[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 98 of about 98
76. Yamamoto K, Yakushijin K, Kawamori Y, Minagawa K, Katayama Y, Matsui T: Translocation (7;9)(q22;q34) in therapy-related myelodysplastic syndrome after allogeneic bone marrow transplantation for acute myeloblastic leukemia. Cancer Genet Cytogenet; 2007 Jul 1;176(1):61-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Translocation (7;9)(q22;q34) in therapy-related myelodysplastic syndrome after allogeneic bone marrow transplantation for acute myeloblastic leukemia.
  • Reciprocal translocations involving the long arm of chromosome 7 are relatively rare cytogenetic aberrations in myelodysplastic syndrome (MDS) and acute myeloblastic leukemia (AML).
  • A 44-year-old woman was initially given a diagnosis of de novo AML M6A with a normal karyotype.
  • Considering two other such reported cases of AML, the t(7;9)(q22;q34) may be a novel recurrent translocation in myeloid malignancies.
  • [MeSH-major] Bone Marrow Transplantation / adverse effects. Chromosomes, Human, Pair 7. Chromosomes, Human, Pair 9. Leukemia, Myeloid, Acute / therapy. Myelodysplastic Syndromes / genetics. Translocation, Genetic
  • [MeSH-minor] Adult. Female. Humans. Spectral Karyotyping


77. Lu SH, Hou YY, Tan YS, Xu JF, Zeng HY, Sujie AK, Wang XD, Bai CX: Clinical and histopathological alterations of lymphangioleiomyomatosis in 14 Chinese patients. Chin Med J (Engl); 2009 Aug 20;122(16):1895-900
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The clinical course of LAM is characterized by progressive dyspnea on exertion, recurrent pneumothorax, and chylous fluid collections.
  • Extrapulmonary findings such as renal angiomyolipoma (AML), enlarged abdominal lymph nodes, liver AML and retroperitoneal lymphangioleiomyoma were seen in 21.4%, 14.3%, 7.14% and 7.14% in 14 cases respectively, which is remarkably lower than in the previously reported.
  • CONCLUSIONS: Women with unexplained recurrent pneumothorax, tuberous sclerosis, or a diagnosis of primary spontaneous pneumothorax or emphysema in the setting of limited or absent tobacco use should undergo high-resolution computed tomography (HRCT) scan screening for LAM.
  • [MeSH-minor] Adolescent. Adult. Aged. Contraceptives, Oral, Synthetic. Female. Humans. Immunohistochemistry. Medroxyprogesterone / therapeutic use. Middle Aged. Ovariectomy. Progesterone / therapeutic use. Progestins / therapeutic use. Young Adult

  • Genetic Alliance. consumer health - Lymphangioleiomyomatosis.
  • Hazardous Substances Data Bank. MEDROXYPROGESTERONE .
  • Hazardous Substances Data Bank. PROGESTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19781367.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Synthetic; 0 / Progestins; 4G7DS2Q64Y / Progesterone; HSU1C9YRES / Medroxyprogesterone
  •  go-up   go-down


78. de Lima M, Giralt S, Thall PF, de Padua Silva L, Jones RB, Komanduri K, Braun TM, Nguyen HQ, Champlin R, Garcia-Manero G: 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. Cancer; 2010 Dec 01;116(23):5420-31
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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


79. Graziano A, Santangelo M, Umana DS: Clinical evaluation of epithelioid angiomyolipoma. Ann Ital Chir; 2008 Mar-Apr;79(2):135-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Kidney Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


80. Arnaud B, Douet-Guilbert N, Morel F, Le Bris MJ, Herry A, Banzakour S, Bourquard P, Morice P, Le Calvez G, Marion V, Abgrall JF, Berthou C, De Braekeleer M: Screening by fluorescence in situ hybridization for MLL status at diagnosis in 239 unselected patients with acute myeloblastic leukemia. Cancer Genet Cytogenet; 2005 Sep;161(2):110-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Screening by fluorescence in situ hybridization for MLL status at diagnosis in 239 unselected patients with acute myeloblastic leukemia.
  • A large number of abnormalities involving the MLL gene have been associated with hematological malignancies, including acute myeloblastic leukemias (AML).
  • Given the overall unfavorable prognosis of AML with an MLL abnormality, its reliable and accurate detection is needed for informed treatment decision.
  • We therefore investigated the occurrence of MLL abnormalities in 239 unselected consecutive AML patients, using conventional cytogenetic and fluorescent in situ hybridization (FISH) analyses.
  • MLL abnormalities were more frequently found in AML-M5 and M4, mainly as rearrangements, and in AML-M2, mainly as overrepresentation.
  • All M2, M4, and M5 AML patients without known recurrent translocations, such as t(8;21) and inv(16), should be investigated by FISH with an MLL probe because it allows the detection of MLL rearrangement that would go undetected by conventional cytogenetics and because it has the ability of detecting multiple copies of the MLL gene in, for example, marker chromosomes and double minutes.
  • [MeSH-major] Chromosome Aberrations. Chromosomes, Human, Pair 11. DNA-Binding Proteins / genetics. Leukemia, Myeloid, Acute / genetics. Proto-Oncogenes / genetics. Transcription Factors / genetics
  • [MeSH-minor] Adult. Aged. Female. Histone-Lysine N-Methyltransferase. Humans. In Situ Hybridization, Fluorescence. Infant, Newborn. Male. Middle Aged. Myeloid-Lymphoid Leukemia Protein

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16102580.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / MLL protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase
  •  go-up   go-down


81. Yang L, Zhang Y, Zhang MR, Xiao ZJ: [Relationship between GSTT1, GSTM1 and NQO1 gene polymorphism and acute myeloid leukemia and recurrent chromosome translocations]. Zhonghua Yi Xue Za Zhi; 2005 Aug 31;85(33):2312-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


82. Balgobind BV, Van Vlierberghe P, van den Ouweland AM, Beverloo HB, Terlouw-Kromosoeto JN, van Wering ER, Reinhardt D, Horstmann M, Kaspers GJ, Pieters R, Zwaan CM, Van den Heuvel-Eibrink MM, Meijerink JP: Leukemia-associated NF1 inactivation in patients with pediatric T-ALL and AML lacking evidence for neurofibromatosis. Blood; 2008 Apr 15;111(8):4322-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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


83. Marcucci G, Maharry K, Wu YZ, Radmacher MD, Mrózek K, Margeson D, Holland KB, Whitman SP, Becker H, Schwind S, Metzeler KH, Powell BL, Carter TH, Kolitz JE, Wetzler M, Carroll AJ, Baer MR, Caligiuri MA, Larson RA, Bloomfield CD: IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study. J Clin Oncol; 2010 May 10;28(14):2348-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IDH1 and IDH2 gene mutations identify novel molecular subsets within de novo cytogenetically normal acute myeloid leukemia: a Cancer and Leukemia Group B study.
  • PURPOSE To analyze the frequency and associations with prognostic markers and outcome of mutations in IDH genes encoding isocitrate dehydrogenases in adult de novo cytogenetically normal acute myeloid leukemia (CN-AML).
  • IDH2 mutations, previously unreported in AML, were detected in 69 patients (19%; 13 with R172 and 56 with R140).
  • The highest expressed gene and microRNAs in R172 IDH2-mutated patients compared with the IDH1/IDH2wt patients were APP (previously associated with complex karyotype AML) and miR-1 and miR-133 (involved in embryonal stem-cell differentiation), respectively.
  • CONCLUSION IDH1 and IDH2 mutations are recurrent in CN-AML and have an unfavorable impact on outcome.
  • The R172 IDH2 mutations, previously unreported in AML, characterize a novel subset of CN-AML patients lacking other prognostic mutations and associate with unique gene- and microRNA-expression profiles that may lead to the discovery of novel, therapeutically targetable leukemogenic mechanisms.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] N Engl J Med. 1995 Jun 22;332(25):1671-7 [7760868.001]
  • [Cites] J Clin Oncol. 2004 Nov 1;22(21):4290-301 [15514371.001]
  • [Cites] Genomics. 1996 Oct 1;37(1):140-1 [8921382.001]
  • [Cites] Cancer Res. 1998 Jan 1;58(1):55-9 [9426057.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):482-93 [15534356.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Nat Cell Biol. 2005 Mar;7(3):255-61 [15723050.001]
  • [Cites] Blood. 2005 Dec 1;106(12):3740-6 [16051734.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9234-42 [16275934.001]
  • [Cites] Leukemia. 2006 Mar;20(3):426-32 [16424866.001]
  • [Cites] Blood. 2006 May 1;107(9):3481-5 [16455952.001]
  • [Cites] J Immunol. 2006 Jul 15;177(2):1078-84 [16818764.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1677-83 [16670265.001]
  • [Cites] Am J Hematol. 2006 Oct;81(10):779-86 [16838325.001]
  • [Cites] J Clin Oncol. 2009 Oct 20;27(30):5031-8 [19752345.001]
  • [Cites] Inflamm Res. 2009 Dec;58(12):909-19 [19603257.001]
  • [Cites] Nature. 2009 Dec 10;462(7274):739-44 [19935646.001]
  • [Cites] Blood. 2010 Jan 21;115(3):453-74 [19880497.001]
  • [Cites] J Clin Oncol. 2010 Feb 1;28(4):596-604 [20026798.001]
  • [Cites] J Inherit Metab Dis. 2008 Apr;31(2):226-9 [18392745.001]
  • [Cites] N Engl J Med. 1994 Oct 6;331(14):896-903 [8078551.001]
  • [Cites] Blood. 2006 Dec 1;108(12):3898-905 [16912223.001]
  • [Cites] Lancet. 2006 Nov 25;368(9550):1894-907 [17126723.001]
  • [Cites] Blood. 2007 Jan 15;109(2):431-48 [16960150.001]
  • [Cites] J Clin Oncol. 2007 May 10;25(14):1908-15 [17488990.001]
  • [Cites] Blood. 2007 Jun 15;109(12):5164-7 [17341662.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3337-43 [17577018.001]
  • [Cites] Blood. 2008 Feb 1;111(3):1552-9 [17940205.001]
  • [Cites] Blood. 2008 Jun 1;111(11):5371-9 [18378853.001]
  • [Cites] Int J Oncol. 2008 Aug;33(2):239-44 [18636143.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):336-45 [18692684.001]
  • [Cites] Semin Oncol. 2008 Aug;35(4):346-55 [18692685.001]
  • [Cites] Science. 2008 Sep 26;321(5897):1807-12 [18772396.001]
  • [Cites] J Clin Oncol. 2008 Oct 1;26(28):4595-602 [18559874.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4934-9 [18591543.001]
  • [Cites] J Exp Med. 2008 Oct 27;205(11):2499-506 [18936236.001]
  • [Cites] J Clin Oncol. 2008 Nov 1;26(31):5078-87 [18809607.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5429-35 [18591546.001]
  • [Cites] Hum Mutat. 2009 Jan;30(1):7-11 [19117336.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):765-73 [19228619.001]
  • [Cites] N Engl J Med. 2009 Feb 19;360(8):813-5 [19228626.001]
  • [Cites] Blood. 2009 Jun 11;113(24):6215-24 [18955566.001]
  • [Cites] J Clin Oncol. 2009 Jul 1;27(19):3198-204 [19451432.001]
  • [Cites] Circ J. 2009 Aug;73(8):1492-7 [19521018.001]
  • [Cites] Best Pract Res Clin Haematol. 2009 Jun;22(2):239-48 [19698931.001]
  • [Cites] N Engl J Med. 2009 Sep 10;361(11):1058-66 [19657110.001]
  • [Cites] Blood. 2009 Oct 1;114(14):2993-3000 [19643984.001]
  • [Cites] J Clin Oncol. 1999 Sep;17(9):2831-9 [10561359.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7233-9 [11585760.001]
  • [Cites] Hypertens Res. 2002 Jan;25(1):135-40 [11924719.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4326-35 [12036858.001]
  • [Cites] J Immunol. 2002 Jul 1;169(1):415-23 [12077272.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]
  • [Cites] Blood. 2003 Sep 1;102(5):1613-8 [12750167.001]
  • [Cites] J Clin Oncol. 2004 Feb 15;22(4):624-33 [14726504.001]
  • [Cites] Blood Rev. 2004 Jun;18(2):115-36 [15010150.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 16;101(11):3915-20 [15007164.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11755-60 [15284443.001]
  • [Cites] Blood. 2004 Oct 1;104(7):1940-51 [15217827.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1418-25 [8640834.001]
  • (PMID = 20368543.001).
  • [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 / CA33601; United States / NCI NIH HHS / CA / P50 CA140158; United States / NCI NIH HHS / CA / CA140158; United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA101140; United States / NCI NIH HHS / CA / U10 CA077658; United States / NCI NIH HHS / CA / U10 CA031946; United States / NCI NIH HHS / CA / R21 CA129657; United States / NCI NIH HHS / CA / U10 CA033601; United States / NCI NIH HHS / CA / U24 CA114725; United States / NCI NIH HHS / CA / U10 CA101140; United States / NCI NIH HHS / CA / P30 CA016058; United States / NCI NIH HHS / CA / CA77658; United States / NCI NIH HHS / CA / CA129657; United States / NCI NIH HHS / CA / CA114725; United States / NCI NIH HHS / CA / CA31946
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; EC 1.1.1.41 / Isocitrate Dehydrogenase; EC 1.1.1.41 / isocitrate dehydrogenase 2, human; EC 1.1.1.42. / IDH1 protein, human
  • [Other-IDs] NLM/ PMC2881719
  •  go-up   go-down


8
Advertisement
4. Falini B, Mecucci C, Tiacci E, Alcalay M, Rosati R, Pasqualucci L, La Starza R, Diverio D, Colombo E, Santucci A, Bigerna B, Pacini R, Pucciarini A, Liso A, Vignetti M, Fazi P, Meani N, Pettirossi V, Saglio G, Mandelli F, Lo-Coco F, Pelicci PG, Martelli MF, GIMEMA Acute Leukemia Working Party: Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype. N Engl J Med; 2005 Jan 20;352(3):254-66
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytoplasmic nucleophosmin in acute myelogenous leukemia with a normal karyotype.
  • METHODS: We used immunohistochemical methods to study the subcellular localization of NPM in bone marrow-biopsy specimens from 591 patients with primary acute myelogenous leukemia (AML).
  • RESULTS: Cytoplasmic NPM was detected in 208 (35.2 percent) of the 591 specimens from patients with primary AML but not in 135 secondary AML specimens or in 980 hematopoietic or extrahematopoietic neoplasms other than AML.
  • It was associated with a wide spectrum of morphologic subtypes of the disease, a normal karyotype, and responsiveness to induction chemotherapy, but not with recurrent genetic abnormalities.
  • There was a high frequency of FLT3 internal tandem duplications and absence of CD34 and CD133 in AML specimens with a normal karyotype and cytoplasmic dislocation of NPM, but not in those in which the protein was restricted to the nucleus.
  • AML specimens with cytoplasmic NPM carried mutations of the NPM gene that were predicted to alter the protein at its C-terminal; this mutant gene caused cytoplasmic localization of NPM in transfected cells.
  • CONCLUSIONS: Cytoplasmic NPM is a characteristic feature of a large subgroup of patients with AML who have a normal karyotype, NPM gene mutations, and responsiveness to induction chemotherapy.
  • [MeSH-major] Bone Marrow / pathology. Cytoplasm / chemistry. Leukemia, Myeloid, Acute / genetics. Mutation. Nuclear Proteins / genetics
  • [MeSH-minor] Adolescent. Adult. Antibodies, Monoclonal. Antineoplastic Agents / therapeutic use. Base Sequence. Cell Nucleolus. DNA Mutational Analysis. Humans. Karyotyping. Middle Aged. Remission Induction. Transfection. Translocation, Genetic


85. Nimer SD: Is it important to decipher the heterogeneity of "normal karyotype AML"? Best Pract Res Clin Haematol; 2008 Mar;21(1):43-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


86. Abbas S, Lugthart S, Kavelaars FG, Schelen A, Koenders JE, Zeilemaker A, van Putten WJ, Rijneveld AW, Löwenberg B, Valk PJ: Acquired mutations in the genes encoding IDH1 and IDH2 both are recurrent aberrations in acute myeloid leukemia: prevalence and prognostic value. Blood; 2010 Sep 23;116(12):2122-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


87. Druhan LJ, Ai J, Massullo P, Kindwall-Keller T, Ranalli MA, Avalos BR: Novel mechanism of G-CSF refractoriness in patients with severe congenital neutropenia. Blood; 2005 Jan 15;105(2):584-91
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Severe congenital neutropenia (SCN) is a rare disease diagnosed at or soon after birth, characterized by a myeloid maturation arrest in the bone marrow, ineffective neutrophil production, and recurrent infections.
  • In the subset of patients with SCN transforming to acute myeloid leukemia (AML), mutations that truncate the cytoplasmic tail of the G-CSF receptor (G-CSFR) have been detected.
  • Here, we report a novel mutation in the extracellular portion of the G-CSFR within the WSXWS motif in a patient with SCN without AML who was refractory to G-CSF treatment.
  • Expression of the mutant receptor in either myeloid or lymphoid cells was shown to alter subcellular trafficking of the wild-type (WT) G-CSFR by constitutively heterodimerizing with it.
  • [MeSH-minor] Adult. Cells, Cultured. Dimerization. Drug Resistance. Female. Gene Expression. Humans. Infant, Newborn. Ligands. Male. Parents. Point Mutation. Signal Transduction / drug effects. Signal Transduction / immunology

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15353486.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16058; United States / NCI NIH HHS / CA / CA75226; United States / NCI NIH HHS / CA / CA82859
  • [Publication-type] Case Reports; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Granulocyte Colony-Stimulating Factor; 143011-72-7 / Granulocyte Colony-Stimulating Factor
  •  go-up   go-down


88. Chou WC, Hou HA, Chen CY, Tang JL, Yao M, Tsay W, Ko BS, Wu SJ, Huang SY, Hsu SC, Chen YC, Huang YN, Chang YC, Lee FY, Liu MC, Liu CW, Tseng MH, Huang CF, Tien HF: Distinct clinical and biologic characteristics in adult acute myeloid leukemia bearing the isocitrate dehydrogenase 1 mutation. Blood; 2010 Apr 8;115(14):2749-54
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


89. Camera A, Rinaldi CR, Palmieri S, Cantore N, Mele G, Mettivier V, Miraglia E, Mastrullo L, Grimaldi F, Luciano L, Guerriero A, Rotoli B, Ferrara F: Sequential continuous infusion of fludarabine and cytarabine associated with liposomal daunorubicin (DaunoXome) (FLAD) in primary refractory or relapsed adult acute myeloid leukemia patients. Ann Hematol; 2009 Feb;88(2):151-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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


90. Shearer BM, Knudson RA, Flynn HC, Ketterling RP: Development of a D-FISH method to detect DEK/CAN fusion resulting from t(6;9)(p23;q34) in patients with acute myelogenous leukemia. Leukemia; 2005 Jan;19(1):126-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


91. Yanada M, Suzuki M, Kawashima K, Kiyoi H, Kinoshita T, Emi N, Saito H, Naoe T: Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience. Eur J Haematol; 2005 May;74(5):418-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcomes for unselected patients with acute myeloid leukemia categorized according to the World Health Organization classification: a single-center experience.
  • The actual utility of a new classification system of acute myeloid leukemia (AML) recently introduced by the World Health Organization (WHO) has not been thoroughly investigated yet.
  • In this study, we evaluated long-term outcomes of unselected AML patients categorized according to the new WHO classification.
  • Between 1990 and 2002, 109 adult AML cases were referred to our hospital.
  • AML with recurrent genetic abnormalities accounted for 26%, AML with multilineage dysplasia for 29%, therapy-related AML for 13%, and AML not otherwise categorized for 32% of classifiable cases.
  • These results indicate that outcomes for AML patients appear to be distinguished on the basis of the WHO classification, but the prognostic significance of multilineage dysplasia and prior therapy is lost after adjusting for cytogenetic risk and age.
  • [MeSH-major] Leukemia, Myeloid / classification. Leukemia, Myeloid / therapy
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Humans. Middle Aged. Palliative Care. Retrospective Studies. Survival Analysis. Survivors. Treatment Outcome. World Health Organization

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15813916.001).
  • [ISSN] 0902-4441
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Denmark
  •  go-up   go-down


92. Sperr WR, Mitterbauer M, Mitterbauer G, Kundi M, Jäger U, Lechner K, Valent P: Quantitation of minimal residual disease in acute myeloid leukemia by tryptase monitoring identifies a group of patients with a high risk of relapse. Clin Cancer Res; 2005 Sep 15;11(18):6536-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


93. Inaba H, Stewart CF, Crews KR, Yang S, Pounds S, Pui CH, Rubnitz JE, Razzouk BI, Ribeiro RC: Combination of cladribine plus topotecan for recurrent or refractory pediatric acute myeloid leukemia. Cancer; 2010 Jan 1;116(1):98-105
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Topotecan .
  • Hazardous Substances Data Bank. CLADRIBINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


94. Pereira FG, Metze K, Costa FP, Lima CS, Lorand-Metze I: Phenotypic quantitative features of patients with acute myeloid leukemia. Neoplasma; 2006;53(2):155-60
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phenotypic quantitative features of patients with acute myeloid leukemia.
  • The recent WHO classification for acute myeloid leukemias (AML) separates entities by recurrent cytogenetic abnormalities and immunophenotypic features presenting prognostic impact.
  • We have examined the expression of several lineage and maturation linked antigens used in routine immunophenotyping of patients with de novo AML, using a 3-color two-step panel.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunophenotyping / methods. Leukemia, Myeloid / diagnosis. Leukemia, Myeloid / metabolism
  • [MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal. Antigens, CD / metabolism. Female. Flow Cytometry. Humans. Male. Middle Aged. Neoplasm, Residual. Phenotype. Prognosis. Survival Analysis

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16575472.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD; 0 / Biomarkers, Tumor
  •  go-up   go-down


95. Hijiya N, Ness KK, Ribeiro RC, Hudson MM: Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues. Cancer; 2009 Jan 1;115(1):23-35
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute leukemia as a secondary malignancy in children and adolescents: current findings and issues.
  • Secondary acute leukemia is a devastating complication in children and adolescents who have been treated for cancer.
  • Secondary acute lymphoblastic leukemia (s-ALL) was rarely reported previously but can be distinguished today from recurrent primary ALL by comparison of immunoglobulin and T-cell receptor rearrangement.
  • Secondary acute myeloid leukemia (s-AML) is much more common, and some cases actually may be second primary cancers.
  • Treatment-related and host-related characteristics and their interactions have been identified as risk factors for s-AML.
  • A high cumulative dose of alkylating agents is well known to predispose to s-AML.
  • The prevalence of alkylator-associated s-AML has diminished among pediatric oncology patients with the reduction of cumulative alkylator dose and limited use of the more leukemogenic alkylators.
  • The best-documented topoisomerase II inhibitor-associated s-AML is s-AML associated with epipodophyllotoxins.
  • The risk of s-AML in these cases is influenced by the schedule of drug administration and by interaction with other antineoplastic agents but is not consistently found to be related to cumulative dose.
  • The unpredictable risk of s-AML after epipodophyllotoxin therapy may discourage the use of these agents, even in patients at a high risk of disease recurrence, although the benefit of recurrence prevention may outweigh the risk of s-AML.
  • Studies in survivors of adult cancers suggest that, contrary to previous beliefs, the outcome of s-AML is not necessarily worse than that of de novo AML when adjusted for cytogenetic features.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PODOFILOX .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2008 American Cancer Society.
  • [Cites] Lancet. 1996 Feb 3;347(8997):295-7 [8569364.001]
  • [Cites] N Engl J Med. 1996 Mar 21;334(12):745-51 [8592547.001]
  • [Cites] J Natl Cancer Inst. 1996 Dec 18;88(24):1840-7 [8961974.001]
  • [Cites] Cancer. 1997 Mar 1;79(5):1049-54 [9041170.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2247-53 [9196137.001]
  • [Cites] Leukemia. 1998 Mar;12(3):346-52 [9529129.001]
  • [Cites] Blood. 1999 Jun 1;93(11):3617-23 [10339466.001]
  • [Cites] Blood. 1999 Jul 15;94(2):803-7 [10397748.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3221-5 [10506622.001]
  • [Cites] Bone Marrow Transplant. 1999 Oct;24(7):735-9 [10516676.001]
  • [Cites] J Clin Oncol. 2004 Dec 15;22(24):4926-33 [15611507.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):926-7 [15681547.001]
  • [Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]
  • [Cites] Leukemia. 2006 Feb;20(2):239-46 [16341039.001]
  • [Cites] Oncogene. 2006 Sep 25;25(43):5875-84 [16998502.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Nov;15(11):2020-6 [17057028.001]
  • [Cites] Blood. 2007 Jan 1;109(1):46-51 [16985182.001]
  • [Cites] Bone Marrow Transplant. 2007 Jan;39(2):59-70 [17143301.001]
  • [Cites] J Clin Oncol. 2007 Jan 20;25(3):292-300 [17159192.001]
  • [Cites] J Natl Cancer Inst. 2007 Feb 7;99(3):196-205 [17284714.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):493-500 [17290056.001]
  • [Cites] Best Pract Res Clin Haematol. 2007 Mar;20(1):29-37 [17336252.001]
  • [Cites] JAMA. 2007 Mar 21;297(11):1207-15 [17374815.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1431-5 [17460701.001]
  • [Cites] Ophthalmology. 2007 Jul;114(7):1378-83 [17613328.001]
  • [Cites] Blood. 2007 Aug 15;110(4):1379-87 [17488876.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3871-6 [17664457.001]
  • [Cites] J Pediatr Hematol Oncol. 2007 Sep;29(9):646-8 [17805043.001]
  • [Cites] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):233-55 [9748598.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):13176-81 [9789061.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3880-9 [9850034.001]
  • [Cites] Bone Marrow Transplant. 1999 Jan;23(1):21-5 [10037046.001]
  • [Cites] J Clin Oncol. 1999 Feb;17(2):569-77 [10080601.001]
  • [Cites] Pediatr Hematol Oncol. 1999 May-Jun;16(3):267-70 [10326227.001]
  • [Cites] Leukemia. 2007 Oct;21(10):2128-36 [17673902.001]
  • [Cites] Haematologica. 2007 Oct;92(10):1389-98 [17768113.001]
  • [Cites] Hematology Am Soc Hematol Educ Program. 2007;:453-9 [18024664.001]
  • [Cites] J Clin Oncol. 2008 Mar 1;26(7):1106-11 [18309945.001]
  • [Cites] Blood. 2008 May 1;111(9):4477-89 [18285545.001]
  • [Cites] Med Pediatr Oncol. 1989;17(6):477-84 [2586362.001]
  • [Cites] Leukemia. 1999 Mar;13(3):335-42 [10086723.001]
  • [Cites] Leukemia. 2000 Feb;14(2):232-7 [10673738.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1588-93 [10688812.001]
  • [Cites] J Clin Oncol. 2000 Mar;18(5):947-55 [10694543.001]
  • [Cites] Br J Haematol. 2000 Apr;109(1):13-23 [10848777.001]
  • [Cites] Br J Cancer. 2000 Jul;83(1):91-4 [10883674.001]
  • [Cites] J Clin Oncol. 2000 Aug;18(15):2836-42 [10920131.001]
  • [Cites] Ann Oncol. 2000 Oct;11(10):1289-94 [11106118.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2196-204 [11187911.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2205-22 [11187912.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2223-33 [11187913.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2234-9 [11187914.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2240-6 [11187915.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2257-66 [11187917.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2267-75 [11187918.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2276-85 [11187919.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2295-306 [11187921.001]
  • [Cites] Leukemia. 2000 Dec;14(12):2307-20 [11187922.001]
  • [Cites] Br J Haematol. 2001 Jan;112(1):109-17 [11225603.001]
  • [Cites] Med Pediatr Oncol. 2001 May;36(5):525-35 [11340607.001]
  • [Cites] Med Pediatr Oncol. 2001 May;36(5):536-40 [11340608.001]
  • [Cites] Leukemia. 2001 Jun;15(6):963-70 [11417484.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11592-7 [11553769.001]
  • [Cites] Lancet Oncol. 2001 Jul;2(7):429-36 [11905737.001]
  • [Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]
  • [Cites] Blood. 2002 Jul 15;100(2):427-34 [12091332.001]
  • [Cites] Blood. 2002 Sep 15;100(6):1972-6 [12200354.001]
  • [Cites] Pharmacogenetics. 2002 Nov;12(8):605-11 [12439220.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1074-81 [12637473.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1195-204 [12663705.001]
  • [Cites] Blood. 2003 May 15;101(10):3862-7 [12531808.001]
  • [Cites] J Clin Oncol. 2003 Jun 1;21(11):2123-37 [12775738.001]
  • [Cites] Leukemia. 2004 Jan;18(1):120-5 [14586477.001]
  • [Cites] Clin Cancer Res. 2004 Apr 15;10(8):2675-80 [15102670.001]
  • [Cites] Int J Hematol. 2004 Apr;79(3):229-34 [15168589.001]
  • [Cites] J Clin Oncol. 2004 Jun 15;22(12):2510-1 [15197216.001]
  • [Cites] Blood. 2004 Aug 1;104(3):822-8 [15090454.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1581-6 [15356657.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]
  • [Cites] J Clin Oncol. 1985 Apr;3(4):532-8 [2984346.001]
  • [Cites] Blood. 1987 Nov;70(5):1412-7 [2822173.001]
  • [Cites] Cancer. 1988 Oct 1;62(7):1364-70 [3046737.001]
  • [Cites] N Engl J Med. 1989 Jul 20;321(3):136-42 [2787477.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):432-7 [1999712.001]
  • [Cites] N Engl J Med. 1991 Dec 12;325(24):1682-7 [1944468.001]
  • [Cites] J Clin Oncol. 1992 Jan;10(1):156-63 [1309379.001]
  • [Cites] J Clin Oncol. 1993 Feb;11(2):209-17 [8426196.001]
  • [Cites] J Clin Oncol. 1993 Jun;11(6):1039-45 [8388919.001]
  • [Cites] Leukemia. 1993 Dec;7(12):1975-86 [8255096.001]
  • [Cites] Leukemia. 1995 Oct;9(10):1680-4 [7564509.001]
  • [Cites] Leukemia. 1996 Jan;10(1):27-31 [8558933.001]
  • (PMID = 19072983.001).
  • [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 / P30 CA021765-31
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] L36H50F353 / Podophyllotoxin
  • [Number-of-references] 99
  • [Other-IDs] NLM/ NIHMS135594; NLM/ PMC2767267
  •  go-up   go-down


96. La Starza R, Matteucci C, Gorello P, Brandimarte L, Pierini V, Crescenzi B, Nofrini V, Rosati R, Gottardi E, Saglio G, Santucci A, Berchicci L, Arcioni F, Falini B, Martelli MF, Sambani C, Aventin A, Mecucci C: NPM1 deletion is associated with gross chromosomal rearrangements in leukemia. PLoS One; 2010;5(9):e12855
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NPM1 deletion is associated with gross chromosomal rearrangements in leukemia.
  • BACKGROUND: NPM1 gene at chromosome 5q35 is involved in recurrent translocations in leukemia and lymphoma.
  • It also undergoes mutations in 60% of adult acute myeloid leukemia (AML) cases with normal karyotype.
  • The incidence and significance of NPM1 deletion in human leukemia have not been elucidated.
  • METHODOLOGY AND PRINCIPAL FINDINGS: Bone marrow samples from 145 patients with myelodysplastic syndromes (MDS) and AML were included in this study.
  • NPM1 deletion was an uncommon event in the "5q- syndrome" but occurred in over 40% of cases with high risk MDS/AML with complex karyotypes and 5q loss.
  • CONCLUSIONS AND SIGNIFICANCE: NPM1/5q35 deletion is a consistent event in MDS/AML with a 5q-/-5 in complex karyotypes.
  • NPM1 deletion and NPM1 exon 12 mutations appear to be mutually exclusive and are associated with two distinct cytogenetic subsets of MDS and AML.
  • [MeSH-major] Gene Deletion. Leukemia, Myeloid / genetics. Nuclear Proteins / genetics. Translocation, Genetic
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Base Sequence. Child. Chromosome Deletion. Chromosomes, Human, Pair 5 / genetics. Chromosomes, Human, Pair 5 / metabolism. Female. Humans. Male. Middle Aged. Molecular Sequence Data. Young Adult

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Leukemia. 2006 Feb;20(2):319-21 [16341035.001]
  • [Cites] Mol Cell Biol. 2005 Oct;25(20):8874-86 [16199867.001]
  • [Cites] Cancer Genet Cytogenet. 2006 May;167(1):66-9 [16682289.001]
  • [Cites] Nat Rev Cancer. 2006 Jul;6(7):493-505 [16794633.001]
  • [Cites] Leukemia. 2006 Nov;20(11):1943-9 [16990778.001]
  • [Cites] J Mol Histol. 2006 Sep;37(5-7):239-51 [16855788.001]
  • [Cites] Cancer Genet Cytogenet. 2007 Jul 1;176(1):1-21 [17574959.001]
  • [Cites] Haematologica. 2008 Jul;93(7):976-82 [18591623.001]
  • [Cites] Leukemia. 2009 Jan;23(1):203-6 [18596741.001]
  • [Cites] PLoS One. 2009;4(2):e4583 [19240791.001]
  • [Cites] Leukemia. 2009 Jul;23(7):1252-6 [19322210.001]
  • [Cites] Oncogene. 2009 Oct 1;28(39):3429-41 [19597464.001]
  • [Cites] Nat Med. 2010 Jan;16(1):49-58 [19898489.001]
  • [Cites] Nat Med. 2010 Jan;16(1):59-66 [19966810.001]
  • [Cites] Leukemia. 1999 Dec;13(12):1901-28 [10602411.001]
  • [Cites] Blood. 2002 Jun 15;99(12):4638-41 [12036901.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2474-86 [14562124.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2318-57 [14562125.001]
  • [Cites] Haematologica. 2004 Mar;89(3):281-5 [15020265.001]
  • [Cites] Cell Cycle. 2004 Aug;3(8):976-9 [15254398.001]
  • [Cites] Nature. 1974 Oct 4;251(5474):437-8 [4421285.001]
  • [Cites] N Engl J Med. 2005 Jan 20;352(3):254-66 [15659725.001]
  • [Cites] Biochim Biophys Acta. 2005 Jul 25;1755(2):71-89 [15921859.001]
  • [Cites] Nature. 2005 Sep 1;437(7055):147-53 [16007073.001]
  • [Cites] Blood. 2006 May 15;107(10):4011-20 [16455956.001]
  • (PMID = 20877721.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 117896-08-9 / nucleophosmin
  • [Other-IDs] NLM/ PMC2943467
  •  go-up   go-down


97. Gong H, Liu WL, Zhou JF, Xu HZ: [Expression of mitosis checkpoint gene CHFR in acute leukemia]. Zhonghua Yi Xue Za Zhi; 2005 Apr 27;85(16):1085-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression of mitosis checkpoint gene CHFR in acute leukemia].
  • OBJECTIVE: To investigate the expression of mitosis checkpoint gene CHFR in adult patients with acute leukemia (AL) and its clinical significance.
  • METHODS: Four ml of bone marrow was extracted from 65 AL patients, 38 males and 27 females, with the median age of 35, 43 with acute myelocytic leukemia (AML) and 22 with acute lymphocytic leukemia (ALL), 45 de novo patients and 20 recurrent patients, and 8 normal donor of allogeneic bone marrow transplantation as controls.
  • (1) The levels of CHFR protein and mRNA were correlated with the cumulative percentages of cells in S phases. (2) The expression level of CHFR protein in 40.6% (13/32) of the AL patients and that of the CHFR mRNA in 60.0% (27/45) of the AL patients were both significantly lower than those of the normal controls. (3) The mean expression level of CHFR protein in the recurrent acute lymphoblastic leukemia (ALL) was 0.71, significantly higher than that of the de novo group (0.38, t = 2.54, P = 0.017). (4) The complete remission (CR) rates in the AL patients with high expression levels of CHFR protein and mRNA were 30.2% and 42.4% respectively, significantly lower than those in the AL patients with low expression levels (88.6% and 85.4% respectively, both P < 0.05).
  • CONCLUSION: By affecting mitotic checkpoint function, CHFR inactivation plays a key role in tumorigenesis in adult patients with acute leukemia.
  • Moreover, the aberrant expression of CHFR appears to be a good molecular marker to predict the sensitivity of acute leukemia to chemotherapy.
  • [MeSH-major] Cell Cycle Proteins / biosynthesis. Leukemia, Myeloid, Acute / genetics. Neoplasm Proteins / biosynthesis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Agents / pharmacology. Cell Cycle. Child. Drug Resistance. Female. HL-60 Cells. Humans. Male. Middle Aged. Mitosis. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16029562.001).
  • [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] 0 / Antineoplastic Agents; 0 / CHFR protein, human; 0 / Cell Cycle Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
  •  go-up   go-down


98. Ahmad F, Dalvi R, Das BR, Mandava S: Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population. Cancer Detect Prev; 2008;32(2):168-77
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Specific chromosomal aberrations in de novo acute myeloid leukemia: a comparative analysis of results with a report of three novel chromosomal rearrangements t(7;14)(q35;q13), t(8;18)(p11.2;q12), t(13;15) in Indian population.
  • BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous disease with regard to morphology, immunophenotype, and genetic rearrangements.
  • Multiple recurrent chromosomal aberrations have been identified by conventional cytogenetic analysis, which is now widely recognized as one of the most important diagnostic and prognostic determinants in AML.
  • METHOD: Conventional cytogenetic analysis was done on 200 de novo AML subjects.
  • Similarly, the frequency of other recurrent FAB associated abnormalities viz.
  • Furthermore, ongoing cytogenetic studies are warranted in larger groups of AML cases to identify newly acquired chromosomal aberrations that may aid in cloning novel genes involved in the neoplastic process, ultimately helping in the development of targeted therapeutic drugs.
  • [MeSH-major] Chromosome Aberrations. Leukemia, Myeloid, Acute / genetics
  • [MeSH-minor] Adolescent. Adult. Age Distribution. Aged. Aged, 80 and over. Child. Child, Preschool. Cytogenetic Analysis. Female. Humans. India. Infant. Karyotyping. Male. Middle Aged

  • Genetic Alliance. consumer health - Leukemia, Myeloid.
  • MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18639991.001).
  • [ISSN] 1525-1500
  • [Journal-full-title] Cancer detection and prevention
  • [ISO-abbreviation] Cancer Detect. Prev.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down






Advertisement