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[Title] Activity of bortezomib in adult de novo and relapsed acute myeloid leukemia.

AIM: The aim of the study was the analysis of in vitro drug resistance to bortezomib and other anticancer drugs in de novo and relapsed adult acute myeloid leukemia (AML).

PATIENTS AND METHODS: The leukemic cells of 46 adult patients with AML were tested for the in vitro drug resistance profile.

The group included 20 de novo and 26 relapsed AML patients, among whom, 12 relapsed after allogeneic hematopoietic stem cell transplantation (HSCT) and 4 after autologous HSCT.

RESULTS: No significant differences in drug resistance were found for all tested drugs between de novo and relapsed AML samples, while expression of PGP, MRP1 and LRP was higher in relapsed patients.

Patients with refractory or relapsed disease, had higher resistance of myeloblasts to cyclophosphamide (RR = 2.4, p = 0.050), and better sensitivity to busulfan (RR = 0.4, p = 0.054) and topotecan (RR = 0.4, p = 0.031).

Those who have died due to refractory/relapsed disease (n = 16) had better sensitivity to bortezomib (RR = 0.6, p = 0.046) and treosulfan (RR = 0.1, p = 0.018).

CONCLUSION: In vitro drug resistance in relapsed adult AML is comparable to that in de novo disease.

Activity in vitro of bortezomib might be a rationale for its use in refractory/relapsed AML adult patients.

[MeSH-major] Antineoplastic Agents / pharmacology. Boronic Acids / pharmacology. Leukemia, Myeloid / drug therapy. Pyrazines / pharmacology

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bortezomib. Drug Resistance, Neoplasm. Female. Flow Cytometry. HL-60 Cells. Humans. Male. Middle Aged. Multidrug Resistance-Associated Proteins / biosynthesis. Multidrug Resistance-Associated Proteins / metabolism. P-Glycoprotein / biosynthesis. P-Glycoprotein / metabolism. Vault Ribonucleoprotein Particles / biosynthesis. Vault Ribonucleoprotein Particles / metabolism

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(PMID = 18225565.001).

[ISSN] 0250-7005

[Journal-full-title] Anticancer research

[ISO-abbreviation] Anticancer Res.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Greece

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Multidrug Resistance-Associated Proteins; 0 / P-Glycoprotein; 0 / Pyrazines; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 0 / multidrug resistance-associated protein 1; 69G8BD63PP / Bortezomib

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Diagnosis of acute myeloid leukemia according to the WHO classification in the Japan Adult Leukemia Study Group AML-97 protocol.

We reviewed and categorized 638 of 809 patients who were registered in the Japan Adult Leukemia Study Group acute myeloid leukemia (AML)-97 protocol using morphological means.

According to the WHO classification, 171 patients (26.8%) had AML with recurrent genetic abnormalities, 133 (20.8%) had AML with multilineage dysplasia (MLD), 331 (51.9%) had AML not otherwise categorized, and 3 (0.5%) had acute leukemia of ambiguous lineage.

The platelet count was higher and the rate of myeloperoxidase (MPO)-positive blasts was lower in AML with MLD than in the other WHO categories.

Our results confirmed that the cytogenetic profile, MLD phenotype, and MPO-positivity of blasts are associated with survival in patients with AML, and showed that each category had the characteristics of the WHO classification such as incidence, clinical features, and OS.

[MeSH-major] Karyotyping. Leukemia, Myeloid, Acute / classification. Leukemia, Myeloid, Acute / genetics. Registries

[MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Japan. Kaplan-Meier Estimate. Male. Middle Aged

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[Cites] J Clin Oncol. 1999 Dec;17(12):3835-49 [10577857.001]

[Cites] Blood. 2006 Dec 15;108(13):4146-55 [16926285.001]

[Cites] Blood. 2001 Sep 1;98(5):1312-20 [11520776.001]

[Cites] J Clin Oncol. 2002 Aug 1;20(15):3254-61 [12149299.001]

[Cites] Blood. 2002 Oct 1;100(7):2292-302 [12239137.001]

[Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]

[Cites] Br J Haematol. 2003 Jan;120(1):56-62 [12492577.001]

[Cites] J Clin Oncol. 2003 Jan 15;21(2):256-65 [12525517.001]

[Cites] Am J Clin Pathol. 2003 May;119(5):672-80 [12760285.001]

[Cites] Leukemia. 2003 Aug;17(8):1538-43 [12886240.001]

[Cites] Blood. 2003 Oct 1;102(7):2395-402 [12805060.001]

[Cites] Blood. 2004 Mar 1;103(5):1901-8 [14604973.001]

[Cites] Eur J Clin Invest. 2004 Aug;34 Suppl 2:12-24 [15291802.001]

[Cites] Haematologica. 2004 Sep;89(9):1082-90 [15377469.001]

[Cites] Br J Haematol. 2004 Oct;127(1):59-66 [15384978.001]

[Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]

[Cites] Ann Intern Med. 1985 Oct;103(4):620-5 [3862359.001]

[Cites] Br J Haematol. 1994 Apr;86(4):767-73 [7918070.001]

[Cites] Baillieres Clin Haematol. 1996 Mar;9(1):87-105 [8730552.001]

[Cites] Blood. 1997 Dec 1;90(11):4532-8 [9373264.001]

[Cites] Cancer. 1997 Dec 1;80(11 Suppl):2191-8 [9395033.001]

[Cites] Leukemia. 1998 May;12(5):788-91 [9593282.001]

[Cites] Blood. 1998 Jun 15;91(12):4662-7 [9616163.001]

[Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]

[Cites] Clin Cancer Res. 2005 Feb 15;11(4):1416-24 [15746041.001]

[Cites] Eur J Haematol. 2005 May;74(5):418-23 [15813916.001]

[Cites] Blood. 2005 Jul 1;106(1):265-73 [15769897.001]

[Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]

[Cites] Haematologica. 2005 Dec;90(12):1626-34 [16330435.001]

[Cites] Cancer. 2005 Dec 15;104(12):2726-34 [16284985.001]

[Cites] Leukemia. 2006 Feb;20(2):247-53 [16408102.001]

[Cites] Eur J Haematol. 2006 Jul;77(1):35-45 [16573742.001]

[Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]

(PMID = 18256787.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Other-IDs] NLM/ PMC2276241

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] KIT-D816 mutations in AML1-ETO-positive AML are associated with impaired event-free and overall survival.

Mutations in codon D816 of the KIT gene represent a recurrent genetic alteration in acute myeloid leukemia (AML).

To clarify the biologic implication of activation loop mutations of the KIT gene, 1940 randomly selected AML patients were analyzed.

In contrast, other activating mutations like FLT3 and NRAS mutations were very rarely detected in AML1-rearranged leukemia.

Our findings clearly indicate that activating mutations of receptor tyrosine kinases are associated with distinct genetic subtypes in AML.

The KIT-D816 mutations confer a poor prognosis to AML1-ETO-positive AML and should therefore be included in the diagnostic workup.

Patients with KIT-D816-positive/AML1-ETO-positive AML might benefit from early intensification of treatment or combination of conventional chemotherapy with KIT PTK inhibitors.

[MeSH-major] Amino Acid Substitution. Core Binding Factor Alpha 2 Subunit / genetics. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins, Fusion / genetics. Point Mutation. Proto-Oncogene Proteins c-kit / genetics

[MeSH-minor] Adult. Aged. Cell Line. Chromosomes, Human, Pair 21 / genetics. Chromosomes, Human, Pair 8 / genetics. Codon / genetics. Disease-Free Survival. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Gene Expression / genetics. Humans. Male. Middle Aged. Prognosis. Protein Kinase Inhibitors / pharmacology. Retrospective Studies. Translocation, Genetic / genetics

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(PMID = 16254134.001).

[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 / AML1-ETO fusion protein, human; 0 / Codon; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Oncogene Proteins, Fusion; 0 / Protein Kinase Inhibitors; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit

   

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Is it important to decipher the heterogeneity of "normal karyotype AML"?

Almost half of adult acute myelogenous leukemia (AML) is normal cytogenetically, and this subgroup shows a remarkable heterogeneity of genetic mutations at the molecular level and an intermediate response to therapy.

The finding of recurrent cytogenetic abnormalities has influenced, in a primary way, the understanding and treatment of leukemias.

Yet "normal karyotype AML" lacks such obvious abnormalities, but has a variety of prognostically important genetic abnormalities.

Although resistance to treatment is associated with specific mutations, the degree to which the leukemia resembles a stem cell in its functional properties may provide greater protection from the effects of treatment.

Although usually all of the circulating leukemia cells are cleared following treatment, a small residual population of leukemic cells in the bone marrow persists, making this disease hard to eradicate.

Increased understanding of the biological consequences of at least some of these mutations in "normal karyotype AML" is leading to more targeted approaches to develop more effective treatments for this disease.

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[Cites] Cancer Genet Cytogenet. 1989 Jul 15;40(2):203-16 [2766244.001]

[Cites] Blood. 1989 Dec;74(8):2668-73 [2479427.001]

[Cites] Clin Lab Med. 1990 Dec;10(4):755-67 [2272173.001]

[Cites] Am J Med Genet Suppl. 1990;7:251-61 [2149958.001]

[Cites] EMBO J. 1993 Dec;12(12):4481-7 [8223458.001]

[Cites] Nat Genet. 1994 Feb;6(2):146-51 [8162068.001]

[Cites] Cancer Genet Cytogenet. 1994 Mar;73(1):1-7 [8174068.001]

[Cites] J Clin Invest. 1994 Aug;94(2):489-96 [8040301.001]

[Cites] Oncogene. 1995 Apr 6;10(7):1423-30 [7731694.001]

[Cites] Leuk Res. 2004 Jan;28(1):43-8 [14630079.001]

[Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]

[Cites] Blood. 2004 Mar 1;103(5):1883-90 [14592841.001]

[Cites] Nature. 1970 Jun 27;226(5252):1209-11 [4316300.001]

[Cites] Nature. 1970 Jun 27;226(5252):1211-3 [4316301.001]

[Cites] Cold Spring Harb Symp Quant Biol. 1975;39 Pt 1:1-7 [50905.001]

[Cites] Br J Haematol. 1976 Aug;33(4):451-8 [188440.001]

[Cites] Proc Natl Acad Sci U S A. 1977 Feb;74(2):560-4 [265521.001]

[Cites] Br J Cancer. 1977 Mar;35(3):265-72 [322689.001]

[Cites] Arch Intern Med. 1983 Sep;143(9):1726-31 [6577818.001]

[Cites] Proc Natl Acad Sci U S A. 1986 May;83(9):2934-8 [3458254.001]

[Cites] Prog Clin Biol Res. 1995;393:169-76 [8545449.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Jan 21;94(2):569-74 [9012825.001]

[Cites] Semin Oncol. 1997 Feb;24(1):17-31 [9045301.001]

[Cites] Am J Clin Pathol. 1997 Jun;107(6):653-60 [9169661.001]

[Cites] Leuk Lymphoma. 1997 Aug;26(5-6):589-93 [9389365.001]

[Cites] Cancer Res. 1998 Sep 15;58(18):4173-9 [9751631.001]

[Cites] Mol Cell Biol. 1999 May;19(5):3635-44 [10207087.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11370-5 [10500183.001]

[Cites] J Natl Cancer Inst. 1961 Nov;27:1013-35 [14480645.001]

[Cites] Trans Assoc Am Physicians. 1955;68:78-81 [13299314.001]

[Cites] Leuk Res. 2006 Aug;30(8):1037-42 [16303180.001]

[Cites] Cancer Res. 2006 Jun 15;66(12):6361-9 [16778214.001]

[Cites] Mol Cell Biol. 2006 Sep;26(17):6395-402 [16914725.001]

[Cites] Br J Haematol. 2006 Sep;134(6):616-9 [16938118.001]

[Cites] Br J Haematol. 2006 Nov;135(4):438-49 [16965385.001]

[Cites] Haematologica. 2006 Dec;91(12):1653-61 [17145602.001]

[Cites] Blood. 2007 Apr 15;109(8):3509-12 [17179228.001]

[Cites] Blood. 2007 Jun 15;109(12):5164-7 [17341662.001]

[Cites] Oncogene. 2007 Jul 5;26(31):4596-9 [17237811.001]

[Cites] J Clin Pathol. 2007 Nov;60(11):1238-43 [17259299.001]

[Cites] Biochem Biophys Res Commun. 2000 Sep 24;276(2):673-9 [11027530.001]

[Cites] Br J Haematol. 2000 Oct;111(1):190-5 [11091200.001]

[Cites] Blood. 2001 Jan 1;97(1):89-94 [11133746.001]

[Cites] Leukemia. 2001 Jul;15(7):1001-10 [11455967.001]

[Cites] Leukemia. 2001 Aug;15(8):1161-4 [11480556.001]

[Cites] Blood. 2001 Sep 15;98(6):1752-9 [11535508.001]

[Cites] J Biol Chem. 2001 Nov 2;276(44):40373-6 [11568179.001]

[Cites] Science. 2002 Feb 22;295(5559):1523-5 [11809937.001]

[Cites] Cancer Immunol Immunother. 2002 Aug;51(6):299-310 [12111118.001]

[Cites] Cell Growth Differ. 2002 Jun;13(6):275-83 [12114217.001]

[Cites] J Clin Oncol. 2002 Aug 1;20(15):3254-61 [12149299.001]

[Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]

[Cites] Leukemia. 2002 Oct;16(10):1974-83 [12357348.001]

[Cites] Hematol J. 2003;4(1):31-40 [12692518.001]

[Cites] Genes Chromosomes Cancer. 2003 Jul;37(3):237-51 [12759922.001]

[Cites] Cold Spring Harb Symp Quant Biol. 1986;51 Pt 1:263-73 [3472723.001]

[Cites] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6131-5 [3476934.001]

[Cites] Science. 1956 Jul 20;124(3212):127-9 [13337365.001]

[Cites] Acta Paediatr Suppl. 1963;:SUPPL146:77-91 [14043522.001]

[Cites] Curr Opin Hematol. 2005 Jan;12(1):68-75 [15604894.001]

[Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]

[Cites] Clin Cancer Res. 2005 Feb 15;11(4):1416-24 [15746041.001]

[Cites] Oncogene. 2005 May 26;24(23):3847-52 [15750627.001]

[Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]

[Cites] Blood. 2005 Jul 1;106(1):318-27 [15784732.001]

[Cites] Science. 2005 Oct 28;310(5748):644-8 [16254181.001]

[Cites] Blood. 2005 Dec 1;106(12):3958-61 [16081693.001]

[Cites] Haematologica. 2005 Dec;90(12):1617-25 [16330434.001]

[Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]

[Cites] Leukemia. 2006 Feb;20(2):212-7 [16357841.001]

[Cites] J Clin Oncol. 2006 Feb 10;24(5):790-7 [16418499.001]

[Cites] J Exp Med. 2006 Feb 20;203(2):371-81 [16446383.001]

[Cites] Cancer Cell. 2006 Mar;9(3):175-87 [16530702.001]

[Cites] Pediatr Res. 2006 Apr;59(4 Pt 2):59R-64R [16549550.001]

[Cites] Cancer Res. 2006 Apr 1;66(7):3737-46 [16585200.001]

(PMID = 18342811.001).

[ISSN] 1521-6926

[Journal-full-title] Best practice & research. Clinical haematology

[ISO-abbreviation] Best Pract Res Clin Haematol

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / R01 DK052621; United States / NIDDK NIH HHS / DK / R01 DK052621-08; United States / NIDDK NIH HHS / DK / R56 DK052208-09A1; United States / NCI NIH HHS / CA / R01 CA102202-01; United States / NCI NIH HHS / CA / CA102202-01; United States / NIDDK NIH HHS / DK / R56 DK052208; United States / NCI NIH HHS / CA / R01 CA102202; United States / NIDDK NIH HHS / DK / DK052208-09A1; United States / NIDDK NIH HHS / DK / DK052621-08

[Publication-type] Journal Article; Review

[Publication-country] Netherlands

[Number-of-references] 76

[Other-IDs] NLM/ NIHMS44325; NLM/ PMC2654590

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis.

Patients with NF1 have a higher risk to develop juvenile myelomonocytic leukemia (JMML) with a possible progression toward acute myeloid leukemia (AML).

In an oligo array comparative genomic hybridization-based screening of 103 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL) and 71 patients with MLL-rearranged AML, a recurrent cryptic deletion, del(17)(q11.2), was identified in 3 patients with T-ALL and 2 patients with MLL-rearranged AML.

Since the NF1 protein is a negative regulator of the RAS pathway (RAS-GTPase activating protein), homozygous NF1 inactivation represent a novel type I mutation in pediatric MLL-rearranged AML and T-ALL with a predicted frequency that is less than 10%.

NF1 inactivation may provide an additional proliferative signal toward the development of leukemia.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Mutation / genetics. Neurofibromatoses / genetics. Neurofibromin 1 / genetics

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(PMID = 18172006.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Neurofibromin 1; 0 / RNA, Messenger

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Sequential continuous infusion of fludarabine and cytarabine associated with liposomal daunorubicin (DaunoXome) (FLAD) in primary refractory or relapsed adult acute myeloid leukemia patients.

A large proportion of adult patients with acute myeloid leukemia (AML) relapse after treatment, and some of them are resistant to primary induction chemotherapy.

Sixty-one patients from seven hematological centers with poor-risk AML, primary refractory (n = 16), or relapsed (n = 45) were treated with a salvage regimen, including fludarabine (2 days) and cytarabine (3 days) in a sequential continuous infusion, associated with liposomal daunorubicin (3 days) (FLAD).

Complete response rate was 44% and 56% for refractory and relapsed patients, respectively, with an overall response rate of 52% (32 of 61).

Twenty patients (62.5%) relapsed after this treatment in a median of 7.3 months; ten patients relapsed after a SCT procedure.

A better response rate was obtained in the subgroup of relapsed patients, compared to patients treated for refractory disease.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cytarabine / therapeutic use. Daunorubicin / administration & dosage. Daunorubicin / therapeutic use. Leukemia, Myeloid, Acute / drug therapy. Vidarabine / analogs & derivatives

[MeSH-minor] Adult. Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Infusions, Intravenous. Liposomes. Male. Middle Aged. Recurrence. Salvage Therapy. Stem Cell Transplantation. Survival Rate. Time Factors

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(PMID = 18709502.001).

[ISSN] 1432-0584

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

[Publication-type] Clinical Trial; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Liposomes; 04079A1RDZ / Cytarabine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; ZS7284E0ZP / Daunorubicin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Complete remission achieved in a case of both primary and recurrent adult acute myelogeneous leukemia by a novel nutritional therapy.

OBJECTIVES: The aim of this study was to determine the possible clinical benefit of molasses-based dietary compositions (designated as MSQ 13, MSQ 15, and MSQ 18) in a case of both primary and recurrent adult AML.

OUTCOME MEASURES: Clinical improvement and regression of AML were the outcome measures.

CONCLUSIONS: Treatment with the MSQ dietary compositions resulted in disease regression and the reversal of clinical manifestations over two episodes of AML.

Therefore, further studies are warranted to evaluate the utility of this approach for the clinical management of AML.

[MeSH-major] Leukemia, Myeloid, Acute / diet therapy. Molasses. Nutrition Therapy / methods

[MeSH-minor] Adult. Female. Humans. Remission Induction. Treatment Outcome

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(PMID = 16646731.001).

[ISSN] 1075-5535

[Journal-full-title] Journal of alternative and complementary medicine (New York, N.Y.)

[ISO-abbreviation] J Altern Complement Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] AML M1 presenting with recurrent acute large arterial vessel thromboembolism.

Acute leukemia may be associated with coagulopathy, predominantly severe bleeding diathesis caused by disseminated intravascular coagulation (DIC) and/or hyperfibrinolysis.

Disordered hemostasis is characteristic for acute promyelocytic leukemia (APL, FAB M3).

We report a case of severe recurrent acute arterial thromboembolism at presentation in AML FAB M1.

Most likely, the ischemic events in our patient resulted from leukemia as the thrombus material included many leukemic blasts.

[MeSH-major] Leukemia, Myeloid, Acute / complications. Thromboembolism / etiology

[MeSH-minor] Adult. Amputation. Disseminated Intravascular Coagulation / etiology. Female. Hemorrhagic Disorders / etiology. Humans. Iliac Artery / pathology. Iliac Artery / radiography. Ischemia / etiology. Ischemia / pathology. Ischemia / radiography. Ischemia / surgery. Leg / blood supply. Leg / pathology. Leg / radiography. Leg / surgery. Leukemia, Promyelocytic, Acute / complications

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(PMID = 17011031.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Immunohistochemical demonstration of mutant nucleophosmin in acute myeloid leukemia: biological and clinical features related to NPMc expression].

[Transliterated title] Mutáns nucleophosmin fehérje kimutatása akut myeloid leukaemiában: az NPMc+ AML biológiai és klinikai jellemzôi.

The mutation of the nucleophosmin gene (NPM1) is the most frequently occurring genetic aberration in acute myeloid leukemia (AML).

Due to the high frequency and the obvious impact on disease outcome, the current WHO classification also defines the new (tentative) entity of "AML with NPM mutation".

The present study focused on further biological and clinical characterization of NPMc+ AML determined by histological and cytological preparations of the bone marrow.

41 adult AML cases were investigated in our center between 2005 and 2008, 6/41 cases were presented with cytoplasmic NPM immunostaining (14.6%).

All but one were female patients, and were diagnosed as de novo AML with no recurrent cytogenetic aberrations (6/23, 26.1%).

In conclusion, immunohistochemistry is well applicable for the identification of NPM mutated AML in the daily hematopathology practice.

[MeSH-major] Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Bone Marrow / chemistry. Leukemia, Myeloid, Acute / metabolism. Mutation. Nuclear Proteins / analysis. Nuclear Proteins / genetics

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(PMID = 19465351.001).

[ISSN] 0030-6002

[Journal-full-title] Orvosi hetilap

[ISO-abbreviation] Orv Hetil

[Language] hun

[Publication-type] English Abstract; Journal Article

[Publication-country] Hungary

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Del (9q) AML: clinical and cytological characteristics and prognostic implications.

Del (9q) is a recurrent cytogenetic abnormality in acute myeloid leukaemia (AML).

We report an analysis of 81 patients with del(9q) as a diagnostic karyotypic abnormality entered into the Medical Research Council AML trials 10, 11 and 12.

It is likely that the deletion of single or multiple tumour suppressor genes located in this region may underlie the pathogenesis of del (9q) AML.

[MeSH-major] Gene Deletion. Genes, Tumor Suppressor. Leukemia, Myeloid / genetics

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Bone Marrow Cells / pathology. Child. Child, Preschool. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Cytogenetic Analysis. Disease-Free Survival. Female. Genetic Markers. Humans. Male. Middle Aged. Survival Rate. Translocation, Genetic

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[CommentIn] Br J Haematol. 2005 Sep;130(6):969; author reply 969 [16156871.001]

(PMID = 15813849.001).

[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 / Genetic Markers

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] K313dup is a recurrent CEBPA mutation in de novo acute myeloid leukemia (AML).

The CEBPA gene codes for a transcription factor that has a pivotal role in controlling proliferation and differentiation of myeloid progenitors.

Acquired CEBPA mutations have been found in acute myeloid leukemias (AML) with a good prognosis, and most of these patients have a normal karyotype.

All four had an AML-M1 with CD7 positivity and T-cell receptor gamma chain (TCR-gamma) rearrangement.

K313dup seems to be selected in leukemic cells, and its frequency in other AML series could be determined using the screening method reported in this paper.

[MeSH-major] CCAAT-Enhancer-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

[MeSH-minor] Adolescent. Adult. Aged. DNA Mutational Analysis. Female. Humans. Male. Middle Aged. Receptors, Antigen, T-Cell, gamma-delta / genetics. Receptors, Antigen, T-Cell, gamma-delta / metabolism

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(PMID = 18587575.001).

[ISSN] 0939-5555

[Journal-full-title] Annals of hematology

[ISO-abbreviation] Ann. Hematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 0 / CEBPA protein, human; 0 / Receptors, Antigen, T-Cell, gamma-delta

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] del(6)(p23) in two cases of de novo AML--a new recurrent primary chromosome abnormality.

OBJECTIVE: Previously, deletion 6p23 was generally reported in therapy-related secondary acute myeloid leukemia (AML) as part of complex karyotypes.

In this report, we present two young adult patients with de novo AML-M2 and a terminal deletion 6p23 as a sole primary abnormality, confirmed by chromosome 6 specific subtelomeric probes.

RESULTS: A diagnosis of AML-M2 was confirmed in both patients by morphological and immunophenotyping studies.

The common morphological, immunophenotypic, and cytogenetic features in our two patients strongly support a separate new entity of de novo AML with deletion 6p23.

[MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 6 / genetics. Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adult. Chromosomal Proteins, Non-Histone / genetics. Cytogenetics. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping. Oncogene Proteins / genetics. Oncogenes. Recurrence

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(PMID = 16856925.001).

[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 / Chromosomal Proteins, Non-Histone; 0 / Dek protein, human; 0 / Oncogene Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Deletion of chromosome arm 15q in a case of minimally differentiated hypoplastic AML-M0.

Deletion of the long arm of chromosome 15 is known as a rare but recurrent chromosomal abnormality in myeloid malignancies.

We report a novel case of minimally differentiated hypoplastic acute myeloid leukemia (AML M0) in a patient who initially had a normal karyotype, but clonal interstitial deletion of chromosome 15, del(15)(q11.2q22), coincided with increment of leukemic cells a year later.

We also summarize 18 published cases with myeloid malignancies and this chromosomal abnormality.

[MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Differentiation. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Recurrence

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(PMID = 18558291.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Primary total hip arthroplasty with Asian-type AML total hip prosthesis: follow-up for more than 10 years.

BACKGROUND: We retrospectively reviewed 137 consecutive total hip arthroplasties performed with AML-A stems and Tri-Lock cups to see whether design modifications made to these components would achieve durable biological fixation in the Japanese population in whom developmental dysplasia of the hip (DDH) is relatively common.

METHODS: Between April 1988 and June 1994, we performed 137 total hip arthroplasties using the AML-A prosthesis for the patients with osteoarthritis of the hip joint.

Another seven hips underwent revision surgery for recurrent dislocation.

[MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Follow-Up Studies. Humans. Japan. Kaplan-Meier Estimate. Male. Middle Aged. Reoperation. Young Adult

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(PMID = 18696190.001).

[ISSN] 0949-2658

[Journal-full-title] Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association

[ISO-abbreviation] J Orthop Sci

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Recurrent steroid-responsive pancreatitis associated with myelodysplastic syndrome and transformations.

However, to date, recurrent acute pancreatitis has never been described in association with MDS.

The vasculitic syndrome responded rapidly to corticosteroids, but soon after tapering of corticosteroids, acute pancreatitis developed.

Finally, his MDS transformed into acute myeloid leukemia (AML); severe acute pancreatitis closely accompanied.

A subsequent pancreatitis attack with pseudocyst formation occurred, but again was controlled with corticosteroids, although this was followed closely by another relapse of AML.

All etiologies for recurrent acute pancreatitis were ruled out.

The dramatic response of his pancreatitis attacks to immunosuppression suggested its autoimmune origin, while the close relationship in both the timing and severity of acute pancreatitis and MDS/AML suggested that the autoimmune pancreatitis was a paraneoplastic phenomenon related to MDS.

[MeSH-minor] Abdomen / pathology. Adult. Cell Transformation, Neoplastic. Humans. Male. Recurrence. Time Factors

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(PMID = 15621795.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Steroids

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations].

OBJECTIVE: To investigate the impact of GSTM1, GSTT1 and NQO1 genotypes on susceptibility to acute myeloid leukemia (AML) and recurrent chromosome translocations of AML.

METHODS: GSTT1, GSTM1 and NQO1 genotypes were detected in 228 adult patients with de novo AML and 241 controls by PCR or PCR-RFLP.

RESULTS: The frequency of GSTM1 null genotype in the AML patients was 62.3%, significantly higher than that in the normal controls (52.7%, P = 0.036), however, no significant difference was found in the incidence of GSTT1 null genotype.

The frequencies of NQO1(C609T) C/T and T/T genotypes were 53.1% and 25.0% respectively among the total AML patients (53.1% and 25.0% respectively), 64.3% and 25.0% respectively among the AML patients with t (8;.

21) (q22; q22)/AML-ETO fusion gene, and 57.1% and 26.0% respectively among the AML patient with t (15;.

21) (q22; q22)/AML-ETO (+) AML was 4.487 (95% CI: 1.282-15.705) for the subjects with NQO1(C609T) C/T genotype, and was 6.293 (95% CI: 1.536-25.782) for the subjects with NQO1(C609T) T/T genotype.

17) (q22; q11)/PML-RARalpha (+) AML was 2.531 (95% CI: 1.286-4.981) for the subjects with NQO1(C609T) C/T genotype, and was 4.149 (95% CI: 1.856-9.275) for the subjects with NQO1(C609T) T/T genotype.

CONCLUSION: Determination of the NQO1(C609T) genotypes may be used as a stratification marker to predict high-risk individuals for AML, especially for AML with t (8;.

21) (q22; q22)/AML-ETO fusion gene and t (15;.

[MeSH-major] Chromosome Aberrations. Glutathione Transferase / genetics. Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Case-Control Studies. Female. Gene Frequency. Genotype. Humans. Male. Middle Aged. NAD(P)H Dehydrogenase (Quinone) / genetics. Translocation, Genetic. Young Adult

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(PMID = 16321221.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] EC 1.6.5.2 / NAD(P)H Dehydrogenase (Quinone); EC 1.6.5.2 / NQO1 protein, human; EC 2.5.1.- / glutathione S-transferase T1; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase M1

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] NF1 inactivation in adult acute myelogenous leukemia.

PURPOSE: This study was conducted to identify novel genes with importance to the biology of adult acute myelogenous leukemia (AML).

EXPERIMENTAL DESIGN: We analyzed DNA from highly purified AML blasts and paired buccal cells from 95 patients for recurrent genomic microdeletions using ultra-high density Affymetrix single nucleotide polymorphism 6.0 array-based genomic profiling.

Sequence analysis of all NF1 coding exons in the 11 AML cases with NF1 copy number changes identified acquired truncating frameshift mutations in two patients.

Subsequent expression analysis of NF1 mRNA in the entire AML cohort using fluorescence-activated cell sorting sorted blasts as a source of RNA identified six patients (one with a NF1 mutation) with absent NF1 expression.

The NF1 null states were associated with increased Ras-bound GTP, and short hairpin RNA-mediated NF1 suppression in primary AML blasts with wild-type NF1 facilitated colony formation in methylcellulose.

Primary AML blasts without functional NF1, unlike blasts with functional NF1, displayed sensitivity to rapamycin-induced apoptosis, thus identifying a dependence on mammalian target of rapamycin (mTOR) signaling for survival.

Finally, colony formation in methylcellulose ex vivo of NF1 null CD34+/CD38- cells sorted from AML bone marrow samples was inhibited by low-dose rapamycin.

CONCLUSIONS: NF1 null states are present in 7 of 95 (7%) of adult AML and delineate a disease subset that could be preferentially targeted by Ras or mammalian target of rapamycin-directed therapeutics.

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[Cites] Cancer Res. 2008 Feb 15;68(4):1012-21 [18281475.001]

[Cites] N Engl J Med. 1997 Jun 12;336(24):1713-20 [9180088.001]

[Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]

[Cites] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6708-13 [18458336.001]

[Cites] Leukemia. 2008 May;22(5):915-31 [18288131.001]

[Cites] Blood. 2008 Aug 1;112(3):814-21 [18490517.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11921-6 [18697940.001]

[Cites] Blood. 2008 Sep 1;112(5):1993-2003 [18436738.001]

[Cites] J Clin Oncol. 2008 Oct 1;26(28):4603-9 [18559876.001]

[Cites] Cancer Res. 2008 Dec 15;68(24):10349-57 [19074904.001]

[Cites] Cancer Cell. 2009 Jul 7;16(1):44-54 [19573811.001]

[Cites] Proc Natl Acad Sci U S A. 2009 Aug 4;106(31):12950-5 [19651600.001]

[Cites] Clin Cancer Res. 2009 Nov 1;15(21):6732-9 [19843663.001]

[Cites] J Exp Med. 2000 Jan 3;191(1):181-8 [10620616.001]

[Cites] Leukemia. 2000 Mar;14(3):513-7 [10720153.001]

[Cites] J Clin Invest. 2001 Sep;108(5):709-15 [11544276.001]

[Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]

[Cites] Blood. 2003 Aug 1;102(3):972-80 [12702506.001]

[Cites] Bioinformatics. 2004 May 22;20(8):1233-40 [14871870.001]

[Cites] Blood. 1991 Mar 1;77(5):925-9 [1704804.001]

[Cites] Am J Clin Pathol. 1993 Nov;100(5):534-40 [8249893.001]

[Cites] N Engl J Med. 1994 Mar 3;330(9):597-601 [8302341.001]

[Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]

[Cites] J Biol Chem. 2004 Dec 3;279(49):50874-85 [15371411.001]

[Cites] Blood. 2005 Mar 15;105(6):2527-34 [15550488.001]

[Cites] Clin Cancer Res. 2005 May 1;11(9):3217-24 [15867216.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8573-8 [15937108.001]

[Cites] Biogerontology. 2005;6(3):185-92 [16041622.001]

[Cites] Cancer Cell. 2005 Oct;8(4):337-48 [16226708.001]

[Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]

[Cites] J Biol Chem. 2005 Nov 25;280(47):39524-33 [16169856.001]

[Cites] Leukemia. 2006 Apr;20(4):635-44 [16467864.001]

[Cites] Leukemia. 2006 May;20(5):840-6 [16498392.001]

[Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]

[Cites] Clin Cancer Res. 2006 Sep 1;12(17):5165-73 [16951235.001]

[Cites] Cancer Cell. 2006 Sep;10(3):179-90 [16959610.001]

[Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]

[Cites] Leukemia. 2007 Jun;21(6):1224-31 [17377590.001]

[Cites] Clin Cancer Res. 2007 Aug 15;13(16):4777-85 [17699855.001]

[Cites] Blood. 2008 Feb 1;111(3):1534-42 [17954704.001]

[Cites] Blood. 2008 Feb 1;111(3):1584-93 [17971485.001]

[Cites] Leukemia. 2008 Feb;22(2):240-8 [18200041.001]

[Cites] Blood. 2008 Apr 15;111(8):4322-8 [18172006.001]

[Cites] Nat Genet. 1996 Feb;12(2):137-43 [8563750.001]

[Cites] Nat Genet. 1996 Feb;12(2):144-8 [8563751.001]

[CommentOn] Clin Cancer Res. 2010 Aug 15;16(16):4074-6 [20587590.001]

(PMID = 20505189.001).

[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 / R01 CA136537; United States / NCI NIH HHS / CA / 1R01 CA136537-01; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / R01 CA136537-02; United States / NCI NIH HHS / CA / CA136537-02

[Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] EC 3.6.5.2 / ras Proteins

[Other-IDs] NLM/ NIHMS210184; NLM/ PMC2921448

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Mechanism of recurrent/persistent ischemic/functional mitral regurgitation in the chronic phase after surgical annuloplasty: importance of augmented posterior leaflet tethering.

BACKGROUND: Surgical annuloplasty can potentially hoist the posterior annulus anteriorly, exaggerate posterior leaflet (PML) tethering, and lead to recurrent ischemic/functional mitral regurgitation (MR).

METHODS AND RESULTS: In 30 patients with surgical annuloplasty for ischemic MR and 20 controls, the anterior leaflet (AML) and PML tethering angles relative to the line connecting annuli, posterior and apical displacement of the coaptation and the MR grade were measured by echocardiography before, early after, and late after surgery.

Early after surgery, grade of MR and AML tethering generally decreased (P<0.01), whereas PML tethering significantly worsened (P<0.01).

Nine of the 30 patients showed recurrent/persistent MR late after surgery.

CONCLUSIONS: Whereas both leaflets tethering is related to preoperative ischemic MR, both leaflets tethering but with predominant contribution from augmented and progressive PML tethering is related to recurrent/persistent ischemic/functional MR late after surgical annuloplasty.

[MeSH-minor] Adult. Aged. Aged, 80 and over. Chronic Disease. Coronary Artery Bypass. Female. Humans. Incidence. Male. Middle Aged. Motion. Papillary Muscles / pathology. Recurrence. Treatment Failure

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(PMID = 16820632.001).

[ISSN] 1524-4539

[Journal-full-title] Circulation

[ISO-abbreviation] Circulation

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia.

BACKGROUND: The prognosis after recurrence of pediatric acute myeloid leukemia (AML) is poor, and effective salvage regimens are urgently needed.

METHODS: In phase 1 and pilot studies, the authors evaluated the maximum tolerated dose (MTD) and dose-limiting toxicities (DLTs) of a 5-day course of cladribine followed by topotecan in pediatric patients with recurrent/refractory AML.

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[Copyright] Copyright 2010 American Cancer Society.

[Cites] J Clin Oncol. 2001 Jun 1;19(11):2804-11 [11387351.001]

[Cites] Cancer. 2008 Jul 15;113(2):376-82 [18459178.001]

[Cites] J Clin Oncol. 2002 Oct 15;20(20):4217-24 [12377965.001]

[Cites] Clin Cancer Res. 2003 Feb;9(2):633-40 [12576429.001]

[Cites] J Clin Oncol. 2003 Aug 1;21(15):2940-7 [12885813.001]

[Cites] Biol Blood Marrow Transplant. 2003 Nov;9(11):706-13 [14652854.001]

[Cites] J Clin Oncol. 2003 Dec 1;21(23):4377-85 [14645428.001]

[Cites] Cancer Res. 1973 Nov;33(11):2834-6 [4748440.001]

[Cites] Biometrics. 1989 Sep;45(3):925-37 [2790129.001]

[Cites] J Clin Invest. 1990 Nov;86(5):1480-8 [1700795.001]

[Cites] J Clin Oncol. 1992 Mar;10(3):364-70 [1346800.001]

[Cites] J Clin Oncol. 1992 Oct;10(10):1514-8 [1357107.001]

[Cites] Cancer Res. 1994 Mar 1;54(5):1235-9 [7906999.001]

[Cites] Blood. 1997 Mar 15;89(6):2098-104 [9058732.001]

[Cites] J Clin Oncol. 1998 Jun;16(6):2233-7 [9626225.001]

[Cites] Clin Cancer Res. 1996 Dec;2(12):1921-30 [9816150.001]

[Cites] Blood. 2005 Apr 15;105(8):3051-7 [15632206.001]

[Cites] Leukemia. 2005 Dec;19(12):2025-9 [16304569.001]

[Cites] J Clin Oncol. 2006 Sep 20;24(27):4499-506 [16983120.001]

[Cites] Biol Blood Marrow Transplant. 2007 Jan;13(1):1-25 [17222748.001]

[Cites] Br J Haematol. 2007 Jan;136(2):229-236 [17278259.001]

[Cites] Blood. 2008 Feb 1;111(3):1044-53 [18000167.001]

[Cites] J Clin Oncol. 2002 Mar 15;20(6):1617-24 [11896112.001]

(PMID = 19885837.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[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] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 47M74X9YT5 / Cladribine; 7M7YKX2N15 / Topotecan

[Other-IDs] NLM/ NIHMS151111; NLM/ PMC2920745

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Recurrent expression signatures of cytokines and chemokines are present and are independently prognostic in acute myelogenous leukemia and myelodysplasia.

We hypothesized that comprehensive profiling of C&Ckine expression in leukemia would provide greater insight compared with individual analyses.

We used multiplex array technology to simultaneously measure the level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndrome (MDS) patients and 19 normal controls.

C&Ckine levels in AML and MDS differed significantly from normal controls (5 higher, 13 lower) but were similar to each other for 24 of 27 analytes, with interleukin-8 and interleukin-13 higher in AML and vascular endothelial growth factor A higher in MDS.

Levels did not correlate with age, gender, infection, or blood counts; however, 3 correlated with specific cytognetic abnormalities in AML.

In newly diagnosed AML, 8 C&Ckine signatures, distinct from the normal control signature, were observed.

These patterns suggest specific therapeutic interventions to investigate in subsets of AML patients.

In conclusion, C&Ckine expression in AML and MDS differs from normal, is similar with one another, and forms recurrent patterns of expression with prognostic relevance.

[MeSH-major] Chemokines / blood. Leukemia, Myeloid, Acute / blood. Leukemia, Myeloid, Acute / diagnosis. Myelodysplastic Syndromes / blood. Myelodysplastic Syndromes / diagnosis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Cluster Analysis. Cytogenetic Analysis. Female. Humans. Male. Middle Aged. Multivariate Analysis. Principal Component Analysis. Prognosis. Survival Analysis. Treatment Outcome. Young Adult

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[Cites] Cancer. 2002 Nov 1;95(9):1923-30 [12404286.001]

[Cites] Acta Haematol. 1996;96(3):155-61 [8876613.001]

[Cites] Clin Diagn Lab Immunol. 2003 Jan;10(1):133-9 [12522051.001]

[Cites] Leukemia. 2003 Apr;17(4):716-30 [12682629.001]

[Cites] Nat Rev Cancer. 2004 Jan;4(1):11-22 [14708024.001]

[Cites] Clin Immunol. 2004 Mar;110(3):206-21 [15047199.001]

[Cites] Best Pract Res Clin Haematol. 2004 Dec;17(4):653-61 [15494301.001]

[Cites] Blood. 1987 Apr;69(4):1161-6 [3103713.001]

[Cites] J Clin Invest. 1991 Mar;87(3):838-41 [1705566.001]

[Cites] Blood. 1992 Apr 15;79(8):1938-45 [1373331.001]

[Cites] Blood Rev. 1992 Sep;6(3):149-56 [1422283.001]

[Cites] Blood. 1993 Jan 15;81(2):281-92 [8422455.001]

[Cites] Leukemia. 1997 Dec;11(12):2049-54 [9447819.001]

[Cites] Br J Haematol. 1998 Sep;102(4):1025-34 [9734654.001]

[Cites] Cytokines Cell Mol Ther. 1998 Sep;4(3):187-98 [9825844.001]

[Cites] J Biopharm Stat. 2005;15(3):437-63 [15920890.001]

[Cites] Leuk Lymphoma. 2005 Jun;46(6):885-91 [16019534.001]

[Cites] Br J Haematol. 2005 Sep;130(5):709-15 [16115126.001]

[Cites] Cancer Treat Res. 2005;126:103-27 [16209064.001]

[Cites] Exp Hematol. 2005 Oct;33(10):1109-17 [16219533.001]

[Cites] Eur J Haematol. 2005 Dec;75(6):485-91 [16313260.001]

[Cites] Ann Clin Lab Sci. 2006 Winter;36(1):7-15 [16501231.001]

[Cites] Blood. 2006 Oct 1;108(7):2358-65 [16763210.001]

[Cites] Cancer Biomark. 2005;1(6):259-69 [17192050.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2007 Jan;16(1):102-7 [17220337.001]

[Cites] Haematologica. 2007 Mar;92(3):332-41 [17339182.001]

[Cites] Clin Cancer Res. 2007 Apr 15;13(8):2385-91 [17438097.001]

[Cites] Oncogene. 2007 Oct 15;26(47):6724-37 [17934481.001]

[Cites] Oncogene. 2007 Oct 15;26(47):6738-49 [17934482.001]

[Cites] Blood. 2008 May 1;111(9):4788-96 [18252861.001]

[Cites] Blood. 2008 May 1;111(9):4797-808 [18270328.001]

[Cites] Cancer. 2008 Oct 1;113(7):1605-13 [18683214.001]

[Cites] Blood. 2009 Jan 1;113(1):154-64 [18840713.001]

[Cites] Leuk Res. 1996 Nov-Dec;20(11-12):891-900 [9009245.001]

[Cites] Br J Cancer. 1999 Dec;81(8):1398-401 [10604739.001]

[Cites] Oncogene. 2000 Feb 3;19(5):624-31 [10698507.001]

[Cites] Cytokine. 2000 Jun;12(6):699-707 [10843748.001]

[Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]

[Cites] Trends Immunol. 2002 Aug;23(8):403-8 [12133803.001]

[Cites] Oncology. 2002;63(1):64-9 [12187073.001]

[Cites] Leukemia. 1994 May;8(5):798-805 [8182937.001]

[Cites] Blood. 1995 Dec 15;86(12):4594-602 [8541550.001]

[Cites] Leukemia. 1996 Jun;10(6):925-31 [8667646.001]

[Cites] Science. 1996 Nov 1;274(5288):782-4 [8864118.001]

[Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]

(PMID = 20679526.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P01 CA108631; United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Chemokines

[Other-IDs] NLM/ PMC4081283

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Characterization of a recurrent translocation t(2;3)(p15-22;q26) occurring in acute myeloid leukaemia.

Six patients with de novo acute myeloid leukemia (AML) and a t(2;3)(p15-21;q26-27) were identified among approximately 1000 cases enrolled in the GIMEMA trial.

The patients showed dysplasia of at least two myeloid cell lineages in all cases; they had a low-to-normal platelet count and displayed an immature CD34+ CD117+ immunophenotype.

We arrived at the following conclusions: (a) the t(2;3) is a recurrent translocation having an approximate 0.5% incidence in adult AML;.

[MeSH-major] Chromosomes, Human, Pair 2 / genetics. Chromosomes, Human, Pair 3 / genetics. Leukemia, Myeloid / genetics. Translocation, Genetic / genetics

[MeSH-minor] Acute Disease. Adult. Cytogenetic Analysis / methods. Female. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Polymerase Chain Reaction. Predictive Value of Tests. Prognosis. Trisomy

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(PMID = 16619048.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Clinical study of 572 adult acute leukemia patients in Shanghai according to WHO classification].

OBJECTIVE: To evaluate WHO classification of acute leukemia (AL) in Shanghai and compare the difference between WHO and FAB classification.

METHODS: Successive and unselected leukemia patients were referred to Sino-US Leukemia Cooperative Group of Shanghai from 2003 to 2006.

A total of 572 adult AL cases were diagnosed and classified according to WHO and FAB classification.

RESULTS: Of the 572 AL patients, 436 (76.2%) were diagnosed as acute myeloid leukemia (AML), 119 (20.8%) acute lymphoblastic leukemia (ALL).

The AML and ALL percentage ratio was 3.66: 1.

AML with recurrent cytogenetic abnormalities accounted for 35.3%, and with multilineage dysplasia for 13.1%, therapy-related AML accounted for 0.9%, and AML not otherwise categorized for 50.7%.

The percentage of therapy-related AML in Shanghai was lower than that in the Western.

According to FAB classification, AML-M4 was the most (38.5%) common subtype.

The percentage of AML-M3 and M4 in Shanghai were higher than that in the Western, but that of AML-M, was lower.

The incidence of karyotypic abnormalities in AML was 60.8%.

The incidence of AML with t (15;17) was higher than that in the Western.

Favorable cytogenetic risk group accounted for 30.6%, intermediate group for 51.5%, unfavorable group for 17.9% of AML.

CONCLUSIONS: The percentages of AML with t (15;17) and AML-M4 in Shanghai and the incidence of cytogenetic favorable group were higher than that in the Western.

It was different in WHO classification and karyotypic abnormalities of AML between Shanghai and the Western.

Comparing to the AL data of Shanghai Leukemia Group between 1984 and 1994, the percentage of AML-M4 was increased, but that of AML-M1 and M5 were decreased.

[MeSH-major] Leukemia / classification

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. China. Female. Humans. Karyotyping. Male. Middle Aged

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(PMID = 18072625.001).

[ISSN] 0253-2727

[Journal-full-title] Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi

[ISO-abbreviation] Zhonghua Xue Ye Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value.

Somatic mutations in isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) were recently demonstrated in acute myeloid leukemia (AML), but their prevalence and prognostic impact remain to be explored in large extensively characterized AML series, and also in various other hematologic malignancies.

Here, we demonstrate in 893 newly diagnosed cases of AML mutations in the IDH1 (6%) and IDH2 (11%) genes.

Moreover, we identified IDH mutations in 2 JAK2 V617F myeloproliferative neoplasias (n = 96), a single case of acute lymphoblastic leukemia (n = 96), and none in chronic myeloid leukemias (n = 81).

In AML, IDH1 and IDH2 mutations are more common among AML with normal karyotype and NPM1(mutant) genotypes.

Thus, IDH1 and IDH2 mutations are common genetic aberrations in AML, and IDH1 mutations may carry prognostic value in distinct subtypes of AML.

[MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Mutation

[MeSH-minor] Adolescent. Adult. Aged. Female. Hematologic Diseases. Humans. Janus Kinase 2 / genetics. Male. Middle Aged. Prevalence. Prognosis. Young Adult

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(PMID = 20538800.001).

[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] EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human; EC 2.7.10.2 / Janus Kinase 2

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acquired copy number alterations in adult acute myeloid leukemia genomes.

Cytogenetic analysis of acute myeloid leukemia (AML) cells has accelerated the identification of genes important for AML pathogenesis.

To complement cytogenetic studies and to identify genes altered in AML genomes, we performed genome-wide copy number analysis with paired normal and tumor DNA obtained from 86 adult patients with de novo AML using 1.85 million feature SNP arrays.

A total of 201 somatic CNAs were found in the 86 AML genomes (mean, 2.34 CNAs per genome), with French-American-British system M6 and M7 genomes containing the most changes (10-29 CNAs per genome).

Twenty-four percent of AML patients with normal cytogenetics had CNA, whereas 40% of patients with an abnormal karyotype had additional CNA detected by SNP array, and several CNA regions were recurrent.

The mRNA expression levels of 57 genes were significantly altered in 27 of 50 recurrent CNA regions <5 megabases in size.

Collectively, 34 of 86 AML genomes (40%) contained alterations not found with cytogenetics, and 98% of these regions contained genes.

In this study of 86 adult AML genomes, the use of an unbiased high-resolution genomic screen identified many genes not previously implicated in AML that may be relevant for pathogenesis, along with many known oncogenes and tumor suppressor genes.

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[Cites] Blood. 2001 Jun 1;97(11):3581-8 [11369654.001]

[Cites] Blood. 1999 Sep 1;94(5):1820-4 [10477709.001]

[Cites] Genes Chromosomes Cancer. 2003 Jan;36(1):90-8 [12461753.001]

[Cites] Leukemia. 2003 Nov;17(11):2244-7 [12931227.001]

[Cites] Blood. 1993 Dec 1;82(11):3241-9 [8241496.001]

[Cites] Cancer Res. 2005 Jan 15;65(2):375-8 [15695375.001]

[Cites] Oncogene. 2005 Jun 9;24(25):4129-37 [15806161.001]

[Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):334-7 [16015648.001]

[Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):305-19 [16075461.001]

[Cites] Cancer Res. 2005 Oct 15;65(20):9152-4 [16230371.001]

[Cites] Leukemia. 2005 Dec;19(12):2355-8 [16239911.001]

[Cites] Leukemia. 2006 Apr;20(4):696-706 [16467868.001]

[Cites] Leukemia. 2006 May;20(5):840-6 [16498392.001]

[Cites] J Clin Oncol. 2006 Aug 20;24(24):3887-94 [16864856.001]

[Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]

[Cites] Leukemia. 2007 Mar;21(3):571-4 [17268525.001]

[Cites] Nature. 2007 Apr 12;446(7137):758-64 [17344859.001]

[Cites] Leukemia. 2007 Jun;21(6):1224-31 [17377590.001]

[Cites] Blood. 2007 Aug 15;110(4):1251-61 [17452517.001]

[Cites] Blood. 2007 Sep 1;110(5):1648-55 [17494858.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]

[Cites] J Exp Med. 2007 Dec 24;204(13):3059-66 [18070937.001]

[Cites] Blood. 2008 May 1;111(9):4797-808 [18270328.001]

[Cites] N Engl J Med. 2008 May 1;358(18):1909-18 [18450602.001]

[Cites] Nat Genet. 2008 Jun;40(6):722-9 [18438408.001]

[Cites] Nature. 2008 Nov 6;456(7218):66-72 [18987736.001]

[Cites] Leukemia. 2009 Jan;23(1):85-94 [18818702.001]

[Cites] Blood. 2009 Feb 19;113(8):1741-8 [19109227.001]

[Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]

(PMID = 19651600.001).

[ISSN] 1091-6490

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / K08 HL083012; United States / NCI NIH HHS / CA / P01 CA101937; United States / NHLBI NIH HHS / HL / T32 HL007088; United States / NCI NIH HHS / CA / U10 CA101140

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / NSD1 protein, human; 0 / Nuclear Pore Complex Proteins; 0 / Nuclear Proteins; 0 / Nup98 protein, human

[Other-IDs] NLM/ PMC2716381

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities: a comparative analysis of 2562 patients with acute myeloid leukemia.

Acute myeloid leukemia carrying NPM1 mutations and cytoplasmic nucleophosmin (NPMc(+) acute myeloid leukemia) represents one-third of adult AML (50-60% of all acute myeloid leukemia with normal karyotype) and shows distinct biological, pathological and clinical features.

We confirm in 2562 patients with acute myeloid leukemia our previous observation that NPM1 mutations and cytoplasmic nucleophosmin are mutually exclusive of recurrent genetic abnormalities.

Taken together, these findings make NPMc+ acute myeloid leukemia a good candidate for inclusion in the upcoming World Health Organization classification.

[MeSH-major] Cytoplasm / chemistry. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics

[MeSH-minor] Acute Disease. Bone Marrow / pathology. Cell Nucleus / chemistry. Chromosome Aberrations. Chromosome Inversion. Cohort Studies. DNA Mutational Analysis. Germany / epidemiology. Humans. In Situ Hybridization, Fluorescence. Oncogene Proteins, Fusion / genetics. Reverse Transcriptase Polymerase Chain Reaction. Translocation, Genetic

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(PMID = 18268276.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Comparative Study; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 117896-08-9 / nucleophosmin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular typing of adult acute myeloid leukaemia: significance of translocations, tandem duplications, methylation, and selective gene expression profiling.

Although a number of molecular aberrations have been described in acute myeloid leukaemia (AML), no study has yet determined their relative prognostic importance.

We have analysed blast cells from 250 adult patients treated at the same institution during a 15-year period.

Compared with normal bone marrow, the chemotherapy resistance protein MRP1 and apoptosis related genes BAX and CASPASE3 were found to be overexpressed in AML blasts.

From these data, which are the first to compare these molecular aberrations directly, we conclude that, when a battery of molecular changes is evaluated for upfront significance in AML, recurrent translocations are of prime importance for treatment outcome.

[MeSH-major] DNA Methylation. Leukemia, Myeloid / genetics. Tandem Repeat Sequences / genetics. Translocation, Genetic

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. DNA, Neoplasm / genetics. Gene Expression Profiling. Genes, MDR. Humans. Middle Aged. Neoplasm Proteins / genetics. Promoter Regions, Genetic / genetics. Proportional Hazards Models. Retrospective Studies. Survival Analysis. fms-Like Tyrosine Kinase 3 / genetics

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(PMID = 16281935.001).

[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 / Biomarkers, Tumor; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Array comparative genomic hybridization analysis of adult acute leukemia patients.

We have performed a retrospective array-based comparative hybridization (array-CGH) study on 41 acute leukemia samples [n=17 acute lymphoblastic leukemia (ALL) patients only at diagnosis, n=3 ALL patients both at diagnosis and relapse; n=20 acute myeloid leukemia (AML) patients only at diagnosis and n=1 AML patient both at diagnosis and relapse] using an Agilent 44K array.

In addition to previously detected cytogenetic aberrations, we observed cryptic aberrations in 95% of ALL and 90.5% of AML cases.

ALL-specific recurrent abnormalities were RB1 (n=3), PAX5 (n=4), and CDKN2B (n=3) deletions; AML-specific recurrent abnormalities were HOXA9 and HOXA10 (n=2) deletions and NOTCH1 duplication (n=2).

Recurrent duplication of the ELK1 oncogene was observed in both ALL (n=2) and AML (n=3) cases.

[MeSH-major] Comparative Genomic Hybridization / methods. Oligonucleotide Array Sequence Analysis / methods. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. Chromosome Aberrations. Female. Humans. In Situ Hybridization, Fluorescence. Leukemia, Myeloid, Acute / genetics. Male. Middle Aged. Mutation. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction

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(PMID = 20193845.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A pericentric inv(9)(p22q34) of the der(9)t(9;22)(q34;q11.2) is a recurrent secondary anomaly in Ph-positive leukemia.

A pericentric inv(9)(p22q34) of the derivative chromosome 9 that resulted from a standard t(9;22)(q34;q11.2) was identified by R-banding karyotypic analysis and fluorescence in situ hybridization (FISH) assays in 4 (0.18%) of 2,200 Philadelphia chromosome (Ph)-positive leukemia patients, including 3 with chronic myeloid leukemia (CML) in chronic phase and 1 with acute myeloid leukemia (AML) in our hospital since 2004.

FISH also found a deletion of partial sequence of BCR on der(9)t(9;22)(q34;q11.2)inv(9)(p22q34) in 67.5% of bone marrow cells in the AML patient, but did not detect the deletion of the sequence of ASS/9q34 in these four patients.

Reverse transcriptase-polymerase chain reaction revealed a b3a2 type of BCR/ABL1 fusion transcript in all of them, proving their disease to be Ph-positive leukemia.

On reviewing the literature, only two solitary Ph-positive leukemia patients have been noticed to have the inv(9)(p22q34) anomaly.

These two patients, together with our four documented patients, indicate that inv(9)(p22q34) is a novel, rare, but recurrent secondary chromosomal abnormality for Ph-positive leukemia.

Despite receiving hydroxyurea therapy (n = 3 patients), combined chemotherapy (n = 2), even imatinib treatment (n = 1), three patients, including one with AML and two with CML (one of whom progressed into the lymphoblastic blast phase), died with survival times of 28 days, 13 months, and 34 months, respectively.

[MeSH-major] Chromosome Inversion. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics

[MeSH-minor] Adult. Bone Marrow Cells / cytology. Chromosome Aberrations. Disease Progression. Female. Gene Deletion. Humans. In Situ Hybridization, Fluorescence. Karyotyping. Male. Middle Aged. Prognosis. Reverse Transcriptase Polymerase Chain Reaction

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[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

(PMID = 21156255.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Nucleophosmin (NPM1) mutations in adult and childhood acute myeloid leukaemia: towards definition of a new leukaemia entity.

Somatic mutations in exon 12 of the NPM gene (NPM1) are the most frequent genetic abnormality in adult acute myeloid leukaemia (AML), found in approximately 35% of all cases and up to 60% of patients with normal karyotype (NK) AML.

In children, NPM1 mutations are far less frequent, occurring in 8-10% of all AML cases, and in approximately 25% of those with a NK.

NPM1 mutations lead to aberrant localization of the NPM protein into the cytoplasm, thus the designation, NPMc+ AML.

NPMc+ AML is seen predominantly in patients with a NK and is essentially mutually exclusive of recurrent chromosomal translocations.

NPMc+ AML is also characterized by a unique gene expression signature and microRNA signature.

NPMc+ AML has important prognostic significance, as NPMc+ AML, in the absence of a coexisting FLT3-ITD mutation, is associated with a favourable outcome.

Given its distinctive biologic and clinical features and its clear clinical relevance, NPMc+ AML is included as a provisional entity in the 2008 WHO classifications.

Further, it represents a potential therapeutic target warranting research aimed at identifying novel small molecules with activity in NPMc+ AML.

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[Copyright] Copyright (c) 2009 John Wiley & Sons, Ltd.

[Cites] Leukemia. 2007 Jul;21(7):1564-6 [17410190.001]

[Cites] Leukemia. 2007 Jul;21(7):1566-70 [17443224.001]

[Cites] Cancer Res. 2007 Jul 1;67(13):6230-7 [17616680.001]

[Cites] Blood. 2007 Aug 1;110(3):979-85 [17440048.001]

[Cites] Leukemia. 2007 Sep;21(9):2000-9 [17597811.001]

[Cites] Int J Hematol. 2007 Aug;86(2):143-6 [17875528.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317.001]

[Cites] Leukemia. 2008 Jan;22(1):195-8 [17637812.001]

[Cites] J Biol Chem. 2008 Feb 29;283(9):5728-37 [18165222.001]

[Cites] Blood. 2008 Mar 1;111(5):2776-84 [17957027.001]

[Cites] Leukemia. 2008 Jun;22(6):1234-40 [18401421.001]

[Cites] Blood. 1996 Feb 1;87(3):882-6 [8562957.001]

[Cites] Oncogene. 1996 Jan 18;12(2):265-75 [8570204.001]

[Cites] J Pathol. 1996 Jan;178(1):48-52 [8778315.001]

[Cites] Mol Cell Biol. 1997 Apr;17(4):2312-25 [9121481.001]

[Cites] Cell. 1997 Nov 28;91(5):649-59 [9393858.001]

[Cites] J Soc Gynecol Investig. 1997 Nov-Dec;4(6):298-304 [9408885.001]

[Cites] FEBS Lett. 1997 Dec 22;420(1):25-7 [9450543.001]

[Cites] Nat Cell Biol. 1999 May;1(1):20-6 [10559859.001]

[Cites] Cell. 2000 Sep 29;103(1):127-40 [11051553.001]

[Cites] Curr Opin Hematol. 2001 Jul;8(4):189-91 [11561153.001]

[Cites] FEBS Lett. 2001 Oct 12;506(3):272-6 [11602260.001]

[Cites] Nat Genet. 2002 Jan;30(1):41-7 [11731795.001]

[Cites] Blood. 2002 Jan 15;99(2):409-26 [11781220.001]

[Cites] Leukemia. 2002 Jun;16(6):1053-68 [12040437.001]

[Cites] Nat Cell Biol. 2002 Jul;4(7):529-33 [12080348.001]

[Cites] Blood. 2002 Sep 1;100(5):1532-42 [12176867.001]

[Cites] Biosci Biotechnol Biochem. 2002 Oct;66(10):2239-42 [12450141.001]

[Cites] Mol Cell. 2003 Feb;11(2):415-24 [12620229.001]

[Cites] Hematol J. 2003;4(1):31-40 [12692518.001]

[Cites] Leukemia. 2003 Sep;17(9):1738-52 [12970773.001]

[Cites] Mol Cell Biol. 2004 Feb;24(3):985-96 [14729947.001]

[Cites] Science. 2004 Apr 23;304(5670):594-6 [15105502.001]

[Cites] Cancer Cell. 2004 May;5(5):465-75 [15144954.001]

[Cites] Genes Dev. 2004 Aug 1;18(15):1862-74 [15289458.001]

[Cites] J Biol Chem. 2004 Aug 20;279(34):35726-34 [15190079.001]

[Cites] FEBS Lett. 2004 Sep 24;575(1-3):112-8 [15388344.001]

[Cites] Blood. 2008 Mar 1;111(5):2527-37 [17965322.001]

[Cites] Haematologica. 2008 Mar;93(3):439-42 [18268276.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]

[Cites] Leuk Lymphoma. 2007 Nov;48(11):2141-4 [17990177.001]

[Cites] Blood. 2008 Apr 1;111(7):3859-62 [18212245.001]

[Cites] Oncogene. 2008 Apr 10;27(17):2382-9 [17968318.001]

[Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]

[Cites] Leukemia. 2008 May;22(5):1075-8 [17972951.001]

[Cites] Curr Opin Hematol. 2008 Jul;15(4):352-8 [18536574.001]

[Cites] Leukemia. 2008 Jun;22(6):1285-9 [18059485.001]

[Cites] Mol Cell Biol. 2004 Nov;24(21):9327-38 [15485902.001]

[Cites] Cell. 1989 Feb 10;56(3):379-90 [2914325.001]

[Cites] J Biol Chem. 1990 Oct 25;265(30):18227-33 [2211699.001]

[Cites] Cancer Res. 1992 Jun 15;52(12):3372-7 [1596895.001]

[Cites] Science. 1994 Mar 4;263(5151):1281-4 [8122112.001]

[Cites] J Biol Chem. 1994 Dec 9;269(49):30994-8 [7527039.001]

[Cites] Cancer Res. 1995 Apr 15;55(8):1625-8 [7712464.001]

[Cites] Nucleic Acids Res. 1995 Oct 11;23(19):3974-9 [7479045.001]

[Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]

[Cites] Oncogene. 2006 Jul 20;25(31):4376-80 [16501600.001]

[Cites] J Cell Biol. 2008 Jul 14;182(1):19-26 [18625840.001]

[Cites] Leukemia. 2008 Nov;22(11):2041-7 [18668134.001]

[Cites] Leukemia. 2009 Feb;23(2):262-70 [19020547.001]

[Cites] Nucleic Acids Res. 1998 Oct 1;26(19):4508-15 [9742256.001]

[Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3706-11 [10097101.001]

[Cites] Protein Sci. 1999 Apr;8(4):905-12 [10211837.001]

[Cites] Prostate. 1999 Jun 1;39(4):298-304 [10344220.001]

[Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]

[Cites] J Biol Chem. 2005 Mar 25;280(12):10988-96 [15644315.001]

[Cites] Biochem J. 2005 May 15;388(Pt 1):7-15 [15737070.001]

[Cites] Blood. 2005 Aug 1;106(3):899-902 [15831697.001]

[Cites] Nat Cell Biol. 2005 Aug;7(8):823-30 [16041368.001]

[Cites] Blood. 2005 Aug 15;106(4):1419-22 [15870172.001]

[Cites] Mol Cell Biol. 2005 Sep;25(17):7534-45 [16107701.001]

[Cites] Nature. 2005 Sep 1;437(7055):147-53 [16007073.001]

[Cites] Mol Cell Biol. 2005 Oct;25(20):8874-86 [16199867.001]

[Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]

[Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]

[Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]

[Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]

[Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]

[Cites] Cell Cycle. 2005 Nov;4(11):1593-8 [16205118.001]

[Cites] Cancer Res. 2006 Mar 15;66(6):3044-50 [16540653.001]

[Cites] Cancer Res. 2006 Mar 15;66(6):3310-6 [16540685.001]

[Cites] Mol Cell Biol. 2006 May;26(10):3798-809 [16648475.001]

[Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]

[Cites] Br J Haematol. 2006 Jun;133(6):638-41 [16704439.001]

[Cites] Blood. 2006 Jun 1;107(11):4514-23 [16455950.001]

[Cites] Leukemia. 2006 Jun;20(6):1103-8 [16541144.001]

[Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]

[Cites] Haematologica. 2006 Aug;91(8):1147-8 [16870548.001]

[Cites] Blood. 2006 Sep 15;108(6):1999-2005 [16720834.001]

[Cites] Leuk Res. 2007 Jan;31(1):109-11 [16678898.001]

[Cites] Trends Mol Med. 2006 Dec;12(12):580-7 [17071139.001]

[Cites] Nature. 2006 Nov 30;444(7119):638-42 [17136094.001]

[Cites] Blood. 2006 Dec 15;108(13):4146-55 [16926285.001]

[Cites] Blood. 2007 Feb 1;109(3):874-85 [17008539.001]

[Cites] Leukemia. 2007 Feb;21(2):366-7 [17151698.001]

[Cites] Leuk Res. 2007 Apr;31(4):427-34 [17161457.001]

[Cites] Leukemia. 2007 May;21(5):1099-103 [17301808.001]

[Cites] Leukemia. 2007 May;21(5):998-1004 [17361227.001]

[Cites] APMIS. 2007 Apr;115(4):341-6 [17504301.001]

[Cites] Leukemia. 2007 Jun;21(6):1307 [17315018.001]

(PMID = 19569254.001).

[ISSN] 1099-1069

[Journal-full-title] Hematological oncology

[ISO-abbreviation] Hematol Oncol

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA111728-05; United States / NCI NIH HHS / CA / K23 CA111728; United States / NCI NIH HHS / CA / T32 CA060441; United States / NCI NIH HHS / CA / K23 CA111728-05

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin

[Number-of-references] 102

[Other-IDs] NLM/ NIHMS234930; NLM/ PMC3069851

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation.

Recent genome-wide screening also revealed IDH1 mutation as a recurrent event in acute myeloid leukemia (AML), but its clinical implications in AML are largely unknown.

We analyzed 493 adult Chinese AML patients in Taiwan and found 27 patients (5.5%) harboring this mutation.

[MeSH-major] Chromosomes, Human, Pair 8 / genetics. Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics. Monosomy. Neoplasm Proteins / genetics

[MeSH-minor] Adult. Aged. Antigens, CD13 / biosynthesis. Antigens, CD13 / genetics. Antigens, CD14 / biosynthesis. Antigens, CD14 / genetics. Female. Gene Expression Regulation, Leukemic / genetics. Genome-Wide Association Study. HLA-DR Antigens / biosynthesis. HLA-DR Antigens / genetics. Humans. Male. Middle Aged. Recurrence. Remission Induction. Taiwan

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[CommentIn] Blood. 2010 Jul 22;116(3):495-6 [20651083.001]

(PMID = 20097881.001).

[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, CD14; 0 / HLA-DR Antigens; 0 / Neoplasm Proteins; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.42. / IDH1 protein, human; EC 3.4.11.2 / Antigens, CD13

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36).

BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia.

In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML).

RESULTS: Six of seven breakpoints in ALL and two in a single case of AML were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe.

INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL.

Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism.

[MeSH-major] Chromosome Breakage. Chromosome Inversion / genetics. Chromosomes, Human, Pair 6 / genetics. Chromosomes, Human, Pair 7 / genetics. Genes, myb. Leukemia, Myeloid / genetics. Leukemia-Lymphoma, Adult T-Cell / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

[MeSH-minor] Acute Disease. Adaptor Proteins, Signal Transducing / genetics. Adolescent. Bone Marrow Cells / ultrastructure. Child. Child, Preschool. Chromosome Banding. Clone Cells / pathology. Female. Humans. In Situ Hybridization, Fluorescence. Infant. Male. Oncogene Proteins, Fusion / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / pathology

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(PMID = 15921375.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / AHI1 protein, human; 0 / Adaptor Proteins, Signal Transducing; 0 / Oncogene Proteins, Fusion

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics.

Acute myeloid leukemia (AML) is a heterogenous disorder that results from a block in the differentiation of hematopoietic progenitor cells along with uncontrolled proliferation.

In approximately 60% of cases, specific recurrent chromosomal aberrations can be identified by modern cytogenetic techniques.

Currently, favorable risk AML patients are usually treated with contemporary chemotherapy while poor risk AML patients receive allogeneic stem cell transplantation if suitable stem cell donors exist.

The largest subgroup of AML patients (aproximately 40%) have no identifiable cytogenetic abnormalities and are classified as intermediate risk.

Recently, it is becoming increasingly evident that it is possible to identify a subgroup of poorer risk patients among those with normal cytogenic AML (NC-AML).

Molecular risk stratification for NC-AML patients may be possible due to mutations of NPM1, FLT3, MLL, and CEBPalpha as well as alterations in expression levels of BAALC, MN1, ERG, and AF1q.

Further prospective studies are needed to confirm if poorer risk NC-AML patients have improved clinical outcomes after more aggressive therapy.

[MeSH-major] Genetic Markers. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adult. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Cytogenetics. Gene Expression Profiling. Gene Expression Regulation, Leukemic. Humans. Neoplasm, Residual. Nuclear Proteins / genetics. Nuclear Proteins / physiology. Prognosis. fms-Like Tyrosine Kinase 3 / genetics. fms-Like Tyrosine Kinase 3 / physiology

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[Cites] Haematologica. 2005 Jul;90(7):881-9 [15996925.001]

[Cites] Exp Hematol. 2009 Jan;37(1):135-42 [19100523.001]

[Cites] Cancer Res. 2005 Sep 1;65(17):7596-602 [16140924.001]

[Cites] Blood. 2005 Oct 15;106(8):2854-61 [15994285.001]

[Cites] Leuk Lymphoma. 2005 Dec;46(12):1679-87 [16263569.001]

[Cites] Blood. 2005 Nov 15;106(10):3618-20 [16046528.001]

[Cites] Blood. 2005 Nov 15;106(10):3658-65 [16076872.001]

[Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]

[Cites] Blood. 2005 Dec 1;106(12):3733-9 [16076867.001]

[Cites] Blood. 2005 Dec 1;106(12):3747-54 [16109776.001]

[Cites] Blood. 2005 Dec 15;106(13):4269-77 [16105979.001]

[Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]

[Cites] Br J Haematol. 2006 Apr;133(1):103-5 [16512836.001]

[Cites] Semin Hematol. 2006 Apr;43(2):89-95 [16616042.001]

[Cites] Blood. 2006 May 1;107(9):3724-6 [16368883.001]

[Cites] Leukemia. 2000 May;14(5):796-804 [10803509.001]

[Cites] Blood. 2000 Dec 15;96(13):4075-83 [11110676.001]

[Cites] Nat Genet. 2001 Mar;27(3):263-70 [11242107.001]

[Cites] Blood. 2001 Apr 15;97(8):2434-9 [11290608.001]

[Cites] Acta Haematol. 2001;105(1):45-8 [11340253.001]

[Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13901-6 [11707601.001]

[Cites] Genes Chromosomes Cancer. 2002 Jun;34(2):137-53 [11979548.001]

[Cites] Haematologica. 2002 Jun;87(6):569-77 [12031912.001]

[Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]

[Cites] J Clin Oncol. 2002 Aug 1;20(15):3254-61 [12149299.001]

[Cites] Blood. 2002 Oct 15;100(8):2717-23 [12351377.001]

[Cites] Blood. 2002 Dec 15;100(13):4372-80 [12393388.001]

[Cites] Hematol J. 2002;3(6):283-9 [12522450.001]

[Cites] Oncogene. 2003 Feb 6;22(5):699-709 [12569362.001]

[Cites] Hematol J. 2003;4(1):31-40 [12692518.001]

[Cites] Genes Chromosomes Cancer. 2003 Jun;37(2):149-58 [12696063.001]

[Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]

[Cites] Exp Hematol. 2003 Nov;31(11):1051-6 [14585369.001]

[Cites] Br J Haematol. 2003 Nov;123(3):413-9 [14616999.001]

[Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]

[Cites] Blood. 2004 Mar 1;103(5):1901-8 [14604973.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20 [15007164.001]

[Cites] Leuk Lymphoma. 2004 Jan;45(1):73-8 [15061200.001]

[Cites] N Engl J Med. 2004 Apr 15;350(16):1605-16 [15084693.001]

[Cites] Ann Hematol. 2004;83 Suppl 1:S81-2 [15124685.001]

[Cites] Expert Opin Emerg Drugs. 2004 May;9(1):55-71 [15155136.001]

[Cites] Am J Med Genet Suppl. 1990;7:251-61 [2149958.001]

[Cites] Nature. 1995 Nov 30;378(6556):505-8 [7477409.001]

[Cites] Semin Oncol. 1997 Feb;24(1):17-31 [9045301.001]

[Cites] Blood. 1997 Aug 1;90(3):1192-9 [9242552.001]

[Cites] Blood. 2004 Nov 15;104(10):3058-63 [15217837.001]

[Cites] Oncogene. 2004 Dec 16;23(58):9381-91 [15543237.001]

[Cites] Curr Opin Hematol. 2005 Jan;12(1):7-13 [15604885.001]

[Cites] Br J Haematol. 2005 Jan;128(2):218-20 [15638856.001]

[Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]

[Cites] Clin Cancer Res. 2005 Feb 15;11(4):1416-24 [15746041.001]

[Cites] Leuk Res. 2005 Jul;29(7):849-53 [15921740.001]

[Cites] Blood. 2005 Jul 1;106(1):345-52 [15774615.001]

[Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]

[Cites] Leukemia. 2006 Jun;20(6):1103-8 [16541144.001]

[Cites] Int J Hematol. 2006 May;83(4):301-8 [16757428.001]

[Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]

[Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]

[Cites] Arch Pathol Lab Med. 2006 Nov;130(11):1687-92 [17076533.001]

[Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]

[Cites] Blood. 2007 Feb 1;109(3):874-85 [17008539.001]

[Cites] Exp Mol Pathol. 2008 Dec;85(3):227-31 [18977345.001]

[Cites] Leukemia. 2005 Aug;19(8):1479-82 [15973451.001]

(PMID = 19490647.001).

[ISSN] 1756-8722

[Journal-full-title] Journal of hematology & oncology

[ISO-abbreviation] J Hematol Oncol

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Genetic Markers; 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3

[Number-of-references] 65

[Other-IDs] NLM/ PMC2700131

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Phase I pharmacokinetic and pharmacodynamic study of temozolomide in pediatric patients with refractory or recurrent leukemia: a Children's Oncology Group Study.

PURPOSE: To determine the tolerability, pharmacokinetics, and mechanisms of temozolomide resistance in children with relapsed or refractory leukemia.

Pretreatment leukemia cell O6-methylguanine-DNA methyltransferase (MGMT) activity, tumor and plasma MGMT promoter methylation, and microsatellite instability (MSI) were examined in 14 of 16 study patients and in tissue bank samples from children with acute leukemia not treated with temozolomide (MGMT, n = 67; MSI, n = 65).

RESULTS: Sixteen patients (nine female, seven male; acute lymphoblastic leukemia [ALL], n = 8; acute myeloid leukemia [AML], n = 8), median age 11 years (range, 1 to 19 years), received either 200 mg/m2/d (nine enrolled, three assessable for toxicity) or 260 mg/m2/d (seven enrolled, three assessable for toxicity) of temozolomide.

MGMT activity in leukemia cells was quite variable and was highest in patients with relapsed ALL.

CONCLUSION: Temozolomide was well tolerated at doses as high as 260 mg/m2/d for 5 days in children with relapsed or refractory leukemia.

Increased MGMT activity may account for the temozolomide resistance in children with relapsed leukemia.

Leukemia cell MGMT activity was higher in pediatric ALL than AML (P < .0001).

[MeSH-major] Antineoplastic Agents, Alkylating / pharmacokinetics. Dacarbazine / analogs & derivatives. Drug Resistance, Neoplasm / genetics. Leukemia / drug therapy. Neoplasm Recurrence, Local / drug therapy

[MeSH-minor] Adolescent. Adult. Child. Child, Preschool. DNA Modification Methylases / metabolism. DNA Repair Enzymes / metabolism. Female. Humans. Infant. Male. Microsatellite Instability. Tumor Suppressor Proteins / metabolism

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(PMID = 17971589.001).

[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

[Grant] United States / NCI NIH HHS / CA / K12CA90433; United States / NCI NIH HHS / CA / P30 CA14599; United States / NCI NIH HHS / CA / U01CA63187; United States / NCI NIH HHS / CA / UO1-CA97452

[Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Suppressor Proteins; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 6.5.1.- / DNA Repair Enzymes

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Genes predictive of outcome and novel molecular classification schemes in adult acute myeloid leukemia.

The pretreatment karyotype of leukemic blasts is currently the key determinant in therapy decision making in acute myeloid leukemia (AML).

The World Health Organization (WHO) has recognized this important information by including, besides clinical, cytological, cytochemical, and immunophenotypical features, recurrent cytogenetic abnormalities in its classification (Table 1).

In addition, novel molecular approaches in genomics, like monitoring the expression levels of thousands of genes in parallel using DNA microarray technology, open possibilities for further refinement of prognostication of AML.

Gene expression profiling in AML is already well established and has proven to be valuable to recognize various cytogenetic subtypes, discover novel AML subclasses, and predict clinical outcome.

The current advances made in molecular understanding of AML will ultimately lead to a further refinement of prognostics of AML.

[MeSH-major] Genes, Neoplasm. Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adult. Chromosome Aberrations. Gene Expression Profiling. Humans. Neoplasm Proteins / genetics. Neoplasm Proteins / physiology. Oligonucleotide Array Sequence Analysis. Prognosis. Treatment Outcome

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(PMID = 20306246.001).

[ISSN] 0927-3042

[Journal-full-title] Cancer treatment and research

[ISO-abbreviation] Cancer Treat. Res.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Neoplasm Proteins

[Number-of-references] 81

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Recurrent finding of the FIP1L1-PDGFRA fusion gene in eosinophilia-associated acute myeloid leukemia and lymphoblastic T-cell lymphoma.

Here, we report on seven FIP1L1-PDGFRA-positive patients who presented with acute myeloid leukemia (AML, n=5) or lymphoblastic T-cell non-Hodgkin-lymphoma (n=2) in conjunction with AML or Eos-MPD.

AML patients were negative for common mutations of FLT3, NRAS, NPM1, KIT, MLL and JAK2; one patient revealed a splice mutation of RUNX1 exon 7.

We conclude that all eosinophilia-associated hematological malignancies should be screened for the presence of the FIP1L1-PDGFRA fusion gene as they are excellent candidates for treatment with tyrosine kinase inhibitors even if they present with an aggressive phenotype such as AML.

[MeSH-major] Eosinophilia / drug therapy. Leukemia, Myeloid / drug therapy. Oncogene Proteins, Fusion / analysis. Piperazines / administration & dosage. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / administration & dosage. Receptor, Platelet-Derived Growth Factor alpha. mRNA Cleavage and Polyadenylation Factors

[MeSH-minor] Acute Disease. Adult. Aged. Benzamides. Disease-Free Survival. Humans. Imatinib Mesylate. Male. Middle Aged. Myeloproliferative Disorders / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Remission Induction / methods

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(PMID = 17377585.001).

[ISSN] 0887-6924

[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

[Chemical-registry-number] 0 / Benzamides; 0 / FIP1L1 protein, human; 0 / Oncogene Proteins, Fusion; 0 / Piperazines; 0 / Pyrimidines; 0 / mRNA Cleavage and Polyadenylation Factors; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Recurrent extramedullary relapse of acute myelogenous leukemia after allogeneic hematopoietic stem cell transplantation in a patient with the chromosomal abnormality t(8;21) and CD56-positivity.

Isolated extramedullary (EM) relapse of acute myelogenous leukemia (AML) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is rare.

We describe an AML patient showing the chromosomal abnormality t(8;21) and CD56 expression who experienced a unique EM relapse after allo-HSCT.

These findings suggest that the graft-versus-leukemia effect may preferentially maintain marrow remission rather than prevent EM relapse.

In addition, our findings show that extended survival is possible after EM relapse following allo-HSCT in patients with marrow hematopoiesis of donor origin, and that augmentation of the graft-versus-leukemia effect may be useful.

[MeSH-major] Graft vs Leukemia Effect. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute. Stomach Neoplasms. Translocation, Genetic

[MeSH-minor] Antigens, CD56 / metabolism. Chromosomes, Human, Pair 21. Chromosomes, Human, Pair 8. Gastric Mucosa / pathology. Humans. Male. Recurrence. Transplantation, Homologous. Young Adult

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(PMID = 19629629.001).

[ISSN] 1865-3774

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD56

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Maintenance therapy with low-dose azacitidine after allogeneic hematopoietic stem cell transplantation for recurrent acute myelogenous leukemia or myelodysplastic syndrome: a dose and schedule finding study.

BACKGROUND: Recurrence is a major cause of treatment failure after allogeneic transplantation for acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS), and treatment options are very limited.

Azacitidine is a DNA methyltransferase inhibitor with activity in myeloid disease.

CONCLUSIONS: Azacitidine at 32 mg/m2 given for 5 days is safe and can be administered after allogeneic transplant for at least 4 cycles to heavily pretreated AML/MDS patients.

[MeSH-major] Azacitidine / administration & dosage. Hematopoietic Stem Cell Transplantation. Leukemia, Myeloid, Acute / drug therapy. Leukemia, Myeloid, Acute / surgery. Myelodysplastic Syndromes / drug therapy. Myelodysplastic Syndromes / surgery

[MeSH-minor] Adult. Aged. DNA Methylation. Disease-Free Survival. Drug Administration Schedule. Female. Graft vs Host Disease / epidemiology. Humans. Male. Middle Aged. Recurrence. Transplantation, Homologous

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[Copyright] Copyright © 2010 American Cancer Society.

(PMID = 20672358.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P30 CA016672

[Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] M801H13NRU / Azacitidine

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The clinical relevance of Wilms Tumour 1 (WT1) gene mutations in acute leukaemia.

Recurrent genetic aberrations are important predictors of outcome in acute myeloid leukaemia (AML).

WT1 mutations occur in approximately 10% of adult AML patients at diagnosis and are most frequent in the cytogenetically normal (CN) AML subgroup.

Herein, we discuss the importance of WT1 mutations in AML.

[MeSH-major] Genes, Wilms Tumor. Leukemia, Myeloid, Acute / genetics. Mutation / genetics

[MeSH-minor] Adult. Humans. Prognosis. WT1 Proteins / genetics. WT1 Proteins / metabolism

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(PMID = 20013787.001).

[ISSN] 1099-1069

[Journal-full-title] Hematological oncology

[ISO-abbreviation] Hematol Oncol

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G0700052; United Kingdom / Cancer Research UK / / ; United Kingdom / Medical Research Council / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / WT1 Proteins

[Number-of-references] 75

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Twenty years of follow-up among survivors of childhood and young adult acute myeloid leukemia: a report from the Childhood Cancer Survivor Study.

BACKGROUND: Limited data exist on the comprehensive assessment of late medical and social effects experienced by survivors of childhood and young adult acute myeloid leukemia (AML).

METHODS: This analysis included 272 5-year AML survivors who participated in the Childhood Cancer Survivor Study (CCSS).

The cumulative incidence of recurrent AML was 6.6% at 10 years (95% CI, 3.7%-9.6%) and 8.6% at 20 years (95% CI, 5.1%-12.1%).

CONCLUSIONS: Long-term survival from childhood AML > or =5-years after diagnosis was favorable.

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(PMID = 18327823.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / K12 RR023247; United States / NCI NIH HHS / CA / U24 CA055727; United States / NCRR NIH HHS / RR / 1 K12 RR 023247; United States / NCI NIH HHS / CA / U24 CA 55727

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Investigator] Robison LL; Hudson M; Armstrong G; Perkins J; O'Leary M; Friedman D; Pendergrass T; Greffe B; Odom L; Ruccione K; Mulvihill J; Ginsberg J; Meadows A; Tersak J; Ritchey A; Blatt J; Reaman G; Packer R; Davies S; Bhatia S; Qualman S; Hammond S; Termuhlen A; Ruymann F; Diller L; Grier H; Li F; Meacham L; Mertens A; Leisenring W; Potter J; Greenberg M; Nathan PC; Boice J; Rodriguez V; Smithson WA; Gilchrist G; Sklar C; Oeffinger K; Finklestein J; Anderson B; Inskip P; Vik TA; Weetman R; Green DM; Hayashi R; Vietti T; Marina N; Donaldson SS; Link MP; Dreyer Z; Whelan K; Sande J; Berkow R; Yasui Y; Casallis J; Zeltzer L; Goldsby R; Ablin A; Hutchinson R; Neglia J; Deapen D; Breslow N; Bowers D; Tomlinson G; Buchanan GR; Strong L; Stovall M

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Cytogenetic studies of a series of 43 consecutive secondary myelodysplastic syndromes/acute myeloid leukemias: conventional cytogenetics, FISH, and multiplex FISH.

We report a series of 43 consecutive therapy-related myelodysplastic syndromes (t-MDS) or acute myeloid leukemias (t-AML) observed for 6 years.

Conventional cytogenetic and fluorescent in situ hybridization (FISH)/ multiplex FISH (M-FISH) methods were used to analyze cytogenetic characteristics of secondary MDS/AML.

A considerable proportion of recurrent balanced translocations characterized t-AML secondary to therapy.

Compared to other series, recurrent translocations appeared to be more numerous (25%), probably reflecting an evolution of therapeutic modalities.

[MeSH-major] In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Myelodysplastic Syndromes / genetics

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Child. Female. Gene Amplification. Gene Deletion. Humans. Karyotyping. Male. Middle Aged. Translocation, Genetic

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(PMID = 16843103.001).

[ISSN] 0165-4608

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse.

PURPOSE: Recent data suggest that tryptase is produced by blast cells in a group of patients with acute myeloid leukemia (AML).

PATIENTS: In this study, we examined the value of tryptase as a marker of minimal residual AML.

In 61 patients with de novo AML exhibiting elevated serum tryptase (>15 ng/mL) at diagnosis, tryptase levels were measured serially during and after chemotherapy by a fluoroenzyme immunoassay.

Thus, AML relapses occurred in 15 of 29 patients with CR + BR (52%) and in 12 of 13 patients with CR without BR (92%), resulting in a significantly reduced probability of continuous CR for patients with CR without BR (P < 0.05).

In all patients with continuous hematologic CR, tryptase levels remained constantly normal, whereas a recurrent elevation of tryptase in CR was invariably followed by a hematologic relapse.

CONCLUSION: A persistently elevated tryptase level in AML in CR is indicative of minimal residual AML and associated with a high risk of relapse.

[MeSH-major] Leukemia, Myeloid / pathology. Neoplasm, Residual / pathology. Serine Endopeptidases / blood

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Neoplasm Proteins / genetics. Neoplasm Recurrence, Local. Oncogene Proteins, Fusion / genetics. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Risk Factors. Survival Analysis. Time Factors. Tryptases

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(PMID = 16166430.001).

[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] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / Neoplasm Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.59 / Tryptases

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Plag1 and Plagl2 are oncogenes that induce acute myeloid leukemia in cooperation with Cbfb-MYH11.

Recurrent chromosomal rearrangements are associated with the development of acute myeloid leukemia (AML).

This fusion protein inhibits the core-binding factor (CBF), resulting in a block of hematopoietic differentiation, and induces leukemia upon the acquisition of additional mutations.

In this study, we demonstrate that Plag1 and Plagl2 independently cooperate with CBF beta-SMMHC in vivo to efficiently trigger leukemia with short latency in the mouse.

Finally, PLAG1 and PLAGL2 expression was increased in 20% of human AML samples.

Interestingly, PLAGL2 was preferentially increased in samples with chromosome 16 inversion, suggesting that PLAG1 and PLAGL2 may also contribute to human AML.

Overall, this study shows that Plag1 and Plagl2 are novel leukemia oncogenes that act by expanding hematopoietic progenitors expressing CbF beta-SMMHC.

[MeSH-major] DNA-Binding Proteins / genetics. Leukemia, Myeloid / genetics. Oncogene Proteins, Fusion / genetics. RNA-Binding Proteins / genetics. Transcription Factors / genetics

[MeSH-minor] Acute Disease. Adolescent. Adult. Animals. Female. G1 Phase / immunology. Gene Expression Regulation, Leukemic. Hematopoietic Stem Cells / cytology. Humans. Male. Mice. Mice, Mutant Strains. Middle Aged. Mutagenesis, Insertional. Retroviridae / genetics. S Phase / immunology

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(PMID = 15585652.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Grant] United States / NCI NIH HHS / CA / R01 CA096983-01

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / CBFbeta-MYH11 fusion protein; 0 / DNA-Binding Proteins; 0 / Oncogene Proteins, Fusion; 0 / PLAG1 protein, human; 0 / PLAGL2 protein, human; 0 / RNA-Binding Proteins; 0 / Transcription Factors

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Secondary prophylaxis of IFI is widely administered, but reliable data on outcome and risk factors for recurrent IFI during subsequent chemotherapy are not available.

This study determines risk factors for recurrent IFI in leukaemia patients.

METHODS: From 25 European cancer centres, 166 consecutive patients with acute myelogenous leukaemia (AML) and a recent history of proven or probable pulmonary IFI were included.

Recurrent IFI occurred in 26 patients (15.7%).

Multiple logistic regressions yielded predisposing factors: duration of neutropenia [per additional day; odds ratio (OR) 1.043, confidence interval (CI) 1.008-1.078], high-dose cytarabine (OR 3.920, CI 1.120-12.706), number of antibiotics (per antibiotic; OR 1.504, CI 1.089-2.086), partial response as outcome of prior IFI (OR 4.037, CI 1.301-12.524) and newly diagnosed AML (OR 3.823, CI 0.953-15.340).

CONCLUSIONS: Duration of neutropenia, high-dose cytarabine, prior antibiotic therapy and a partial response to the first IFI therapy were risk factors for recurrent IFI and should be considered in AML patients with prior pulmonary IFI undergoing further chemotherapy.

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chemoprevention. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid, Acute / complications. Leukemia, Myeloid, Acute / drug therapy. Logistic Models. Male. Middle Aged. Recurrence. Risk Factors. Treatment Outcome

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(PMID = 18272515.001).

[ISSN] 1460-2091

[Journal-full-title] The Journal of antimicrobial chemotherapy

[ISO-abbreviation] J. Antimicrob. Chemother.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antifungal Agents

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Deletion 15q as the sole abnormality in acute myeloid leukemia: report of three cases and review of the literature.

Deletions within the long arm of chromosome 15, a recurrent abnormality in myeloid malignancies, have been reported previously as a sole abnormality in only eight cases of acute myeloid leukemia (AML).

We describe three new cases of AML with this abnormality, all adult women (age, 41-66 years).

Two cases were acute myelomonocytic leukemia (FAB AML-M4), and one was acute myeloblastic leukemia with maturation (FAB AML-M2).

Taken together with the eight previously reported cases, we conclude that deletions in chromosome 15 are associated with AML, both in cases that arise de novo or in the setting of a myeloproliferative disorder or myelodysplastic syndrome.

The prognosis is poor, with survival similar to other AML cases with unfavorable cytogenetic changes.

[MeSH-major] Chromosomes, Human, Pair 15. Leukemia, Myeloid, Acute / genetics. Sequence Deletion

[MeSH-minor] Adult. Aged. Chromosome Banding. Fatal Outcome. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Karyotyping

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(PMID = 19100517.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article; Review

[Publication-country] United States

[Number-of-references] 20

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute Myelogeneous Leukemia (M0/M1) with novel chromosomal abnormality of t(14;17) (q32; q11.2).

Acute Myelogeneous Leukemia (AML) is a heterogeneous disease with respect to morphology, immunophenotype, and genetic rearrangements.

Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis.

In this study, we report a case whose clinical features were suggestive of AML-M1 subtype with t(14;17) (q32; q11.2) karyotype involving rearrangement of chromosomal segments 17q11.2 and 14q32.

This is the first report of novel chromosomal translocation in this subset of AML and has not yet been reported elsewhere.

[MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 17 / genetics. Leukemia, Myeloid, Acute / genetics. Translocation, Genetic / genetics

[MeSH-minor] Adult. Female. Humans. Karyotyping

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(PMID = 17177193.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic impact of isocitrate dehydrogenase enzyme isoforms 1 and 2 mutations in acute myeloid leukemia: a study by the Acute Leukemia French Association group.

PURPOSE: Recently, whole-genome sequencing in acute myeloid leukemia (AML) identified recurrent isocitrate dehydrogenase enzyme isoform (IDH1) mutations (IDH1m), previously reported to be involved in gliomas as well as IDH2 mutations (IDH2m).

The prognosis of both IDH1m and IDH2m in AML remains unclear.

PATIENTS AND METHODS: The prevalence and the prognostic impact of R132 IDH1 and R172 IDH2 mutations were evaluated in a cohort of 520 adults with AML homogeneously treated in the French Acute Leukemia French Association (ALFA) -9801 and -9802 trials.

In patients with CN-AML, IDH1m were associated with NPM1m (P = .008), but exclusive of CEBPAm (P = .03).

In CN-AML patients, IDH1m were found in 19% of favorable genotype ([NPM1m or CEBPAm] without fms-related tyrosine kinase 3 [FLT3] internal tandem duplication [ITD]) and were associated with a higher risk of relapse (RR) and a shorter overall survival (OS).

Favorable genotype in CN-AML could thus be defined by the association of NPM1m or CEBPAm with neither FLT3-ITD nor IDH1m.

In IDH2m CN-AML patients, we observed a higher risk of induction failure, a higher RR and a shorter OS.

CONCLUSION: Contrarily to what is reported in gliomas, IDH1m and IDH2m in AML are associated with a poor prognosis.

Screening of IDH1m could help to identify high-risk patients within the subset of CN-AML with a favorable genotype.

[MeSH-major] Isocitrate Dehydrogenase / genetics. Leukemia, Myeloid, Acute / genetics

[MeSH-minor] Adolescent. Adult. Aged. Humans. Middle Aged. Mutation. Prevalence. Prognosis. Protein Isoforms / genetics. Randomized Controlled Trials as Topic. Retrospective Studies. Young Adult

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(PMID = 20625116.001).

[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

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00880243/ NCT00931138

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Protein Isoforms; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Cost of hospital-based management of acute myeloid leukemia: from analytical to procedure-based tarification].

The confrontation of the macro- and micro-economic approaches of hospital costs is a recurrent question, in particular for pathologies where length of stay is highly variable, like acute myeloid leukemias (AML).

This monocentric and retrospective study compares direct hospital medical costs of induction and relapse treatment sequences for AML, valued according to four different approaches: the analytic accounting system of our hospital, the French Diagnosis Related Group (DRG) cost databases of hospital discharges (readjusted, or not, to actual hospital stay duration), and official tariffs from the new French DRG prospective payment system.

The average cost of hospital AML care valued by the analytic accounting system of our hospital is 61,248 euros for the induction phase and 91,702 euros for the relapse phase.

[MeSH-major] Hospital Costs. Leukemia, Myeloid / economics. Prospective Payment System / economics

[MeSH-minor] Acute Disease. Adolescent. Adult. Diagnosis-Related Groups / economics. Female. France. Humans. Length of Stay / economics. Male. Middle Aged. Recurrence. Remission Induction. Retrospective Studies

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(PMID = 16935786.001).

[ISSN] 1769-6917

[Journal-full-title] Bulletin du cancer

[ISO-abbreviation] Bull Cancer

[Language] fre

[Publication-type] English Abstract; Journal Article

[Publication-country] France

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute myelomonocytic leukemia with abnormal eosinophils: a case report with multi-modality diagnostic work-up.

Acute myeloid leukemia (AML) with recurrent genetic abnormalities often carries a favorable prognosis.

AML with inv(16)(p13q22) occurs predominantly in younger patients and usually shows granulocytic and monocytic differentiation with abnormal eosinophils.

It is referred to as acute myelomonocytic leukemia with abnormal eosinophils (AMML Eo).

[MeSH-major] Eosinophils / pathology. Leukemia, Myelomonocytic, Acute / diagnosis

[MeSH-minor] Adult. Bone Marrow Examination. Flow Cytometry. Humans. Immunohistochemistry. Male

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(PMID = 17214400.001).

[ISSN] 2072-0939

[Journal-full-title] Chang Gung medical journal

[ISO-abbreviation] Chang Gung Med J

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] China (Republic : 1949- )

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

OBJECTIVE: Epithelioid angiomyolipomas (AML) of the kidney are malignant tumors with aggressive clinical behavior.

The diagnosis of epithelioid AML was established by positive staining for melanoma and smooth muscle cell markers, and presence of perivascular epithelioid cells.

Two patients developed recurrent, metastatic disease following nephrectomy.

Epithelioid AML, may be locally aggressive and metastasized.

[MeSH-minor] Adult. Aged. Carcinoma, Renal Cell / diagnosis. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Kidney / pathology. Male. Middle Aged. Nephrectomy. Tomography, X-Ray Computed

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(PMID = 18727277.001).

[ISSN] 0003-469X

[Journal-full-title] Annali italiani di chirurgia

[ISO-abbreviation] Ann Ital Chir

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] Italy

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with acute myelogenous leukemia.

The t(6;9)(p23;q34)-DEK/CAN fusion occurs with an incidence of 1-5% in adult patients with acute myelogenous leukemia (AML) and tends to have an unfavorable prognosis at diagnosis.

Unfortunately, no commercial or previously published fluorescence in situ hybridization (FISH) strategies exist for this recurrent anomaly.

The development of this sensitive D-FISH strategy for the detection of the t(6;9)(p23;q34) adds to the AML FISH testing repertoire, and is effective in the detection of low-level disease in post-treatment samples in these patients.

[MeSH-major] Chromosomes, Human, Pair 6. Chromosomes, Human, Pair 9. In Situ Hybridization, Fluorescence / methods. Leukemia, Myeloid, Acute / genetics. Oncogene Proteins / genetics. Recombinant Fusion Proteins / genetics. Translocation, Genetic

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(PMID = 15510206.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / DEK-CAN fusion protein, recombinant; 0 / Oncogene Proteins; 0 / Oncogene Proteins, Fusion; 0 / Recombinant Fusion Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Gene expression profile of refractory acute myeloid leukemia (M2a)].

BACKGROUND & OBJECTIVE: Recurrence is the major cause of treatment failure of acute myeloid leukemia (AML).

Drug resistance, the main cause of refractoriness of AML, is related to abnormal genes expression.

This study was to detect differential expression of genes in naive and recurrent/refractory AML, and explore potential mechanisms of recurrent/refractory AML.

METHODS: Differential gene expressions of bone marrow mononuclear cells between naive and recurrent/refractory diseases in 5 self-paired patients with AML-M(2a) were detected by DNA microarray.

RESULTS: In 925 tested genes, 14 were differentially expressed between naive and recurrent/refractory diseases in the 5 self-paired patients.

Of the 14 genes, 12 (involved in signal transduction, DNA replication, regulation of transcription, RNA processing, and regulation of cell cycle) were obviously up-regulated in recurrent diseases, and up-regulation of RRM1 (involved in DNA replication) was the most obvious.

CONCLUSIONS: Development of recurrent/refractory AML-M(2a) is concerned with various genes.

Up-regulation of these genes suggests that proliferation of recurrent/refractory AML-M(2a) blasts may be higher than that of naive AML-M(2a) blasts.

[MeSH-major] Gene Expression Profiling. Immunophenotyping. Leukemia, Myeloid / genetics

[MeSH-minor] Acute Disease. Adult. Antigens, CD / metabolism. Cell Proliferation. Female. Humans. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Recurrence. Tumor Suppressor Proteins / metabolism. Up-Regulation

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(PMID = 15946477.001).

[Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer

[ISO-abbreviation] Ai Zheng

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD; 0 / RRM1 protein, human; 0 / Tumor Suppressor Proteins

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Novel regions of acquired uniparental disomy discovered in acute myeloid leukemia.

The acquisition of uniparental disomy (aUPD) in acute myeloid leukemia (AML) results in homozygosity for known gene mutations.

We therefore aimed to develop a map of the regions of aUPD in AML.

Here, we have analyzed a large set of diagnostic AML samples (n = 454) from young adults (age: 15-55 years) using genotype arrays.

Novel recurrent regions of aUPD were uncovered at 2p, 17p, 2q, 17q, 1p, and Xq.

This study demonstrates aUPD is a frequent and significant finding in AML and pinpoints regions that may contain novel mutational targets.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Uniparental Disomy / genetics

[MeSH-minor] Adult. Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 13 / genetics. DNA Mutational Analysis. Humans. Middle Aged. Models, Genetic. Mutation

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[Copyright] 2008 Wiley-Liss, Inc.

(PMID = 18506749.001).

[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; United Kingdom / Cancer Research UK / /

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States