in the modern petrochemical industry and related fields.
  • [MeSH-major] Attitude of Health Personnel. Benzene / adverse effects. Developed Countries. Drug-Related Side Effects and Adverse Reactions. Leukemia, Myeloid / etiology
  • [MeSH-minor] Acute Disease. Chromosome Aberrations / chemically induced. Chromosome Inversion. Chromosomes, Human, Pair 15. Chromosomes, Human, Pair 16. Chromosomes, Human, Pair 17. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Humans. Occupational Diseases / chemically induced. Occupational Diseases / epidemiology. Occupational Exposure / adverse effects. Occupational Exposure / analysis. Petroleum / adverse effects. Translocation, Genetic

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  • [Copyright] 2007 Wiley-Liss, Inc
  • (PMID = 17506065.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Petroleum; J64922108F / Benzene
  • [Number-of-references] 79
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95. Grudeva-Popova J, Yaneva M, Zisov K, Ananoshtev N: Therapy-related acute promyelocytic leukemia after treatment with radioiodine for thyroid cancer: case report with literature review. J BUON; 2007 Jan-Mar;12(1):129-32
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  • [Title] Therapy-related acute promyelocytic leukemia after treatment with radioiodine for thyroid cancer: case report with literature review.
  • Therapy-related acute promyelocytic leukemia (t-APL) is a rare but known complication of chemotherapy and/or radiation therapy.
  • The patient's excellent response to treatment supports the data of the relevant literature that t-APL is associated with a better therapeutic result than the other subtypes of secondary acute myeloid leukemia (AML).
  • [MeSH-major] Iodine Radioisotopes / adverse effects. Leukemia, Promyelocytic, Acute / etiology. Neoplasms, Radiation-Induced / etiology. Thyroid Neoplasms / radiotherapy

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  • (PMID = 17436415.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Iodine Radioisotopes
  • [Number-of-references] 19
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96. Leung W, Neale G, Behm F, Iyengar R, Finkelstein D, Kastan MB, Pui CH: Deficient innate immunity, thymopoiesis, and gene expression response to radiation in survivors of childhood acute lymphoblastic leukemia. Cancer Epidemiol; 2010 Jun;34(3):303-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deficient innate immunity, thymopoiesis, and gene expression response to radiation in survivors of childhood acute lymphoblastic leukemia.
  • BACKGROUND: Survivors of childhood acute lymphoblastic leukemia (ALL) are at an increased risk of developing secondary malignant neoplasms.
  • In contrast, patients had lower numbers of all lymphocyte subsets involved in innate immunity (gammadeltaT cells and all NK subsets, including KIR2DL1+ cells, KIR2DL2/L3+ cells, and CD16+ cells), and lower natural cytotoxicity against K562 leukemia cells.

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  • [Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.
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  • (PMID = 20413363.001).
  • [ISSN] 1877-783X
  • [Journal-full-title] Cancer epidemiology
  • [ISO-abbreviation] Cancer Epidemiol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA021765-24; United States / NCI NIH HHS / CA / CA-21765; United States / NCI NIH HHS / CA / P30 CA-21765-24
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Other-IDs] NLM/ NIHMS193817; NLM/ PMC2874127
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97. Ko M, Huang Y, Jankowska AM, Pape UJ, Tahiliani M, Bandukwala HS, An J, Lamperti ED, Koh KP, Ganetzky R, Liu XS, Aravind L, Agarwal S, Maciejewski JP, Rao A: Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2. Nature; 2010 Dec 9;468(7325):839-43
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  • [Title] Impaired hydroxylation of 5-methylcytosine in myeloid cancers with mutant TET2.
  • The gene encoding TET2 resides at chromosome 4q24, in a region showing recurrent microdeletions and copy-neutral loss of heterozygosity (CN-LOH) in patients with diverse myeloid malignancies.
  • Somatic TET2 mutations are frequently observed in myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN), MDS/MPN overlap syndromes including chronic myelomonocytic leukaemia (CMML), acute myeloid leukaemias (AML) and secondary AML (sAML).
  • We show here that TET2 mutations associated with myeloid malignancies compromise catalytic activity.
  • Our results demonstrate that Tet2 is important for normal myelopoiesis, and suggest that disruption of TET2 enzymatic activity favours myeloid tumorigenesis.
  • Measurement of 5hmC levels in myeloid malignancies may prove valuable as a diagnostic and prognostic tool, to tailor therapies and assess responses to anticancer drugs.


98. Ayala RM, Martínez-López J, Albízua E, Diez A, Gilsanz F: Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia. Am J Hematol; 2009 Feb;84(2):79-86
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  • [Title] Clinical significance of Gata-1, Gata-2, EKLF, and c-MPL expression in acute myeloid leukemia.
  • The aim of this study was to evaluate the biological correlation and prognostic impact of Gata-1, Gata-2, EKLF, and c-MPL transcript level in a group of 41 acute myeloid leukemia (AML) patients.
  • Expression of c-MPL was associated with CD34+ AML and M2 FAB AML subtype.
  • A higher expression of EKLF was found in secondary AML versus primary AML.
  • Our study has identified expression of EKLF as a factor with a favorable impact on prognosis in AML.
  • [MeSH-major] GATA1 Transcription Factor / physiology. GATA2 Transcription Factor / physiology. Gene Expression Regulation, Neoplastic. Kruppel-Like Transcription Factors / physiology. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / physiology. Receptors, Thrombopoietin / physiology

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  • (PMID = 19097174.001).
  • [ISSN] 1096-8652
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GATA1 Transcription Factor; 0 / GATA1 protein, human; 0 / GATA2 Transcription Factor; 0 / GATA2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / Neoplasm Proteins; 0 / Receptors, Thrombopoietin; 0 / erythroid Kruppel-like factor; 143641-95-6 / MPL protein, human
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99. Tsuchida M, Ohara A, Manabe A, Kumagai M, Shimada H, Kikuchi A, Mori T, Saito M, Akiyama M, Fukushima T, Koike K, Shiobara M, Ogawa C, Kanazawa T, Noguchi Y, Oota S, Okimoto Y, Yabe H, Kajiwara M, Tomizawa D, Ko K, Sugita K, Kaneko T, Maeda M, Inukai T, Goto H, Takahashi H, Isoyama K, Hayashi Y, Hosoya R, Hanada R, Tokyo Children's Cancer Study Group: Long-term results of Tokyo Children's Cancer Study Group trials for childhood acute lymphoblastic leukemia, 1984-1999. Leukemia; 2010 Feb;24(2):383-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term results of Tokyo Children's Cancer Study Group trials for childhood acute lymphoblastic leukemia, 1984-1999.
  • We report the long-term results of Tokyo Children's Cancer Study Group's studies L84-11, L89-12, L92-13, and L95-14 for 1846 children with acute lymphoblastic leukemia, which were conducted between 1984 and 1999.
  • Secondary brain tumors developed in 12 patients at 8-22 years after cranial irradiation.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cranial Irradiation. Neoplasm Recurrence, Local / therapy. Neoplasms, Second Primary / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy

  • Genetic Alliance. consumer health - Childhood Cancer.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.
  • Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia, Childhood.
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  • (PMID = 20033052.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Investigator] Kigasawa H; Hashiyama M; Migita M; Matsui A; Yoshihawa H; Kawaguchi H; Makimoto A; Hosono A; Takagi K; Morinaga S; Kiyotani C; Shiota Y; Moriwaki K; Mochizuki S; Toyama D; Kato Y; Hoshi Y; Gunji Y; Kashii Y; Morimoto T; Saito M; Fujimura J; Ishimoto K; Isoyama K; Yamamoto M; Hirota T; Koike K; Yanagisawa R; Ishii E; Kinoshita A; Kondo K; Morimoto M; Ishida Y; Ozawa M; Hasegawa D; Kamiya T; Ochiai H; Sato Y; Sakao E; Ito K; Sunami K; Igarashi T; Komori I; Kakuta H; Kato S; Morimoto K; Yabe M; Mizutani S; Nagasawa M; Koana S; Kashiwagi Y; Takita J; Kato KM; Ooki K; Wada E; Kato F; Kojima Y; Mitsui K; Uchino Y; Watanabe A; Fukushima K; Kurosawa H; Hagisawa S; Sato Y; Fukuoka K; Sugita M; Kaku H; Kawamura M; Fukunaga Y; Migita S; Ueda T; Asano K; Sugita K; Goi K; Fugii H; Ikuta K; Yanagimachi M; Yokosuka T; Kai S; Goto A; Tanaka F; Tsuji K; Ebihara Y; Nakadate N; Ishiguro Y; Suzuki T; Nakao S; Sotomatsu M; Paku A; Bessho F; Yoshino H; Ishii M; Genma Y; Kogawa K; Tsuji Y; Imai K; Sawa F
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100. Dale DC: Advances in the treatment of neutropenia. Curr Opin Support Palliat Care; 2009 Sep;3(3):207-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Current guidelines recommend the prophylactic use of the myeloid growth factors for the first cycle of chemotherapy for patients with more than a 20% risk of febrile neutropenia.
  • Meta analysis from randomized trials shows that granulocyte colony-stimulating factor prophylaxis is associated with patients receiving more intensive chemotherapy, having better survival, but also having a higher risk of secondary acute myeloid leukemia.
  • SUMMARY: The myeloid growth factor granulocyte colony-stimulating factor has radically changed our approach to the prevention of febrile neutropenia.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
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  • (PMID = 19550332.001).
  • [ISSN] 1751-4266
  • [Journal-full-title] Current opinion in supportive and palliative care
  • [ISO-abbreviation] Curr Opin Support Palliat Care
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / R24 AI049393; United States / NIAID NIH HHS / AI / R24 AI049393-09
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  • [Number-of-references] 48
  • [Other-IDs] NLM/ NIHMS202938; NLM/ PMC3390973
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