BioMedLib Search Engine [ goto HOMEPAGE ]

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

[Title] Expression of IAP-family proteins in adult acute mixed lineage leukemia (AMLL).

To determine the apoptosis-resistant mechanism in adult acute mixed lineage leukemia (AMLL) with biphenotypic blasts responsible for resistance against chemotherapy, the expression levels of IAP-family proteins in AMLL bone marrow cells were analyzed by quantitative RT-PCR.

These findings suggest that higher expression of various IAPs is associated with the chemotherapy-resistant nature of this specific type of leukemia.

[MeSH-major] Apoptosis. Biomarkers, Tumor / metabolism. Bone Marrow Cells / metabolism. Leukemia, Biphenotypic, Acute / metabolism. Proteins / metabolism

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Female. Flow Cytometry. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Leukemia, Monocytic, Acute / drug therapy. Leukemia, Monocytic, Acute / metabolism. Leukemia, Monocytic, Acute / pathology. Male. Microtubule-Associated Proteins / analysis. Microtubule-Associated Proteins / metabolism. Middle Aged. Neoplasm Proteins. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / metabolism. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15726601.001).

[ISSN] 0361-8609

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proteins; 0 / RNA, Messenger

   

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

BACKGROUND: Fusion of the MOZ and TIF2 genes by an inv (8) (p11q13) translocation has been identified in patients with acute mixed-lineage leukemia.

Stable expression of MOZ-TIF2 inhibited retinoic acid (RA) inducible endogenous CD11b and C/EBPbeta gene response.

[MeSH-minor] Acute Disease. Blotting, Western. Carrier Proteins / genetics. Carrier Proteins / metabolism. Corticosterone. Genes, Reporter. Humans. Leukemia, Myeloid / genetics. Receptors, Androgen / genetics. Receptors, Estrogen / genetics

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Genes Dev. 2000 May 15;14(10):1209-28 [10817756.001]

[Cites] Genes Chromosomes Cancer. 2000 Jun;28(2):138-44 [10824998.001]

[Cites] Genes Chromosomes Cancer. 2000 Aug;28(4):415-24 [10862050.001]

[Cites] Genes Dev. 2000 Jul 1;14(13):1553-77 [10887150.001]

[Cites] J Cell Biol. 2000 Jul 10;150(1):265-73 [10893273.001]

[Cites] J Mol Biol. 2000 Oct 20;303(2):243-53 [11023789.001]

[Cites] Cancer Cell. 2004 Dec;6(6):587-96 [15607963.001]

[Cites] Mol Cell Biol. 2005 Feb;25(3):988-1002 [15657427.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Mar 8;102(10):3611-6 [15731352.001]

[Cites] Genes Dev. 2006 May 1;20(9):1175-86 [16651658.001]

[Cites] Genes Dev. 2006 May 15;20(10):1321-30 [16702405.001]

[Cites] J Biol Chem. 2006 Jun 23;281(25):17124-33 [16613851.001]

[Cites] Mol Endocrinol. 1997 Feb;11(2):148-61 [9013762.001]

[Cites] Nature. 1997 Jun 12;387(6634):733-6 [9192902.001]

[Cites] Cell. 1997 Jun 27;89(7):1175-84 [9215639.001]

[Cites] Recent Prog Horm Res. 1997;52:103-19; discussion 119-20 [9238849.001]

[Cites] EMBO J. 1998 Jan 15;17(2):507-19 [9430642.001]

[Cites] Mol Endocrinol. 1998 Feb;12(2):302-13 [9482670.001]

[Cites] Blood. 1998 May 1;91(9):3127-33 [9558366.001]

[Cites] Recept Signal Transduct. 1997;7(4):241-56 [9633825.001]

[Cites] Mol Endocrinol. 1998 Aug;12(8):1172-83 [9717843.001]

[Cites] Blood. 1998 Sep 15;92(6):2118-22 [9731070.001]

[Cites] Mol Endocrinol. 1998 Oct;12(10):1605-18 [9773983.001]

[Cites] Genes Dev. 1998 Nov 1;12(21):3357-68 [9808623.001]

[Cites] J Virol. 1999 May;73(5):3574-81 [10196247.001]

[Cites] Science. 1999 Jun 25;284(5423):2174-7 [10381882.001]

[Cites] Mol Cell Biol. 1999 Sep;19(9):6085-97 [10454556.001]

[Cites] Mol Cell Biol. 1999 Sep;19(9):6164-73 [10454563.001]

[Cites] Cancer Genet Cytogenet. 1999 Aug;113(1):70-2 [10459350.001]

[Cites] J Biol Chem. 1999 Sep 3;274(36):25756-68 [10464314.001]

[Cites] Mol Cell Biol. 1999 Dec;19(12):8383-92 [10567563.001]

[Cites] Gene. 2000 Mar 7;245(1):1-11 [10713439.001]

[Cites] Mol Cell Biol. 2001 Jan;21(1):39-50 [11113179.001]

[Cites] J Biol Chem. 2000 Dec 29;275(52):40810-6 [11010967.001]

[Cites] Hum Mol Genet. 2001 Feb 15;10(4):395-404 [11157802.001]

[Cites] J Biol Chem. 2001 Mar 2;276(9):6695-702 [11078741.001]

[Cites] Leukemia. 2001 Jan;15(1):89-94 [11243405.001]

[Cites] EMBO Rep. 2000 Aug;1(2):151-7 [11265755.001]

[Cites] J Biol Chem. 2001 Apr 27;276(17):13505-8 [11279224.001]

[Cites] J Biol Chem. 2001 May 25;276(21):18375-83 [11279135.001]

[Cites] J Biol Chem. 2001 Mar 9;276(10):7493-9 [11102454.001]

[Cites] Oncogene. 2001 May 28;20(24):3047-54 [11420720.001]

[Cites] J Biol Chem. 2001 Oct 5;276(40):36865-8 [11459854.001]

[Cites] EMBO J. 2001 Nov 1;20(21):6084-94 [11689448.001]

[Cites] EMBO J. 2001 Dec 17;20(24):7184-96 [11742995.001]

[Cites] Cell Growth Differ. 2002 Feb;13(2):69-75 [11864910.001]

[Cites] J Biol Chem. 2002 Mar 22;277(12):10226-35 [11779876.001]

[Cites] Cell. 2002 Feb 22;108(4):465-74 [11909518.001]

[Cites] Mol Cell Biol. 2002 Aug;22(16):5923-37 [12138202.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14789-94 [12397173.001]

[Cites] J Biol Chem. 2002 Nov 29;277(48):46066-72 [12351636.001]

[Cites] Cell. 2002 Dec 27;111(7):931-41 [12507421.001]

[Cites] Br J Haematol. 2003 Jan;120(2):271-3 [12542485.001]

[Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):402-5 [12619164.001]

[Cites] Genes Chromosomes Cancer. 2003 Apr;36(4):413-9 [12619166.001]

[Cites] Cancer Cell. 2003 Mar;3(3):259-71 [12676584.001]

[Cites] Nucleic Acids Res. 2003 Jun 1;31(11):2735-44 [12771199.001]

[Cites] Mol Endocrinol. 2003 Sep;17(9):1681-92 [12805412.001]

[Cites] Nucleic Acids Res. 2004;32(3):959-76 [14960713.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4453-8 [15070739.001]

[Cites] Development. 2004 May;131(10):2443-61 [15128673.001]

[Cites] Oncogene. 2004 May 24;23(24):4225-31 [15156177.001]

[Cites] Genes Dev. 2004 Jul 15;18(14):1753-65 [15256502.001]

[Cites] Proc Natl Acad Sci U S A. 1996 May 14;93(10):4948-52 [8643509.001]

[Cites] Nature. 1996 Jul 25;382(6589):319-24 [8684459.001]

[Cites] EMBO J. 1996 Jul 15;15(14):3667-75 [8670870.001]

[Cites] Nat Genet. 1996 Sep;14(1):33-41 [8782817.001]

[Cites] Cell. 1996 Nov 29;87(5):953-9 [8945521.001]

[Cites] Nature. 1996 Dec 19-26;384(6610):641-3 [8967953.001]

[Cites] J Biol Chem. 1999 Oct 1;274(40):28528-36 [10497217.001]

(PMID = 17697320.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] eng

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

[Publication-country] England

[Chemical-registry-number] 0 / Carrier Proteins; 0 / NCOA2 protein, human; 0 / Nuclear Receptor Coactivator 2; 0 / Oncogene Proteins, Fusion; 0 / Receptors, Androgen; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Estrogen; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / KAT6A protein, human; W980KJ009P / Corticosterone

[Other-IDs] NLM/ PMC2048977

   

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

[Title] Dic (17;20) (p11;q11) preceded MLL gene amplification in a patient with de novo mixed-lineage leukemia.

We report a case of acute mixed-lineage leukemia, as seen in a 65 year-old female with MLL gene amplification and biallelic loss of wild type p53 gene.

The diagnosis was based on the findings that her bone marrow (BM) blasts expressed cytoplasmic CD3 (cyCD3), B-lineage antigens and myeloid antigens accompanied by clonal rearrangements of IgH gene.

Add (11q23) abnormality was found in sideline karyotypes as well as the stemline abnormality of dic(17;20) (p11;q11).

[MeSH-major] Gene Amplification. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20505276.001).

[ISSN] 1880-9952

[Journal-full-title] Journal of clinical and experimental hematopathology : JCEH

[ISO-abbreviation] J Clin Exp Hematop

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Japan

   

Advertisement

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

[Title] Acute mixed lineage leukemia in children: the experience of St Jude Children's Research Hospital.

To characterize the biology and optimal therapy of acute mixed-lineage leukemia in children, we reviewed the pathologic and clinical features, including response to therapy, of 35 patients with mixed-lineage leukemia.

The majority of cases (91%) had blasts cells that simultaneously expressed either T-lineage plus myeloid markers (T/myeloid, n = 20) or B-lineage plus myeloid markers (B/myeloid, n = 12).

Overall survival rates for the B/myeloid and T/myeloid subgroups were not significantly different from each other or from the rate for acute myeloid leukemia (AML) but were inferior to the outcome in children with acute lymphoblastic leukemia (ALL).

Analysis of gene-expression patterns identified a subset of biphenotypic leukemias that did not cluster with T-cell ALL, B-progenitor ALL, or AML.

We propose that treatment for biphenotypic leukemia begin with one course of AML-type induction therapy, with a provision for a switch to lymphoid-type induction therapy with a glucocorticoid, vincristine, and L-asparaginase if the patient responds poorly.

We also suggest that hematopoietic stem cell transplantation is often not required for cure of these patients.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Immunol Methods. 2000 Sep 21;243(1-2):59-75 [10986407.001]

[Cites] Leukemia. 2000 Dec;14(12):2286-94 [11187920.001]

[Cites] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295.001]

[Cites] Cancer Cell. 2002 Mar;1(2):133-43 [12086872.001]

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

[Cites] J Clin Oncol. 2003 Aug 15;21(16):3084-91 [12915598.001]

[Cites] Br J Haematol. 2003 Dec;123(5):842-9 [14632775.001]

[Cites] Cancer. 2003 Dec 15;98(12):2715-22 [14669294.001]

[Cites] Br J Haematol. 2004 Jun;125(6):814-5 [15180872.001]

[Cites] Br J Cancer. 1977 Jan;35(1):1-39 [831755.001]

[Cites] Blood. 1985 Nov;66(5):1115-23 [3931724.001]

[Cites] Blood. 1990 Jan 1;75(1):198-202 [2294988.001]

[Cites] Leukemia. 1990 Feb;4(2):121-6 [2137547.001]

[Cites] N Engl J Med. 1991 Mar 21;324(12):800-8 [1997852.001]

[Cites] Blood. 1991 Sep 1;78(5):1327-37 [1878594.001]

[Cites] J Clin Oncol. 1992 Sep;10(9):1419-29 [1517785.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] Blood. 1995 Oct 15;86(8):3097-108 [7579404.001]

[Cites] Leukemia. 1996 Aug;10(8):1283-7 [8709632.001]

[Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]

[Cites] Blood. 1997 Jul 1;90(1):28-35 [9207434.001]

[Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]

[Cites] Leukemia. 1998 Dec;12(12):2038 [9844938.001]

[Cites] J Clin Oncol. 1998 Dec;16(12):3768-73 [9850020.001]

[Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]

[Cites] Blood. 2004 Dec 1;104(12):3679-87 [15226186.001]

[Cites] Leukemia. 2005 Dec;19(12):2125-9 [16281077.001]

[Cites] N Engl J Med. 2006 Jan 12;354(2):166-78 [16407512.001]

[Cites] Bioinformatics. 2006 Aug 15;22(16):1979-87 [16777905.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

[Cites] Blood. 2007 Aug 15;110(4):1271-7 [17456722.001]

[Cites] Leukemia. 2007 Nov;21(11):2264-70 [17611554.001]

[CommentIn] Blood. 2009 May 21;113(21):5036 [19470432.001]

(PMID = 19131545.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA021765; United States / NCI NIH HHS / CA / P30 CA-21765

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

[Publication-country] United States

[Other-IDs] NLM/ PMC2686179

   

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

[Title] Comparison between CD19 and CD20 expression patterns on acute leukemic cells.

In order to provide the evidences for CD19 as a better antibody targeting molecule for B lineage acute leukemias than CD20 through the multi-parameter flow-cytometry analysis of leukemia cells, the samples from 321 patients with acute leukemia (AL) were immunophenotyped by multi-color flow cytometry and CD45/SSC gating strategy followed by the analysis of CD19 and CD20 expression.

The results showed that the positive rate of CD19 (115/116, 99.1%) in 116 cases with B lineage acute lymphoblastic leukemia (B lineage ALL) was significantly higher than that of CD20 (33/116, 28.4%) (P < 0.01); in 17 patients with B lineage/Myeloid (B/My) acute mixed lineage leukemia (AMLL), the former positive rate (17/17, 100%) was also higher than the latter (5/17, 29.4%) (P < 0.01).

Both of the two antigens were negative in 29 patients with acute T lymphoblastic leukemia and 7 patients with T/My AMLL.

The positive rates of CD19 and CD20 in 152 patients with acute myeloid leukemia (AML) were 7.2% and 2.0%, respectively.

The difference of the fluorescence intensity between the two antigens on the cells from each patient with B lineage ALL or B/My AMLL was statistically significant (t = 20.68, P < 0.001).

The specificity of CD19 and CD20 in B lymphocytic lineage was 92.3% (132/143) and 92.7% (38/41), respectively, while the sensitivity was 99.2% (132/133) and 28.6% (38/133), respectively, the former sensitivity was significantly higher than the latter (chi(2) = 144.018, P = 0.001).

It is concluded that CD19 continuously and steadily express on almost all subtypes of B lineage leukemic cells with homogeneous pattern while only a small number of leukemias express CD20.

These indicate that CD19 may be a better antibody targeting molecule than CD20 for patients with B-lineage acute leukemia.

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16403255.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] ENG

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

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD19; 0 / Antigens, CD20

   

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

[Title] Acute mixed lineage leukemia and a t(6;14)(q25;q32) in two adults.

Acute mixed lineage leukemia (AMLL) is a rare form of leukemia in which both myeloid and lymphoid markers are present.

Few chromosome abnormalities have been identified associated with this form of leukemia.

A translocation involving the long arms of chromosomes 6 and 14 was previously described in four young individuals with acute leukemia and in three of these cases the diagnosis was mixed lineage.

[MeSH-major] Chromosomes, Human, Pair 14. Chromosomes, Human, Pair 6. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18656690.001).

[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] [Major molecular response to imatinib in a patient with acute mixed lineage leukemia expressing a novel BCR/ABL transcript].

OBJECTIVE: To identify the novel BCR/ABL transcript in a patient with acute mixed lineage leukemia (AMLL), and to evaluate the imatinib treatment response by quantitatively monitoring the aberrant BCR/ABL.

Morphological analysis of the bone marrow showed the myeloid blast cells accounted for 66%, and immunophenotyping analysis showed 2 groups of aberrant blast cells: myeloid and B lineage.

Chemical therapy and bone marrow transplantation failed to control the disease, and a novel BCR/ABL transcript (GenBank: EF423615) was found by using several detection protocols.

[MeSH-major] Fusion Proteins, bcr-abl / genetics. Leukemia, Biphenotypic, Acute / drug therapy. Leukemia, Biphenotypic, Acute / genetics. Piperazines / therapeutic use. Pyrimidines / therapeutic use

Hazardous Substances Data Bank. IMATINIB MESYLATE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19552835.001).

[ISSN] 0376-2491

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

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

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

[Publication-country] China

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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

[Title] Detection of FLT3 gene and FLT3/ITD mutation by polymerase chain reaction-single-strand conformation polymorphism in patients with acute lymphoblastic leukemia.

OBJECTIVE: To analyze Fms-like tyrosine kinase 3 (FLT3) gene and FLT3 internal tandem duplication (ITD) mutation in acute lymphoblastic leukemia (ALL) patients of different immunological subtypes.

The positivity rate of FLT3 gene in pre-pre B-lineage ALL, pre-B-ALL, B-lineage ALL and T-lineage ALL cases were 93.3% (14/15), 77.8% (14/18), 41.7% (5/12) and 28.6% (4/14), respectively.

Two cases (3.2%) were found to have FLT3/ITD mutation, which were also positive for myeloid antigen expression and diagnosed as acute mixed-lineage leukemia, showing leukocytosis and high percentage of bone marrow blast cells with poor prognosis.

CONCLUSIONS: FLT3 gene can be detected in both B-and T-lineage ALL patients, but more frequently in the former.

In B-lineage ALL patients, FLT3 gene is more frequent in cases with undifferentiated than those with differentiated blast cells.

FLT3/ITD is rarely detected in ALL patients and FLT3/ITD mutation detection might be helpful to identify the genotypes and evaluate the prognosis of acute leukemia.

[MeSH-major] Mutation. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Receptor Protein-Tyrosine Kinases / genetics. Tandem Repeat Sequences / genetics. fms-Like Tyrosine Kinase 3 / genetics

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16234090.001).

[ISSN] 1000-2588

[Journal-full-title] Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA

[ISO-abbreviation] Di Yi Jun Yi Da Xue Xue Bao

[Language] eng

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

[Publication-country] China

[Chemical-registry-number] EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; 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] Therapy-related, mixed phenotype acute leukemia with t(1;21)(p36;q22) and RUNX1 rearrangement.

We describe here a new case of therapy-related acute leukemia with t(1;21)(p36;q22).

Immunophenotypic analyses revealed that blasts were positive for CD19, CD79a, and cytCD22, as well as MPO, CD13, and CD33, fulfilling the diagnostic criteria of mixed phenotype acute leukemia, B/myeloid.

The patient died of disease progression after 10 months.

Thus, acute leukemia with t(1;21) and RUNX1 rearrangement could be associated with B/myeloid mixed phenotype as well as previous topoisomerase II inhibitor therapy and poor prognoses.

[MeSH-major] Chromosomes, Human, Pair 1. Chromosomes, Human, Pair 21. Core Binding Factor Alpha 2 Subunit / genetics. Gene Rearrangement. Leukemia, Myeloid, Acute / genetics. Neoplasms, Second Primary / genetics

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

[Copyright] 2010 Elsevier Inc. All rights reserved.

(PMID = 20682397.001).

[ISSN] 1873-4456

[Journal-full-title] Cancer genetics and cytogenetics

[ISO-abbreviation] Cancer Genet. Cytogenet.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Core Binding Factor Alpha 2 Subunit; 0 / RUNX1 protein, human

   

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

[Title] [Successful treatment with clarithromycin for Mixed phenotype acute leukemia, T/myeloid, NOS].

The diagnosis was Mixed phenotype acute leukemia, T/myeloid, NOS.

This clinical course suggests CAM is effective for this leukemia.

[MeSH-major] Anti-Bacterial Agents / administration & dosage. Clarithromycin / administration & dosage. Leukemia / drug therapy. Leukemia, Myeloid, Acute / drug therapy. Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy

[MeSH-minor] Acute Disease. Aged. Drug Synergism. Drug Therapy, Combination. Female. Humans. Pneumonia, Bacterial / complications. Pneumonia, Bacterial / drug therapy. Prednisolone / administration & dosage

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Acute Myeloid Leukemia.

MedlinePlus Health Information. consumer health - Antibiotics.

MedlinePlus Health Information. consumer health - Leukemia.

Hazardous Substances Data Bank. PREDNISOLONE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20467229.001).

[ISSN] 0485-1439

[Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology

[ISO-abbreviation] Rinsho Ketsueki

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Anti-Bacterial Agents; 9PHQ9Y1OLM / Prednisolone; H1250JIK0A / Clarithromycin

   

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

[Title] Results of a phase I study of clofarabine (CLO) plus cyclophosphamide (CY) in adult patients (pts) with relapsed and/or refractory acute lymphoblastic leukemia (ALL).

METHODS: Pts ≥ 21 years (yrs) with primary refractory or relapsed ALL, NYHA class < 3, and a cardiac ejection fraction ≥ 45% were eligible.

Twenty-one pts had pre-B ALL, 5 pts pre-T/T ALL, 1 pt mature B ALL, and 3 pts biphenotypic acute leukemias.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 27961382.001).

[ISSN] 1527-7755

[Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology

[ISO-abbreviation] J. Clin. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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

[Title] [Clinical characteristics and immunophenotypes of mixed-lineage acute leukemia].

The aim of study was to analyze the clinical, biological features, treatment outcome and prognosis of mixed-lineage acute leukemia (MAL).

48 MAL patients diagnosed according to European Group of International Leukemia (EGIL) scoring system were retrospectively analyzed and the analysis results were compared with that from 68 cases of AML and 61 cases of ALL.

The results showed that the incidence of MAL in acute leukemia was 9.6%.

The median of white blood cell count in MAL was significantly higher than that of non-mixed-lineage cases (AML and ALL) observed during the same period (P < 0.05).

Coexpression of myeloid and B lymphoid antigens in MAL patients was predominant, its rate was 70.9%.

The coexpression rate of T lymphoid and myeloid antigens was 20.8%, coexpression of B, T lymphoid and myeloid antigens was 8.3%.

In MAL Ph chromosome abnormality incidence was 25% and was significantly higher than that in AML group (0%) (P < 0.01), but was not statistical defference with that in ALL group (16.7%) (P > 0.05).

It is concluded that MAL is supposed to be originated from stem cells, coexpression of lymphoid/myeloid antigens is the major feature of MAL which accompanies many poor prognosis factors and lower CR rate.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17605883.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD34

   

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

[Title] [Successful selection of chemotherapy based on cell surface antigens in a patient with mixed phenotype acute leukemia].

The patient was diagnosed as having mixed phenotype acute leukemia, T/myeloid, NOS, according to the WHO classification.

After initial treatment, residual leukemic cells with CD13, CD33 and MPO were detected by FCM; therefore, he received re-induction chemotherapy for AML, and achieved CR.

Acute leukemia of ambiguous lineage is a relatively rare subtype in acute leukemia and standard chemotherapy has not been established.

[MeSH-major] Antigens, Surface. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia / drug therapy. Leukemia / immunology

[MeSH-minor] Acute Disease. Cyclophosphamide. Cytarabine / administration & dosage. Daunorubicin / administration & dosage. Humans. Male. Middle Aged. Prednisolone / administration & dosage. Treatment Outcome. Vincristine / administration & dosage

MedlinePlus Health Information. consumer health - Leukemia.

Hazardous Substances Data Bank. CYTARABINE .

Hazardous Substances Data Bank. DAUNORUBICIN .

Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

Hazardous Substances Data Bank. PREDNISOLONE .

Hazardous Substances Data Bank. VINCRISTINE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20534955.001).

[ISSN] 0485-1439

[Journal-full-title] [Rinshō ketsueki] The Japanese journal of clinical hematology

[ISO-abbreviation] Rinsho Ketsueki

[Language] jpn

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / Antigens, Surface; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; ZS7284E0ZP / Daunorubicin

   

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

[Title] Mixed phenotype acute leukemia with t(11;19)(q23;p13.3)/ MLL-MLLT1(ENL), B/T-lymphoid type: A first case report.

The majority of cases of acute leukemia belong to a specific lineage origin, either lymphoid or myeloid, and therefore are classified as acute lymphoblastic leukemia (ALL) or acute myelogenous leukemia (AML), based on morphologic features and cytochemical and immunophenotypic profile of the blast cells.

A minority of acute leukemias however, show no clear evidence of differentiation along a single lineage.

These are now classified under acute leukemias of ambiguous lineage by the most recent WHO classification and account for <4% of all cases of acute leukemia [1].

They include leukemias with no lineage specific antigens (acute undifferentiated leukemias) and those with blasts that express antigens of more than one lineage to such degree that it is not possible to assign the leukemia to any one particular lineage with certainty (mixed phenotype acute leukemias).

The latter can either be leukemias with two distinct populations of blasts, each expressing antigens of a different lineage (historically referred to as "bilineal" leukemias) or a single blast population expressing antigens of multiple lineages (historically referred to as "biphenotypic" acute leukemias) [2].

Acute leukemias of ambiguous lineage may harbor a variety of genetic lesions.

Those with t(9;22)(q34;q11) or translocations associated with mixed lineage leukemias (MLL) gene, i.e., t(11;V)(q23;V), occur frequently enough and are associated with distinct features, that are considered as separate entities according to the recent WHO classification.

Co-expression of myeloid and B-lymphoid antigens is most common in mixed phenotype acute leukemia (MPAL), followed by co-expression of myeloid and T-lymphoid antigens, accounting for 66-70% and 23-24% of MLLs, respectively.

Coexpression of B- and T-lineage associated antigens or antigens of all three lineages is exceedingly rare, accounting for <5% of MLLs [3,4].

The requirements for assigning more than one lineage to a single blast population has been established by current WHO classification [1].

[MeSH-major] Antigens, Neoplasm / blood. Chromosomes, Human, Pair 11 / ultrastructure. Chromosomes, Human, Pair 19 / ultrastructure. Immunophenotyping. Leukemia / classification. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

[MeSH-minor] Acute Disease. Adult. Antigens, CD / analysis. Bone Marrow / pathology. Cell Lineage. Gene Rearrangement. Humans. In Situ Hybridization, Fluorescence. Male. Neoplasm Proteins / genetics. Nuclear Proteins / genetics. Transcription Factors / genetics

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20513125.001).

[ISSN] 1096-8652

[Journal-full-title] American journal of hematology

[ISO-abbreviation] Am. J. Hematol.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / MLL-ENL oncoprotein, human; 0 / MLLT1 protein, human; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

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

[Title] Prognosis of children with mixed phenotype acute leukemia treated on the basis of consistent immunophenotypic criteria.

BACKGROUND: Mixed phenotype acute leukemia (MPAL) represents a diagnostic and therapeutic dilemma.

The European Group for the Immunological Classification of Leukemias (EGIL) scoring system unambiguously defines MPAL expressing aberrant lineage markers.

DESIGN AND METHODS: Simple immunophenotypic criteria were used to classify all cases of childhood acute leukemia in order to provide therapy directed against acute lymphoblastic leukemia or acute myeloid leukemia.

Prognosis, genotype and immunoglobulin/T-cell receptor gene rearrangement status were analyzed.

RESULTS: The incidences of MPAL were 28/582 and 4/107 for children treated with acute lymphoblastic leukemia and acute myeloid leukemia regimens, respectively.

In immunophenotypic principal component analysis, MPAL treated as T-cell acute lymphoblastic leukemia clustered between cases of non-mixed T-cell acute lymphoblastic leukemia and acute myeloid leukemia, while other MPAL cases were included in the respective non-mixed B-cell progenitor acute lymphoblastic leukemia or acute myeloid leukemia clusters.

Analogously, immunoglobulin/T-cell receptor gene rearrangements followed the expected pattern in patients treated as having acute myeloid leukemia (non-rearranged, 4/4) or as having B-cell progenitor acute lymphoblastic leukemia (rearranged, 20/20), but were missing in 3/5 analyzed cases of MPAL treated as having T-cell acute lymphobastic leukemia.

In patients who received acute lymphoblastic leukemia treatment, the 5-year event-free survival of the MPAL cases was worse than that of the non-mixed cases (53+/-10% and 76+/-2% at 5 years, respectively, P=0.0075), with a more pronounced difference among B lineage cases.

The small numbers of MPAL cases treated as T-cell acute lymphoblastic leukemia or as acute myeloid leukemia hampered separate statistics.

CONCLUSIONS: Simple immunophenotypic criteria are useful for therapy decisions in MPAL.

In B lineage leukemia, MPAL confers poorer prognosis.

However, our data do not justify a preferential use of current acute myeloid leukemia-based therapy in MPAL.

[MeSH-major] Immunophenotyping. Leukemia / diagnosis. Leukemia / therapy. Phenotype

[MeSH-minor] Adolescent. Child. Child, Preschool. Diagnosis, Differential. Follow-Up Studies. Humans. Infant. Infant, Newborn. Leukemia, Myeloid, Acute / diagnosis. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / therapy. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Prognosis. Receptors, Antigen, T-Cell / immunology

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Leukemia. 2005 Jun;19(6):1092-4 [15830012.001]

[Cites] J Immunol. 2005 Aug 15;175(4):2495-500 [16081821.001]

[Cites] Blood. 2005 Dec 15;106(13):4414-5 [16326981.001]

[Cites] Leukemia. 2006 Mar;20(3):410-6 [16424874.001]

[Cites] Leukemia. 2006 Apr;20(4):620-6 [16437134.001]

[Cites] Blood. 2006 Jun 1;107(11):4508-13 [16493009.001]

[Cites] Curr Opin Pediatr. 2007 Feb;19(1):1-8 [17224655.001]

[Cites] Leukemia. 2007 Nov;21(11):2264-70 [17611554.001]

[Cites] Clin Cancer Res. 2008 Feb 15;14(4):977-83 [18281529.001]

[Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]

[Cites] Haematologica. 2009 Jul;94(7):919-27 [19454497.001]

[Cites] Am J Clin Pathol. 2009 Aug;132(2):182-5; quiz 306 [19605811.001]

[Cites] Pediatr Blood Cancer. 2010 Jan;54(1):62-70 [19760767.001]

[Cites] J Immunol Methods. 2000 Sep 21;243(1-2):59-75 [10986407.001]

[Cites] Br J Haematol. 2001 Jun;113(3):757-62 [11380467.001]

[Cites] Leukemia. 2002 Mar;16(3):368-75 [11896540.001]

[Cites] Leukemia. 2002 Jul;16(7):1233-58 [12094248.001]

[Cites] Med Pediatr Oncol. 2003 Jul;41(1):95-6 [12764763.001]

[Cites] Nat Immunol. 2003 Jun;4(6):533-9 [12717433.001]

[Cites] J Immunol. 2003 Jul 15;171(2):524-7 [12847212.001]

[Cites] Leukemia. 2003 Nov;17(11):2149-56 [14576730.001]

[Cites] Blood. 2004 Jul 15;104(2):558-60 [15044257.001]

[Cites] Cancer Genet Cytogenet. 2004 Aug;153(1):88-9 [15325104.001]

[Cites] Haematologica. 1991 May-Jun;76(3):215-25 [1743592.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] Am J Hematol. 1996 Feb;51(2):147-51 [8579056.001]

[Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]

[Cites] Br J Haematol. 1997 Oct;99(1):101-6 [9359509.001]

[Cites] Blood. 1998 Jul 15;92(2):596-9 [9657760.001]

[Cites] Leukemia. 1999 Feb;13(2):196-205 [10025893.001]

[Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]

[Cites] Leuk Res. 2005 Jun;29(6):633-9 [15863202.001]

[Cites] BMC Cancer. 2005;5:38 [15826304.001]

(PMID = 20145275.001).

[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 / Receptors, Antigen, T-Cell

[Other-IDs] NLM/ PMC2878790

   

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

[Title] [A study of mixed phenotype acute leukemia based on the 2008 World Health Organization classification].

BACKGROUND: We evaluated the clinical significance of revised 2008 WHO classification needed to diagnose mixed phenotype acute leukemia (MPAL).

METHODS: A total of 22 MPAL patients, previously diagnosed by applying the scoring system of the European Group for Immunological Classification of Acute Leukemias (EGIL) were reclassified based on the 2008 WHO classification.

RESULTS: In 2008 WHO classification, the number of monoclonal antibodies (mAbs) required for assigning more than one lineage was markedly decreased, from 26 to 11, compared with that of EGIL.

Seventeen of the 22 MPAL patients were reclassified as MPAL with following details: 6 MPAL with t(9;22)(q34;q11.2); BCR-ABL1, 1 MPAL with t(v;11q23); MLL rearranged, 7 MPAL, B/Myeloid, not otherwise specified (NOS) and 3 MPAL, T/Myeloid, NOS.

Five patients were excluded from MPAL in the revised classification: 4 cytoplasmic myeloperoxidase (cMPO)-negative and 1 CD19-negative.

One patient with cCD79a, CD20, CD38, cMPO and CD15, whose diagnosis was reclassified from MPAL to AML has survived during the study period.

CONCLUSIONS: Because of decreased number of mAbs needed, it is possible that acute leukemia panel is designed to include all mAbs required to diagnose MPAL according to 2008 WHO classification.

When diagnosing MPAL, it is critical to figure out positivity in either cMPO or CD19, and AML expressing more than 2 lymphoid antigens are considered as MPAL.

[MeSH-major] Leukemia / diagnosis

[MeSH-minor] Acute Disease. Adolescent. Adult. Aged. Antibodies, Monoclonal / immunology. Child. Chromosomes, Human. Female. Fusion Proteins, bcr-abl / metabolism. Humans. Infant. Male. Middle Aged. Phenotype. Philadelphia Chromosome. Survival Analysis. World Health Organization

MedlinePlus Health Information. consumer health - Childhood Leukemia.

MedlinePlus Health Information. consumer health - Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21157134.001).

[ISSN] 1598-6535

[Journal-full-title] The Korean journal of laboratory medicine

[ISO-abbreviation] Korean J Lab Med

[Language] kor

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.7.10.2 / Fusion Proteins, bcr-abl

   

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

[Title] Mixed-phenotype acute leukemia relapse in the iris.

Mixed-phenotype acute leukemia is a rare condition with no previously reported intraocular involvement.

We present clinical, radiologic, and cytologic findings of leukemic intraocular relapse in a 23-month-old girl, with lineage switch presenting as conjunctivitis after allogeneic bone marrow transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright © 2010 American Association for Pediatric Ophthalmology and Strabismus. Published by Mosby, Inc. All rights reserved.

(PMID = 20863726.001).

[ISSN] 1528-3933

[Journal-full-title] Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus

[ISO-abbreviation] J AAPOS

[Language] ENG

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

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

[Title] Mixed-phenotype acute leukemia: historical overview and a new definition.

Acute leukemia with a mixed phenotype is a rare disease and comprises 2-5% of all acute leukemias.

These disorders have been known historically by a variety of names, such as mixed lineage leukemia, bilineal leukemia and biphenotypic leukemia, and the criteria for diagnosis have often been arbitrary.

The scoring criteria proposed by the European Group for the Immunological Characterization of Leukemias represented a major attempt to define this disorder.

However, the relative weight given to some markers and the lack of lineage specificity of most markers have raised questions regarding the significance of this approach.

In 2008, the World Health Organization classification of hematopoietic and lymphoid tumors proposed a simpler diagnostic algorithm, which relies on fewer and more lineage-specific markers to define mixed-phenotype acute leukemia (MPAL).

MPAL with t(9;22) and MLL rearrangement have been separated.

Several studies have suggested that patients with acute leukemia of mixed phenotype have a worse clinical outcome when compared with matched controls with acute myeloid leukemia or acute lymphoblastic leukemia.

Further studies are needed to confirm the significance of MPAL as currently defined, to determine a standardized treatment approach and to better understand the biological and clinical aspects of this disease.

[MeSH-major] Leukemia / genetics

[MeSH-minor] Acute Disease. Antigens, CD / analysis. Biomarkers, Tumor / analysis. Blast Crisis / pathology. Gene Rearrangement. Humans. Leukemia, B-Cell / classification. Leukemia, B-Cell / genetics. Leukemia, T-Cell / classification. Leukemia, T-Cell / genetics. Phenotype

MedlinePlus Health Information. consumer health - Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20844566.001).

[ISSN] 1476-5551

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor

   

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

[Title] Infantile mixed phenotype acute leukemia (bilineal and biphenotypic) with t(10;11)(p12;q23);MLL-MLLT10.

We report a case of a 6-month-old boy with a mixed phenotype acute leukemia (MPAL), bilineal and biphenotypic immunophenotype (B-lymphoid lineage and combined B-lymphoid and monocytic lineage) with t(10;11)(p12;q23);MLL-MLLT10.

He was treated with acute myeloid leukemia protocol and in complete remission at 7-month follow-up.

To the best of our knowledge, this is the first reported MLL-MLLT10 rearranged case presenting as MPAL in an infant.

From a clinical practice standpoint, this case illustrates the importance of detection of MLL rearrangement due to its prognostic implication and the effectiveness of flow cytometry immunophenotyping in diagnosing MPAL and monitoring minimal residual disease.

[MeSH-major] Chromosomes, Human, Pair 10 / genetics. Chromosomes, Human, Pair 11 / genetics. Leukemia, Biphenotypic, Acute / genetics. Leukemia, Monocytic, Acute / genetics. Myeloid-Lymphoid Leukemia Protein / genetics. Oncogene Proteins, Fusion / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Translocation, Genetic / genetics

[MeSH-minor] Flow Cytometry. Gene Rearrangement. Humans. Immunophenotyping. Infant. Karyotyping. Male. Neoplasm, Residual / genetics. Neoplasm, Residual / pathology. Neoplasm, Residual / therapy. Phenotype. Prognosis. Remission Induction

Genetic Alliance. consumer health - Acute Biphenotypic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2010 Elsevier Ltd. All rights reserved.

(PMID = 20299091.001).

[ISSN] 1873-5835

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / MLL-AF10 fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

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

[Title] Clinical characteristics and outcome of children with biphenotypic acute leukemia.

BACKGROUND: Knowledge concerning the clinical and biological presentation, as well as the outcome of treatment, of biphenotypic acute leukemia in children is limited.

DESIGN AND METHODS: This retrospective review analyzes the clinical features and outcome of children with biphenotypic acute leukemia diagnosed and treated over an 8-year period.

According to the EGIL scoring system 24 (3.7%) of 633 patients with acute leukemia were classified as having biphenotypic acute leukemia.

The diagnostic work-up and results were reviewed specifically for this study in the light of the newly published WHO criteria for the diagnosis of leukemia of ambiguous lineage.

Based on these criteria, 11 (1.7%) patients were categorized according to the new nomenclature as having mixed phenotype acute leukemia.

The majority of the patients (58.3%) had a B-lymphoid/myeloid phenotype, followed by the T-lymphoid/myeloid phenotype.

The most frequent chromosomal abnormality involved the 14q32 locus.

Patients received therapy based on a treatment regimen for acute lymphocytic leukemia regimen, which included myeloid-effective agents.

The survival of those patients who underwent hematopoietic stem cell transplantation in first complete remission was not different from that of the patients who were treated with chemotherapy alone (overall survival: 70.1% versus 81.1%, respectively, p=0.39; event-free survival: 70.1% versus 76.2%, respectively, p=0.75).

The outcome of the 11 patients who were retrospectively classified as having mixed phenotype acute leukemia according to the new WHO criteria was excellent, with no relapses or deaths occurring among these patients.

CONCLUSIONS: An acute lymphocytic leukemia type of induction therapy, using agents that are active against lymphoid and myeloid leukemias, appears to be more effective in achieving and maintaining complete remissions regardless of whether the patients are classified according to EGIL criteria or the new WHO criteria.

Hematopoietic stem cell transplantation may not be necessary for all patients in first complete remission.

[MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis. Leukemia, Biphenotypic, Acute / therapy

[MeSH-minor] Antigens, CD / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Child. Child, Preschool. Female. Flow Cytometry. Follow-Up Studies. Hematopoietic Stem Cell Transplantation. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Infant. Kaplan-Meier Estimate. Karyotyping. Male. Outcome Assessment (Health Care) / methods. Remission Induction. Retrospective Studies

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Clin Pathol. 2002 Mar;117(3):380-9 [11888077.001]

[Cites] Pediatr Blood Cancer. 2009 Sep;53(3):444-52 [19489056.001]

[Cites] Blood. 2004 Nov 1;104(9):2690-6 [15251979.001]

[Cites] Am J Clin Pathol. 1990 Jul;94(1):54-8 [1694392.001]

[Cites] Blood. 1990 Jul 1;76(1):150-6 [2364166.001]

[Cites] Br J Haematol. 1990 Jun;75(2):202-7 [2372506.001]

[Cites] Leukemia. 1993 Jun;7(6):919-27 [8501986.001]

[Cites] J Clin Pathol. 1993 Oct;46(10):903-7 [8227405.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] Blood. 1997 Apr 1;89(7):2488-93 [9116293.001]

[Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]

[Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]

[Cites] Blood. 1998 Aug 1;92(3):795-801 [9680347.001]

[Cites] J Clin Oncol. 1998 Dec;16(12):3768-73 [9850020.001]

[Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]

[Cites] Leukemia. 2006 Apr;20(4):620-6 [16437134.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

[Cites] J Chin Med Assoc. 2007 Jul;70(7):269-73 [17631462.001]

[Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]

[Cites] Br J Haematol. 2003 Dec;123(5):842-9 [14632775.001]

(PMID = 19713227.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article

[Publication-country] Italy

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

[Other-IDs] NLM/ PMC2791935

   

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

[Title] PAX-5: a valuable immunohistochemical marker in the differential diagnosis of lymphoid neoplasms.

OBJECTIVE: Undifferentiated tumors and hematolymphoid neoplasms can be diagnostically challenging due to potential overlap of morphologic features and variant antigen expression.

PAX-5, a transcription factor expressed throughout B-cell maturation, is detected in most B-cell neoplasms including those that lack expression of mature B-cell markers, such as classical Hodgkin lymphoma (cHL), B-lymphoblastic leukemia and B-cell lymphomas following rituximab therapy.

The lack of PAX-5 expression in most CD30-positive non-hematopoietic malignancies (embryonal carcinoma and seminoma) and T-cell lymphomas, such as anaplastic large cell lymphoma (ALCL), suggests that the absence of PAX-5 may be used to confirm non-B-cell lineage.

DESIGN: Diagnostic lymph node, decalcified core bone marrow biopsies and tissue sections from 111 archived paraffin-embedded tissue blocks and a tissue lymphoma microarray were immunostained using a monoclonal antibody to PAX-5.

RESULTS: Nuclear PAX-5 immunoreactivity was detected in 88% (36/41) of Hodgkin lymphoma, all cases of diffuse large B-cell lymphoma (n=72), small B-cell lymphomas (n=5), B-lymphoblastic leukemia/lymphoma and mixed phenotype acute leukemia with B-cell lineage (n=5).

PAX-5 was not detected in ALCL (n=22), T-cell lymphoblastic leukemia/lymphoma, mixed phenotype acute leukemia with T-cell lineage (n=5), acute myeloid leukemia (n=4), carcinoid tumors with typical morphology (n=5), melanoma (n=3), and undifferentiated/metastatic tumors (n=8).

Non-neoplastic bone marrow sections showed scattered nuclear staining in small B-cell lymphocytes/hematogones.

CONCLUSION: Overall, our results demonstrate that including PAX-5 in a panel with other immunomarkers helps establish B-cell lineage and increases diagnostic yield.

[MeSH-major] B-Cell-Specific Activator Protein / analysis. Biomarkers, Tumor / analysis. Lymphoma / diagnosis

[MeSH-minor] Diagnosis, Differential. Hodgkin Disease / diagnosis. Humans. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large-Cell, Anaplastic / diagnosis

MedlinePlus Health Information. consumer health - Lymphoma.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Br J Haematol. 2001 Sep;114(4):881-3 [11564080.001]

[Cites] Immunity. 2001 Jun;14(6):779-90 [11420047.001]

[Cites] Leuk Lymphoma. 2002 Dec;43(12):2335-41 [12613521.001]

[Cites] Cancer Res. 2003 Aug 1;63(15):4620-5 [12907641.001]

[Cites] Am J Clin Pathol. 2003 Nov;120(5):767-77 [14608905.001]

[Cites] Carcinogenesis. 2004 Oct;25(10):1839-46 [15155532.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7399-404 [15492262.001]

[Cites] Genomics. 1991 Oct;11(2):424-34 [1685142.001]

[Cites] Blood. 1992 Jul 15;80(2):470-7 [1378322.001]

[Cites] Genes Dev. 1992 Sep;6(9):1589-607 [1516825.001]

[Cites] Blood. 1998 Aug 15;92(4):1308-16 [9694719.001]

[Cites] Clin Cancer Res. 1999 Mar;5(3):611-5 [10100713.001]

[Cites] Arch Pathol Lab Med. 2005 Jan;129(1):32-8 [15628906.001]

[Cites] Am J Surg Pathol. 2005 May;29(5):687-92 [15832095.001]

[Cites] Mod Pathol. 2005 Dec;18(12):1542-9 [16056244.001]

[Cites] Mod Pathol. 2006 Jul;19(7):1010-8 [16648862.001]

[Cites] Am J Clin Pathol. 2006 Aug;126(2):235-40 [16891199.001]

[Cites] Am J Clin Pathol. 2006 Oct;126(4):534-44 [16938666.001]

[Cites] Oncol Rep. 2006 Nov;16(5):1003-8 [17016584.001]

[Cites] Am J Clin Pathol. 2006 Nov;126(5):798-804 [17050077.001]

[Cites] Leuk Lymphoma. 2007 Jun;48(6):1127-38 [17577776.001]

[Cites] Mod Pathol. 2007 Aug;20(8):871-7 [17529924.001]

[Cites] Lab Invest. 2009 Mar;89(3):301-14 [19139719.001]

[Cites] Am J Surg Pathol. 2009 May;33(5):775-80 [19145202.001]

[Cites] J Clin Pathol. 2007 Jun;60(6):709-14 [16837628.001]

[Cites] Am J Surg Pathol. 2002 Oct;26(10):1343-50 [12360049.001]

(PMID = 20660931.001).

[ISSN] 1554-6179

[Journal-full-title] Clinical medicine & research

[ISO-abbreviation] Clin Med Res

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / Biomarkers, Tumor; 0 / PAX5 protein, human

[Other-IDs] NLM/ PMC2910102

   

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

[Title] The ultrastructure of hybrid acute leukemia: a study of 15 cases.

The objective of this study was to investigate the ultrastructural characteristics of hybrid acute leukemia (HAL).

By TEM, 5 out 15 cases of HAL were consistent with immunophenotyping (3 cases of biphenotypic type, and 2 cases of biclonal type with granulocytes and lymphocytes); 2 cases were suspected as HAL.

Most of the blast cells of biphenotypic HAL showed lymphoid features, except some cases containing MPO positive granules in blasts, while a few cases exhibited monocytic or nonspecific features.

TEM offers advantages in the diagnosis of biclonal type HAL and biphenotypic HAL positive for MPO.

However, it is difficult to differentiate MPO-negative cases of biphenotypic HAL from ALL and a few cases may be misinterpreted as M5 by TEM.

[MeSH-major] Granulocyte Precursor Cells / ultrastructure. Leukemia, Myeloid, Acute / diagnosis. Lymphocytes / ultrastructure. Precursor Cell Lymphoblastic Leukemia-Lymphoma / diagnosis

[MeSH-minor] Adolescent. Adult. Child. Female. Humans. Immunophenotyping. Male. Microscopy, Electron, Transmission. Middle Aged. Peroxidase / metabolism. Phenotype

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16257860.001).

[ISSN] 0191-3123

[Journal-full-title] Ultrastructural pathology

[ISO-abbreviation] Ultrastruct Pathol

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 1.11.1.7 / Peroxidase

   

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

A 52-year-old man was diagnosed with acute leukemia of mixed phenotype.

[MeSH-minor] Adult. Chromosomes, Human, Pair 22. Chromosomes, Human, Pair 9. Humans. Interphase. Karyotyping. Leukemia / diagnosis. Leukemia / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / diagnosis. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Male. Metaphase. Middle Aged. Phenotype. Translocation, Genetic

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 21157160.001).

[ISSN] 1598-6535

[Journal-full-title] The Korean journal of laboratory medicine

[ISO-abbreviation] Korean J Lab Med

[Language] kor

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Korea (South)

   

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

[Title] Discrepant immunophenotypic characteristics between the lymph node and bone marrow in two mixed-phenotype acute leukemia patients.

The immunophenotypic profile of hematological malignancies is usually consistent among different sites of involvement; this consistency allows reliable diagnosis from peripheral blood, bone marrow, or lymph node, especially in cases of acute leukemia.

Here, we report two Korean patients with acute leukemia where the results of immunophenotypic analysis of the bone marrow specimen were different from those of immunohistochemical studies of a biopsy sample of a cervical lymph node, particularly with respect to myeloperoxidase and CD3.

The clinical significance of the immunophenotypic disparity found in the patients still remains unknown; however, discrepancies between the different anatomic sites that are simultaneously involved can occur in a subset of leukemia patients.

Therefore, integration of all the relevant results, including those of the bone marrow studies, may be helpful for accurate diagnosis and selecting appropriate treatment modalities.

[MeSH-major] Bone Marrow / pathology. Immunophenotyping / methods. Leukemia / diagnosis. Lymph Nodes / pathology

[MeSH-minor] Acute Disease. Adolescent. Adult. Antigens, CD3 / metabolism. Female. Flow Cytometry. Humans. Male. Peroxidase / metabolism. Phenotype

MedlinePlus Health Information. consumer health - Childhood Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19893347.001).

[ISSN] 1598-6535

[Journal-full-title] The Korean journal of laboratory medicine

[ISO-abbreviation] Korean J Lab Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Antigens, CD3; EC 1.11.1.7 / Peroxidase

   

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

The aim of this study was to assess the results of surgical treatment of multiple primary adenocarcinomas of the lung (MPAL) analyzing the radiological and histological features.

METHODS: From 1988 to 2005, 26 patients underwent surgical treatment for MPAL at our department, for a total of 52 tumors.

RESULTS: Thirty-seven tumors were classified as solid, two as ground-glass opacities (GGO) and 13 as mixed solid/GGO tumors on the basis of CT scan evaluation.

CONCLUSIONS: Surgical treatment of MPAL is associated with favorable results.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19169994.001).

[ISSN] 0171-6425

[Journal-full-title] The Thoracic and cardiovascular surgeon

[ISO-abbreviation] Thorac Cardiovasc Surg

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

   

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

METHODS: One hundred thirty-four patients with congenital heart disease were randomly allocated to one of 3 groups according to the cardioplegia formula used: the high-potassium (HP) group (K(+), 20 mmol/L), 46 patients; the high-potassium adenosine-lidocaine (HPAL) group (K(+), 20 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients; and the moderate-potassium adenosine-lidocaine (MPAL) group (K(+), 10 mmol/L; adenosine, 0.7 mmol/L; and lidocaine, 0.7 mmol/L), 44 patients.

RESULTS: At the end of cardiopulmonary bypass and modified ultrafiltration, the systolic and pulse pressures of the MPAL group were significantly increased compared with the respective values of the HP group.

At the time points of 1 to 12 hours after reperfusion, the levels of serum cardiac troponin I were significantly decreased in the MPAL group compared with those in the HP and HPAL groups.

CONCLUSIONS: The MPAL cardioplegia formula was associated with better myocardial protective effects.

MedlinePlus Health Information. consumer health - Congenital Heart Defects.

Hazardous Substances Data Bank. LIDOCAINE .

Hazardous Substances Data Bank. Adenosine .

Hazardous Substances Data Bank. POTASSIUM, ELEMENTAL .

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

(PMID = 19114188.001).

[ISSN] 1097-685X

[Journal-full-title] The Journal of thoracic and cardiovascular surgery

[ISO-abbreviation] J. Thorac. Cardiovasc. Surg.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Cardioplegic Solutions; 0 / Cardiotonic Agents; 98PI200987 / Lidocaine; K72T3FS567 / Adenosine; RWP5GA015D / Potassium

   

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

[Title] [Report of a case of hybrid acute leukemia with t (12; 22) and literature review].

OBJECTIVE: To report a hybrid acute leukemia (HAL) patient with t (12;.

Leukemia surface markers were detected by anti-biotin-biotin complex and monoclonal antibodies.

RESULTS: The clinical and hematological findings were compatible with the diagnosis of HAL.

Lymphoid and myeloid markers were positive on the leukemia cells.

22) translocation is a rare chromosome abnormality in leukemia.

This translocation as a cytogenetic marker for poor-prognosis in leukemia needs to be further studied.

[MeSH-major] Chromosomes, Human, Pair 12 / genetics. Chromosomes, Human, Pair 22 / genetics. Leukemia, Biphenotypic, Acute / genetics. Translocation, Genetic

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16875585.001).

[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] Case Reports; English Abstract; Journal Article; Review

[Publication-country] China

[Number-of-references] 20

   

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

[Title] Diagnosis of biphenotypic acute leukemia: a paradigmatic approach.

Biphenotypic acute leukemia (BAL), or acute leukemia with a single population of blasts coexpressing markers of two different lineages, is a rare clinical entity.

To define BAL, a scoring system was proposed by the European Group of Immunological Markers for Leukemias (EGIL) in 1995.

However, increasing evidence suggests that this system has limitations, as acknowledged by the 2008 World Health Organization (WHO) Classification of Tumors of Hematopoietic and Lymphoid Tissues.

We propose a new paradigmatic approach to defining BAL based on recent clinical studies of BAL and advances in immunologic marker definition and cytogenetics, and applied our new approach to 8 cases of "BAL" among a cohort of 742 new acute leukemias in our Cancer Center.

By our new criteria, 6 cases were reclassified as acute lymphoblastic leukemia (ALL), while only 2 were still classified as BAL.

[MeSH-major] Leukemia, Biphenotypic, Acute / diagnosis

[MeSH-minor] Adolescent. Adult. Aged, 80 and over. Antigens, Neoplasm / analysis. Biomarkers, Tumor / genetics. Biomarkers, Tumor / immunology. Child. Female. Humans. Immunophenotyping. Male. Middle Aged. Phenotype. Retrospective Studies. World Health Organization. Young Adult

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Arch Pathol Lab Med. 2001 Jul;125(7):948-50 [11419984.001]

[Cites] Am J Clin Pathol. 1998 Feb;109(2):211-20 [9583894.001]

[Cites] Am J Hematol. 2001 Oct;68(2):69-74 [11559944.001]

[Cites] Exp Hematol. 2002 Mar;30(3):205-11 [11882357.001]

[Cites] Br J Haematol. 2003 Dec;123(5):842-9 [14632775.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7399-404 [15492262.001]

[Cites] Nature. 1975 Dec 4;258(5534):454-6 [1059878.001]

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

[Cites] Blood. 1981 Sep;58(3):648-52 [6973348.001]

[Cites] Blood. 1983 Apr;61(4):718-25 [6572534.001]

[Cites] Blood. 1983 Jun;61(6):1138-45 [6404327.001]

[Cites] Hum Pathol. 1998 May;29(5):498-504 [9596274.001]

[Cites] Am J Hematol. 1998 Jul;58(3):241-3 [9662278.001]

[Cites] Cytometry. 1998 Aug 15;34(4):198-202 [9725460.001]

[Cites] Haematologica. 1999 Aug;84(8):699-706 [10457405.001]

[Cites] Cancer. 2004 Dec 15;101(12):2788-801 [15481055.001]

[Cites] Exp Mol Pathol. 2005 Aug;79(1):39-41 [16005710.001]

[Cites] Cancer Genet Cytogenet. 2005 Nov;163(1):62-7 [16271957.001]

[Cites] Blood. 2007 May 1;109(9):3697-705 [17218387.001]

[Cites] Exp Mol Pathol. 2007 Aug;83(1):138-41 [17434163.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

[Cites] Exp Mol Pathol. 2007 Dec;83(3):471-3 [17963747.001]

[Cites] Trends Biochem Sci. 2008 Feb;33(2):51-7 [18201888.001]

[Cites] Int J Hematol. 2008 Mar;87(2):132-6 [18288568.001]

[Cites] Leuk Lymphoma. 2008 Apr;49(4):700-9 [18398737.001]

[Cites] Cancer Genet Cytogenet. 2008 Aug;185(1):28-31 [18656690.001]

[Cites] Blood. 2009 May 21;113(21):5083-9 [19131545.001]

[Cites] J Biol Chem. 2000 Mar 24;275(12):8633-40 [10722703.001]

[Cites] Am J Clin Pathol. 2000 Jun;113(6):823-30 [10874883.001]

[Cites] J Chin Med Assoc. 2007 Jul;70(7):269-73 [17631462.001]

[Cites] Leukemia. 2007 Nov;21(11):2264-70 [17611554.001]

[Cites] Pathology. 1986 Jan;18(1):99-110 [3014425.001]

[Cites] EMBO J. 1988 Nov;7(11):3457-64 [2463161.001]

[Cites] Leukemia. 1989 Mar;3(3):170-81 [2465463.001]

[Cites] Br J Haematol. 1990 Jun;75(2):202-7 [2372506.001]

[Cites] Blood. 1990 Aug 15;76(4):808-13 [2166608.001]

[Cites] Blood. 1992 Jul 15;80(2):470-7 [1378322.001]

[Cites] J Immunol. 1992 Oct 1;149(7):2281-5 [1382094.001]

[Cites] Leukemia. 1993 Apr;7(4):489-98 [7681917.001]

[Cites] Blood. 1993 Aug 1;82(3):853-7 [8338949.001]

[Cites] J Exp Med. 1993 Sep 1;178(3):1049-55 [7688784.001]

[Cites] Blood. 1993 Sep 1;82(5):1599-607 [8395912.001]

[Cites] J Pathol. 1993 Oct;171(2):99-104 [7506772.001]

[Cites] Am J Clin Pathol. 1994 Mar;101(3):296-9 [7510927.001]

[Cites] Br J Haematol. 1994 Jun;87(2):273-81 [7947267.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] Am J Clin Pathol. 1996 Jun;105(6):761-8 [8659452.001]

[Cites] Am J Clin Pathol. 1996 Aug;106(2):185-91 [8712171.001]

[Cites] Br J Haematol. 1997 Oct;99(1):101-6 [9359509.001]

[Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]

[Cites] Am J Clin Pathol. 2001 Jul;116(1):25-33 [11447748.001]

(PMID = 19918331.001).

[ISSN] 1936-2625

[Journal-full-title] International journal of clinical and experimental pathology

[ISO-abbreviation] Int J Clin Exp Pathol

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor

[Other-IDs] NLM/ PMC2776262

[Keywords] NOTNLM ; ALL / AML / Biphenotypic acute leukemia / EGIL / classification

   

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

[Title] Molecular basis of the mixed lineage leukemia-menin interaction: implications for targeting mixed lineage leukemias.

Chromosomal translocations targeting the mixed lineage leukemia (MLL) gene result in MLL fusion proteins that are found in aggressive human acute leukemias.

Disruption of MLL by such translocations leads to overexpression of Hox genes, resulting in a blockage of hematopoietic differentiation that ultimately leads to leukemia.

Altogether, our work establishes the molecular basis of the menin interaction with MLL and MLL fusion proteins and provides the necessary foundation for development of small molecule inhibitors targeting this interaction in leukemias with MLL translocations.

[MeSH-major] Myeloid-Lymphoid Leukemia Protein / chemistry. Proto-Oncogene Proteins / chemistry

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Hematol Oncol. 2005 Mar;23(1):1-9 [16118769.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8603-8 [15941828.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Jan 24;103(4):1018-23 [16415155.001]

[Cites] J Am Chem Soc. 2006 Mar 29;128(12):3918-9 [16551093.001]

[Cites] Cancer Res. 2007 Aug 1;67(15):7275-83 [17671196.001]

[Cites] J Magn Reson. 2009 Jun;198(2):275-81 [19307141.001]

[Cites] Cancer Cell. 2010 Feb 17;17(2):148-59 [20159607.001]

[Cites] Curr Opin Struct Biol. 2003 Oct;13(5):581-8 [14568612.001]

[Cites] Mol Cell Biol. 2004 Jan;24(2):617-28 [14701735.001]

[Cites] Int J Hematol. 2003 Dec;78(5):390-401 [14704031.001]

[Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]

[Cites] Mol Cell Biol. 2004 Jul;24(13):5639-49 [15199122.001]

[Cites] Am J Clin Pathol. 2004 Aug;122(2):298-306 [15323147.001]

[Cites] Cell. 1992 Nov 13;71(4):691-700 [1423624.001]

[Cites] J Clin Invest. 1994 Jan;93(1):429-37 [8282816.001]

[Cites] Development. 1994 Jul;120(7):1907-17 [7924996.001]

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

[Cites] J Biomol NMR. 1995 Nov;6(3):277-93 [8520220.001]

[Cites] Leukemia. 1996 Feb;10(2):372-7 [8637251.001]

[Cites] J Mol Graph. 1996 Feb;14(1):51-5, 29-32 [8744573.001]

[Cites] Science. 1997 Apr 18;276(5311):404-7 [9103196.001]

[Cites] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107.001]

[Cites] Crit Rev Eukaryot Gene Expr. 2004;14(4):235-54 [15663355.001]

[Cites] Nat Rev Cancer. 2005 May;5(5):367-75 [15864278.001]

[Cites] Angew Chem Int Ed Engl. 2005 May 13;44(20):3089-92 [15832397.001]

[Cites] Cell. 2005 Oct 21;123(2):207-18 [16239140.001]

(PMID = 20961854.001).

[ISSN] 1083-351X

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Other-IDs] NLM/ PMC3003368

   

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

[Title] V(D)J targeting mistakes occur at low frequency in acute lymphoblastic leukemia.

Translocations of proto-oncogenes to the B-cell or T-cell antigen receptor loci in acute T- or B-cell leukemia and lymphoma have been, in most cases, accredited to V(D)J or switch recombination depending on the location of the breakpoint at the receptor locus.

[MeSH-major] Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Proto-Oncogenes / genetics. Recombination, Genetic. Translocation, Genetic. VDJ Recombinases / metabolism

[MeSH-minor] Adaptor Proteins, Signal Transducing. Animals. Cells, Cultured. DNA Breaks. DNA-Binding Proteins / genetics. Fibroblasts. Genes, T-Cell Receptor. Homeodomain Proteins / genetics. LIM Domain Proteins. Lymphocyte Specific Protein Tyrosine Kinase p56(lck) / genetics. Metalloproteins / genetics. Mice. Receptors, Antigen, B-Cell / genetics. TCF Transcription Factors / genetics. Transcription Factor 7-Like 1 Protein

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19455608.001).

[ISSN] 1098-2264

[Journal-full-title] Genes, chromosomes & cancer

[ISO-abbreviation] Genes Chromosomes Cancer

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / Homeodomain Proteins; 0 / LIM Domain Proteins; 0 / Lmo2 protein, mouse; 0 / Metalloproteins; 0 / Receptors, Antigen, B-Cell; 0 / TCF Transcription Factors; 0 / Tcf7l1 protein, mouse; 0 / Tlx1 protein, mouse; 0 / Transcription Factor 7-Like 1 Protein; EC 2.7.10.2 / Lymphocyte Specific Protein Tyrosine Kinase p56(lck); EC 2.7.7.- / VDJ Recombinases

   

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

[Title] B-Lymphoid and myeloid lineages biphenotypic acute leukemia with t(8;21)(q22;q22).

By analyzing the characteristics of morphology, immune phenotype, chromosome karyotype and clinical manifestations of six cases of B-lymphoid and myeloid lineages biphenotypic acute leukemia (BAL) with t(8;21)(q22;q22), a new subgroup of BAL was reported.

Immunophenotype revealed B-lymphoid and myeloid lineages positive, together with frequent and high expression of CD34 and CD33, and weak expression of HLA-DR.

Chemotherapy for myeloid and lymphoid leukemia simultaneously produced good response in the patients.

q22) might be a new subgroup of BAL, and it was suggested that the leukemia clone with t(8;21)(q22;q22) might have originated from an early phase of hematopoiesis, and AML1/ETO fusion gene might be related to differentiation of B lymphocyte.

[MeSH-major] Leukemia, Myeloid, Acute / genetics. Leukemia, Myeloid, Acute / pathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics. Precursor Cell Lymphoblastic Leukemia-Lymphoma / pathology. Translocation, Genetic

Genetic Alliance. consumer health - Acute Biphenotypic Leukemia.

Genetic Alliance. consumer health - Acute Lymphoblastic Leukemia.

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

[Cites] J Biol Chem. 1994 May 27;269(21):15310-7 [8195169.001]

[Cites] Genes Dev. 1996 Sep 1;10 (17 ):2198-211 [8804314.001]

[Cites] Cell Cycle. 2005 Dec;4(12):1716-8 [16294039.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7521-6 [10861016.001]

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

[Cites] Br J Haematol. 1998 Jan;100(1):147-55 [9450804.001]

[Cites] Haematologica. 2002 Mar;87(3):306-19 [11869944.001]

[Cites] Leukemia. 1995 Oct;9(10):1783-6 [7564526.001]

[Cites] J Biol Chem. 1999 Aug 27;274(35):24671-6 [10455134.001]

[Cites] Mol Cell Biol. 1992 Jun;12 (6):2662-72 [1375324.001]

[Cites] Blood. 2000 Jun 15;95(12 ):3845-52 [10845919.001]

[Cites] EMBO J. 1998 Apr 15;17 (8):2319-33 [9545244.001]

[Cites] Leukemia. 1996 Aug;10(8):1283-7 [8709632.001]

[Cites] Nature. 1999 Oct 7;401(6753):556-62 [10524622.001]

[Cites] Cancer Genet Cytogenet. 2005 Nov;163(1):62-7 [16271957.001]

[Cites] Br J Haematol. 1996 Mar;92(4):855-65 [8616078.001]

(PMID = 18288568.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

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

[Publication-country] Japan

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD79; 0 / Antigens, Differentiation, Myelomonocytic; 0 / CD33 protein, human; 0 / CD79A protein, human; 0 / Sialic Acid Binding Ig-like Lectin 3

   

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

[Title] Induction of apoptosis in lymphoid and myeloid leukemia.

Defects in the core machinery of the apoptosis pathway contribute to chemoresistance and poor outcomes in patients with acute leukemia.

This review highlights compounds that target the mitochondrial, death receptor, and convergence pathways of caspase activation that are being developed for the treatment of acute leukemia.

[MeSH-major] Apoptosis / physiology. Leukemia, Lymphoid / therapy. Leukemia, Myeloid / therapy

Genetic Alliance. consumer health - Leukemia, Myeloid.

MedlinePlus Health Information. consumer health - Chronic Lymphocytic Leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Biol Chem. 1998 Mar 20;273(12):6916-20 [9506996.001]

[Cites] J Med Chem. 2003 Sep 25;46(20):4259-64 [13678404.001]

[Cites] Cancer Res. 2003 Nov 15;63(22):7724-32 [14633697.001]

[Cites] J Med Chem. 2004 Aug 12;47(17):4147-50 [15293984.001]

[Cites] Cancer Cell. 2005 May;7(5):457-68 [15894266.001]

[Cites] Nature. 1999 Oct 21;401(6755):818-22 [10548111.001]

[Cites] Curr Treat Options Oncol. 2003 Jun;4(3):211-8 [12718798.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1252-6 [9990010.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7183-90 [15492230.001]

[Cites] EMBO J. 2005 Feb 9;24(3):645-55 [15650747.001]

[Cites] Haematologica. 2004 Mar;89(3):363-4 [15020280.001]

[Cites] Cancer Res. 1999 Jan 15;59(2):336-41 [9927043.001]

[Cites] Cell Death Differ. 2002 Sep;9(9):881-92 [12181739.001]

[Cites] Science. 1998 Aug 28;281(5381):1312-6 [9721091.001]

[Cites] J Mol Biol. 2000 Sep 8;302(1):171-88 [10964568.001]

[Cites] Chem Biol. 2003 Aug;10(8):759-67 [12954335.001]

[Cites] Blood. 2005 May 15;105(10):4043-50 [15687241.001]

[Cites] Leukemia. 2003 Nov;17(11):2122-9 [12931220.001]

[Cites] Mol Cell. 2003 Feb;11(2):519-27 [12620238.001]

[Cites] Cell. 2001 Mar 9;104(5):781-90 [11257231.001]

[Cites] Cell. 2001 Mar 9;104(5):769-80 [11257230.001]

[Cites] EMBO J. 1999 Oct 1;18(19):5242-51 [10508158.001]

[Cites] J Biol Chem. 1999 Jun 18;274(25):17941-5 [10364241.001]

[Cites] Science. 2004 Sep 3;305(5689):1471-4 [15353805.001]

[Cites] Cell. 2001 Mar 9;104(5):791-800 [11257232.001]

[Cites] Leukemia. 1995 Jan;9(1):131-8 [7845007.001]

[Cites] J Am Chem Soc. 2004 Dec 29;126(51):16686-7 [15612682.001]

[Cites] Science. 1997 Feb 21;275(5303):1132-6 [9027315.001]

[Cites] Cancer Cell. 2004 Jan;5(1):25-35 [14749124.001]

[Cites] Nature. 1998 Dec 10;396(6711):580-4 [9859993.001]

[Cites] Br J Haematol. 2003 Jun;121(5):730-8 [12780787.001]

[Cites] Blood. 2001 Dec 15;98(13):3541-53 [11739155.001]

[Cites] J Biol Chem. 2000 Oct 27;275(43):33777-81 [10934209.001]

[Cites] Cell Death Differ. 2004 Apr;11(4):372-80 [14765132.001]

[Cites] Cancer Gene Ther. 2005 May;12(5):509-14 [15706355.001]

[Cites] Cancer Res. 2004 Nov 1;64(21):7927-35 [15520199.001]

[Cites] J Biol Chem. 1999 Apr 23;274(17):11549-56 [10206961.001]

[Cites] Cell. 1997 Nov 14;91(4):443-6 [9390553.001]

[Cites] J Med Chem. 2004 Aug 26;47(18):4417-26 [15317454.001]

[Cites] Br J Haematol. 2001 Mar;112(3):706-13 [11260076.001]

[Cites] Leukemia. 1999 Oct;13(10):1574-80 [10516759.001]

[Cites] Mol Cell Biol. 2000 Jun;20(11):3781-94 [10805722.001]

[Cites] J Biol Chem. 2002 Jun 21;277(25):22320-9 [11940602.001]

[Cites] J Med Chem. 2004 May 6;47(10):2430-40 [15115387.001]

[Cites] Trends Neurosci. 2000 May;23(5):222-9 [10782128.001]

[Cites] Clin Cancer Res. 2003 Jul;9(7):2826-36 [12855663.001]

[Cites] Science. 2004 Sep 3;305(5689):1466-70 [15353804.001]

[Cites] Cell Growth Differ. 2000 May;11(5):261-7 [10845427.001]

[Cites] Nat Med. 1999 Feb;5(2):157-63 [9930862.001]

[Cites] Mol Cell Biol. 2004 Aug;24(16):7003-14 [15282301.001]

[Cites] Leuk Res. 1998 Jan;22(1):81-7 [9585084.001]

[Cites] Leukemia. 2002 Jan;16(1):67-73 [11840265.001]

[Cites] Cancer Res. 2004 Oct 15;64(20):7570-8 [15492284.001]

[Cites] J Biol Chem. 1998 Oct 16;273(42):27084-90 [9765224.001]

[Cites] Ann N Y Acad Sci. 2005 Nov;1058:215-34 [16394139.001]

[Cites] Nature. 2005 Jun 2;435(7042):677-81 [15902208.001]

[Cites] Leukemia. 1997 Dec;11(12):2075-8 [9447823.001]

[Cites] Cancer Res. 2002 May 1;62(9):2462-7 [11980633.001]

[Cites] EMBO J. 1999 Jul 1;18(13):3586-95 [10393175.001]

[Cites] Nat Med. 2000 May;6(5):564-7 [10802713.001]

[Cites] J Biol Chem. 1999 Jan 29;274(5):3189-98 [9915859.001]

[Cites] Cancer Res. 2005 Mar 15;65(6):2378-86 [15781653.001]

[Cites] Genes Dev. 1998 Jun 1;12(11):1551-70 [9620844.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Jun 20;97(13):7124-9 [10860979.001]

[Cites] Cell Death Differ. 2006 Feb;13(2):179-88 [16322751.001]

[Cites] Mol Biol Cell. 2003 Jan;14(1):78-92 [12529428.001]

[Cites] Br J Haematol. 2000 Jul;110(1):154-60 [10930993.001]

(PMID = 17040621.001).

[ISSN] 1523-3790

[Journal-full-title] Current oncology reports

[ISO-abbreviation] Curr Oncol Rep

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Receptors, Death Domain; EC 3.4.22.- / Caspases

[Number-of-references] 68

   

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

[Transliterated title] Porphyrie cutanée tardive chez un enfant greffé de moelle.

His past medical history revealed acute biphenotypic leukaemia with complete remission after allogeneic hematopoietic stem cell transplantation (unrelated donor).

Complications of bone marrow transplant comprised anaemia (treated by blood transfusions), primary cytomegalovirus (CMV) infection, pulmonary aspergillosis and acute digestive graft-versus-host disease.

The diagnosis of type I sporadic PCT was based on high levels of porphyria and normal erythrocytic uroporphyrinogen decarboxylase activity.

The causative role of bone marrow transplantation in the development of PCT could be related to several triggering factors: primary CMV infection, hepatotoxic drugs, blood transfusion and possible chronic hepatic graft-versus-host disease.

[MeSH-major] Bone Marrow Transplantation / adverse effects. Hematopoietic Stem Cell Transplantation / adverse effects. Leukemia, Biphenotypic, Acute / therapy. Porphyria Cutanea Tarda / diagnosis. Porphyria Cutanea Tarda / therapy

Genetic Alliance. consumer health - Porphyria.

Genetic Alliance. consumer health - Porphyria cutanea tarda.

MedlinePlus Health Information. consumer health - Bone Marrow Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright © 2010 Elsevier Masson SAS. All rights reserved.

(PMID = 20932445.001).

[ISSN] 0151-9638

[Journal-full-title] Annales de dermatologie et de vénéréologie

[ISO-abbreviation] Ann Dermatol Venereol

[Language] fre

[Publication-type] Case Reports; 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] Constitutional pericentric inversion 9 in Korean patients with chronic myelogenous leukemia.

BACKGROUND: Although the pericentric inversion of chromosome 9, inv(9)(p11q13), is generally considered a normal variation, it is also associated with solid tumors and several hematologic malignancies such as biphenotypic acute leukemia, ALL, AML, and myeloproliferative neoplasms.

The purpose of this retrospective study was to investigate the frequency and clinical features of CML patients with concomitant inv(9) and t(9;22)(q34;q11.2) variation at our institution.

METHODS: We reviewed the bone marrow chromosome database entries between October 2006 and December 2008 to identify patients with concomitant inv(9) and t(9;22) variations.

RESULTS: Among the 51 CML patients, 4 (7.8%) had concomitant inv(9) and t(9;22) variations.

[MeSH-major] Asian Continental Ancestry Group / genetics. Chromosome Inversion. Chromosomes, Human, Pair 9. Leukemia, Myeloid, Acute / genetics

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20603579.001).

[ISSN] 1598-6535

[Journal-full-title] The Korean journal of laboratory medicine

[ISO-abbreviation] Korean J Lab Med

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Korea (South)

   

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

[Title] Mixed lineage leukemia: a structure-function perspective of the MLL1 protein.

Several acute lymphoblastic and myelogenous leukemias are correlated with alterations in the human mixed lineage leukemia protein-1 (MLL1) gene.

Despite the important biological role of SET1 family enzymes and their involvement in human leukemias, relatively little is understood about how these enzymes work.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. L-Lysine .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Genet Couns. 1999;10(3):305-13 [10546104.001]

[Cites] J Biol Chem. 2008 Nov 21;283(47):32158-61 [18829459.001]

[Cites] Genes Dev. 2000 Jul 1;14(13):1553-77 [10887150.001]

[Cites] Nature. 2000 Aug 10;406(6796):593-9 [10949293.001]

[Cites] Mol Cell Biol. 2001 Apr;21(7):2249-58 [11259575.001]

[Cites] Nucleic Acids Res. 2002 Feb 15;30(4):958-65 [11842107.001]

[Cites] Cell. 2002 Oct 4;111(1):117-27 [12372305.001]

[Cites] Nat Struct Biol. 2002 Nov;9(11):828-32 [12389037.001]

[Cites] Blood. 2002 Nov 15;100(10):3710-8 [12393701.001]

[Cites] J Biol Chem. 2002 Nov 8;277(45):43168-74 [12205094.001]

[Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]

[Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]

[Cites] Mol Cell Biol. 2003 Jan;23(1):186-94 [12482972.001]

[Cites] Genes Dev. 2003 Apr 1;17(7):896-911 [12670868.001]

[Cites] Nat Struct Biol. 2003 Jul;10(7):545-52 [12819771.001]

[Cites] Mol Cell. 2003 Jul;12(1):177-85 [12887903.001]

[Cites] Curr Opin Struct Biol. 2003 Dec;13(6):699-705 [14675547.001]

[Cites] Br J Cancer. 2004 Feb 23;90(4):756-60 [14970849.001]

[Cites] Methods Enzymol. 2004;376:221-34 [14975309.001]

[Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]

[Cites] J Mol Biol. 2004 Mar 26;337(3):521-34 [15019774.001]

[Cites] Mol Cell Biol. 2004 Jul;24(13):5639-49 [15199122.001]

[Cites] PLoS Biol. 2004 Jul;2(7):E171 [15252442.001]

[Cites] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10735-9 [1720549.001]

[Cites] Curr Opin Genet Dev. 1995 Jun;5(3):309-14 [7549424.001]

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

[Cites] Cancer Res. 1996 Apr 15;56(8):1766-9 [8620491.001]

[Cites] Cell Mol Life Sci. 1998 Jan;54(1):80-93 [9487389.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4152-7 [9539705.001]

[Cites] Mol Cell Biol. 2004 Dec;24(23):10470-8 [15542854.001]

[Cites] J Biol Chem. 2005 Feb 18;280(7):5563-70 [15590646.001]

[Cites] Cell. 2005 Jun 17;121(6):859-72 [15960974.001]

[Cites] Cell. 2005 Jun 17;121(6):873-85 [15960975.001]

[Cites] Genes Dev. 2005 Jun 15;19(12):1444-54 [15933069.001]

[Cites] Genome Biol. 2005;6(8):227 [16086857.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14765-70 [16199523.001]

[Cites] Cell. 2005 Oct 21;123(2):207-18 [16239140.001]

[Cites] Nature. 2005 Nov 17;438(7066):374-8 [16292313.001]

[Cites] J Mol Biol. 2006 Feb 3;355(5):1005-13 [16253272.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6629-34 [16618927.001]

[Cites] J Mol Biol. 2006 May 26;359(1):86-96 [16603186.001]

[Cites] Nat Struct Mol Biol. 2006 Aug;13(8):704-12 [16829959.001]

[Cites] Nat Struct Mol Biol. 2006 Aug;13(8):698-703 [16829960.001]

[Cites] Nat Struct Mol Biol. 2006 Aug;13(8):713-9 [16878130.001]

[Cites] Nat Struct Mol Biol. 2006 Sep;13(9):852-4 [16892064.001]

[Cites] EMBO J. 2006 Sep 20;25(18):4245-52 [16946699.001]

[Cites] EMBO J. 2006 Oct 4;25(19):4503-12 [16990798.001]

[Cites] J Biol Chem. 2008 Dec 12;283(50):35258-64 [18840606.001]

[Cites] Mol Cell. 2009 Jan 30;33(2):181-91 [19187761.001]

[Cites] Nat Struct Mol Biol. 2009 Mar;16(3):312-7 [19219047.001]

[Cites] Mol Cell Biol. 2009 Jul;29(13):3478-86 [19398585.001]

[Cites] Nat Struct Mol Biol. 2009 Jul;16(7):678-80 [19578375.001]

[Cites] J Biol Chem. 2009 Sep 4;284(36):24242-56 [19556245.001]

[Cites] FEBS J. 2010 Apr;277(8):1822-31 [20236311.001]

[Cites] FEBS J. 2010 Apr;277(8):1805-21 [20236312.001]

[Cites] FEBS J. 2010 Apr;277(8):1790-804 [20236313.001]

[Cites] J Biol Chem. 2007 May 4;282(18):13419-28 [17355966.001]

[Cites] J Biol Chem. 2007 Jul 13;282(28):20395-406 [17500065.001]

[Cites] Curr Opin Cell Biol. 2008 Jun;20(3):341-8 [18508253.001]

[Cites] J Biol Chem. 2008 Nov 21;283(47):32162-75 [18829457.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Dec 21;96(26):14967-72 [10611321.001]

(PMID = 20236310.001).

[ISSN] 1742-4658

[Journal-full-title] The FEBS journal

[ISO-abbreviation] FEBS J.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA140522-02; United States / NCI NIH HHS / CA / R01 CA140522; United States / NCI NIH HHS / CA / R01 CA140522-02; United States / NCI NIH HHS / CA / R01CA140522

[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 / Histones; 0 / Ligands; 0 / MLL protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine

[Number-of-references] 61

[Other-IDs] NLM/ NIHMS209384; NLM/ PMC2892832

   

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

The chromosomal translocation t(4;11)(q21;q23) is the most frequent genetic aberration of the human MLL gene, resulting in high-risk acute lymphoblastic leukemia (ALL).

Recipients of AF4.MLL- or double-transduced LSPCs developed pro-B ALL, B/T biphenotypic acute leukemia, or mixed lineage leukemia.

Transplantation of MLL.AF4- or mock-transduced LSPCs did not result in disease development during an observation period of 13 months.

These findings indicate that the expression of the AF4.MLL fusion protein is capable of inducing acute lymphoblastic leukemia even in the absence of the MLL.AF4 fusion protein.

In view of recent findings, these results may imply that t(4;11) leukemia is based on 2 oncoproteins, providing an explanation for the very early onset of disease in humans.

[MeSH-major] Cell Transformation, Neoplastic / metabolism. DNA-Binding Proteins / metabolism. Gene Expression Regulation, Leukemic. Myeloid-Lymphoid Leukemia Protein / metabolism. Nuclear Proteins / metabolism. Oncogene Proteins, Fusion / metabolism. Precursor B-Cell Lymphoblastic Leukemia-Lymphoma / metabolism

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20194896.001).

[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 / Aff1 protein, mouse; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.1.1.43 / Mll protein, mouse

   

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

[Title] c-Myb binds MLL through menin in human leukemia cells and is an important driver of MLL-associated leukemogenesis.

Mixed-lineage leukemia (MLL) is a proto-oncogene frequently involved in chromosomal translocations associated with acute leukemia.

Recent data suggest that the MYB proto-oncogene, which is an important regulator of hematopoietic cell development, has a role in leukemogenesis driven by the MLL-ENL fusion protein, but exactly how is unclear.

Silencing MYB in human leukemic cell lines and primary patient material evoked a global decrease in H3K4 methylation, an unexpected decrease in HOXA9 and MEIS1 gene expression, and decreased MLL and menin occupancy in the HOXA9 gene locus.

The finding that c-Myb has the ability to direct epigenetic marks, along with its participation in an autoregulatory feedback loop with genes known to transform hematopoietic cells, lends mechanistic and translationally relevant insight into its role in MLL-associated leukemogenesis.

[MeSH-major] Leukemia / metabolism. Myeloid-Lymphoid Leukemia Protein / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-myb / metabolism

MedlinePlus Health Information. consumer health - Leukemia.

COS Scholar Universe. author profiles.

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4394-8 [3520570.001]

[Cites] Science. 1988 Dec 2;242(4883):1303-6 [2461588.001]

[Cites] Transgenic Res. 1993 Jul;2(4):199-207 [8364603.001]

[Cites] Br J Haematol. 1994 Feb;86(2):275-83 [8199015.001]

[Cites] Oncogene. 1996 Jul 18;13(2):223-35 [8710361.001]

[Cites] Cell Growth Differ. 1997 Jan;8(1):35-45 [8993832.001]

[Cites] EMBO J. 1997 Jul 16;16(14):4226-37 [9250666.001]

[Cites] Crit Rev Oncog. 1996;7(3-4):245-60 [9258605.001]

[Cites] Curr Opin Genet Dev. 1998 Feb;8(1):76-81 [9529609.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Sep 1;95(18):10632-6 [9724755.001]

[Cites] J Cell Physiol. 1999 Jun;179(3):245-50 [10228942.001]

[Cites] Oncogene. 1999 May 13;18(19):3017-33 [10378697.001]

[Cites] Oncogene. 1999 May 13;18(19):3034-8 [10378698.001]

[Cites] Dev Cell. 2005 Feb;8(2):153-66 [15691758.001]

[Cites] Cell. 2005 Jun 17;121(6):859-72 [15960974.001]

[Cites] Cell. 2005 Jun 17;121(6):873-85 [15960975.001]

[Cites] Nature. 2005 Sep 15;437(7057):436-9 [16079795.001]

[Cites] Immunity. 2005 Sep;23(3):275-86 [16169500.001]

[Cites] Genes Dev. 2005 Oct 15;19(20):2447-57 [16195416.001]

[Cites] Cell. 2005 Oct 21;123(2):207-18 [16239140.001]

[Cites] Nat Rev Mol Cell Biol. 2005 Nov;6(11):838-49 [16261189.001]

[Cites] PLoS Genet. 2006 Apr;2(4):e51 [16604156.001]

[Cites] Blood. 2006 Jun 15;107(12):4703-10 [16484593.001]

[Cites] Blood. 2006 Jul 1;108(1):297-304 [16507773.001]

[Cites] Blood. 2006 Aug 1;108(3):896-903 [16597594.001]

[Cites] Nat Struct Mol Biol. 2006 Aug;13(8):713-9 [16878130.001]

[Cites] Nat Struct Mol Biol. 2006 Sep;13(9):852-4 [16892064.001]

[Cites] Mol Cell. 2007 Jan 12;25(1):15-30 [17218268.001]

[Cites] Cell. 2007 Feb 23;128(4):693-705 [17320507.001]

[Cites] Mol Cell Biol. 2007 Mar;27(6):2048-58 [17242210.001]

[Cites] Nat Genet. 2007 May;39(5):593-5 [17435759.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Jun 26;104(26):10980-5 [17581865.001]

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

[Cites] Cell. 2007 Oct 5;131(1):146-59 [17923094.001]

[Cites] Nat Rev Cancer. 2007 Nov;7(11):823-33 [17957188.001]

[Cites] Nat Rev Mol Cell Biol. 2007 Dec;8(12):983-94 [18037899.001]

[Cites] Int J Hematol. 2008 Jan;87(1):10-8 [18224408.001]

[Cites] Mol Cell Biol. 2008 Mar;28(6):2091-101 [18195038.001]

[Cites] Blood. 2008 May 1;111(9):4771-9 [18227349.001]

[Cites] Proc Natl Acad Sci U S A. 2008 May 27;105(21):7517-22 [18483194.001]

[Cites] PLoS One. 2008;3(6):e2478 [18575582.001]

[Cites] Cancer Cell. 2008 Jul 8;14(1):3-5 [18598937.001]

[Cites] Cancer Cell. 2008 Jul 8;14(1):36-46 [18598942.001]

[Cites] Oncogene. 2008 Aug 7;27(34):4644-56 [18408764.001]

[Cites] Blood. 2008 Sep 1;112(5):1942-50 [18550858.001]

[Cites] Cell Stem Cell. 2009 Feb 6;4(2):129-40 [19200802.001]

[Cites] Blood. 1989 Feb 15;73(3):782-6 [2644989.001]

[Cites] Blood. 1989 May 1;73(6):1444-51 [2469491.001]

[Cites] Proc Natl Acad Sci U S A. 1989 May;86(9):3379-83 [2541445.001]

[Cites] Science. 1989 Jul 14;245(4914):180-3 [2665077.001]

[Cites] J Clin Invest. 1990 Jan;85(1):55-61 [2404028.001]

[Cites] Cell. 1990 Dec 21;63(6):1289-97 [2261644.001]

[Cites] Cell. 1991 May 17;65(4):677-89 [1709592.001]

[Cites] Curr Opin Genet Dev. 1992 Apr;2(2):249-55 [1638119.001]

[Cites] Cell. 1992 Nov 13;71(4):691-700 [1423624.001]

[Cites] Cell. 1992 Nov 13;71(4):701-8 [1423625.001]

[Cites] Nat Genet. 1992 Oct;2(2):113-8 [1303259.001]

[Cites] Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7884-8 [7689231.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Jun 25;99(13):8695-700 [12060701.001]

[Cites] Nature. 2002 Sep 26;419(6905):407-11 [12353038.001]

[Cites] Nature. 2002 Oct 17;419(6908):738-43 [12384703.001]

[Cites] Blood. 2002 Nov 15;100(10):3710-8 [12393701.001]

[Cites] J Biol Chem. 2002 Nov 8;277(45):43168-74 [12205094.001]

[Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]

[Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]

[Cites] Mol Cell Biol. 2003 Jan;23(1):186-94 [12482972.001]

[Cites] Mech Dev. 2003 Jun;120(6):711-20 [12834870.001]

[Cites] Cancer Res. 2003 Jul 15;63(14):4204-10 [12874027.001]

[Cites] EMBO J. 2003 Sep 1;22(17):4478-88 [12941699.001]

[Cites] Oncogene. 2004 Feb 19;23(7):1392-404 [14973551.001]

[Cites] Blood. 2004 Mar 1;103(5):1676-84 [14604967.001]

[Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]

[Cites] Mol Cell Biol. 2004 Jul;24(13):5639-49 [15199122.001]

[Cites] Nat Immunol. 2004 Jul;5(7):721-9 [15195090.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Oct 12;101(41):14853-8 [15466706.001]

[Cites] J Biol Chem. 1975 Nov 25;250(22):8681-5 [1184585.001]

[Cites] Cell. 1982 Dec;31(2 Pt 1):453-63 [6297766.001]

[Cites] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386.001]

[Cites] Proc Natl Acad Sci U S A. 1985 Oct;82(20):6937-41 [2413449.001]

(PMID = 20093773.001).

[ISSN] 1558-8238

[Journal-full-title] The Journal of clinical investigation

[ISO-abbreviation] J. Clin. Invest.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / P01 CA072765; United States / NCI NIH HHS / CA / 2P01CA072765-11

[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 / DNA-Binding Proteins; 0 / Histones; 0 / Homeodomain Proteins; 0 / MEN1 protein, human; 0 / MLL protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-myb; 0 / Recombinant Fusion Proteins; 0 / homeobox protein HOXA9; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase

[Other-IDs] NLM/ PMC2810070

   

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

[Title] Acute myelogenous leukemia cells with the MLL-ELL translocation convert morphologically and functionally into adherent myofibroblasts.

We show in this paper that non-adherent leukemia blasts can change into myofibroblasts.

When myeloblasts from two cases of acute myelogenous leukemia with a fusion product comprising mixed lineage leukemia and RNA polymerase II elongation factor, were cultured long term, their morphology changed to that of myofibroblasts with similar molecular characteristics to the parental myeloblasts.

The original leukemia blasts, when cultured on the leukemia blast-derived myofibroblasts, grew extensively.

Leukemia blasts can create their own microenvironment for proliferation.

[MeSH-major] Chromosomes, Human, Pair 11 / genetics. Fibroblasts / pathology. Leukemia, Myeloid, Acute / pathology. Myeloid-Lymphoid Leukemia Protein / genetics. Myoblasts / pathology. Oncogene Proteins, Fusion / genetics. Translocation, Genetic

[MeSH-minor] Cell Adhesion. Cell Line, Tumor. Humans. Karyotyping

Genetic Alliance. consumer health - Acute Myeloid Leukemia, Adult.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2009 Elsevier Inc. All rights reserved.

(PMID = 19932689.001).

[ISSN] 1090-2104

[Journal-full-title] Biochemical and biophysical research communications

[ISO-abbreviation] Biochem. Biophys. Res. Commun.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / MLL-ELL fusion protein, human; 0 / Oncogene Proteins, Fusion; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein

   

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

[Title] Non-specific interstitial pneumonia as the initial presentation of biphenotypic acute leukemia: a case report.

We present a 46-year-old woman with recent-onset rheumatologic illness who developed pulmonary symptoms as the presenting feature of biphenotypic acute leukaemia.

Corticosteroid therapy resulted in resolution of both her pulmonary and rheumatologic symptoms, and her pulmonary symptoms did not recur following treatment of her leukemia.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Leuk Lymphoma. 2002 Nov;43(11):2083-92 [12533032.001]

[Cites] J Am Acad Dermatol. 2001 Mar;44(3):530-1 [11209130.001]

[Cites] Am J Respir Crit Care Med. 2008 Jun 15;177(12):1338-47 [18388353.001]

[Cites] Crit Rev Oncol Hematol. 2007 Aug;63(2):100-10 [17391977.001]

[Cites] Intern Med. 2004 Aug;43(8):721-6 [15468974.001]

[Cites] Semin Respir Crit Care Med. 2006 Dec;27(6):652-8 [17195141.001]

[Cites] Respiration. 2005 Jan-Feb;72(1):39-45 [15753633.001]

[Cites] Haematologica. 1997 Jan-Feb;82(1):64-6 [9107085.001]

[Cites] Br J Haematol. 2007 Jul;138(2):213-6 [17593028.001]

(PMID = 19918465.001).

[ISSN] 1757-1626

[Journal-full-title] Cases journal

[ISO-abbreviation] Cases J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC2769415

   

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

[Title] On the mechanism of multiple lysine methylation by the human mixed lineage leukemia protein-1 (MLL1) core complex.

The mixed lineage leukemia protein-1 (MLL1) is a member of the SET1 family of H3K4 methyltransferases and is frequently rearranged in acute leukemias.

COS Scholar Universe. author profiles.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

Hazardous Substances Data Bank. L-Lysine .

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] Biophys J. 2000 Mar;78(3):1606-19 [10692345.001]

[Cites] J Biol Chem. 2008 Dec 12;283(50):35258-64 [18840606.001]

[Cites] Nature. 2000 Aug 10;406(6796):593-9 [10949293.001]

[Cites] Science. 2001 Sep 28;293(5539):2453-5 [11498546.001]

[Cites] Genes Dev. 2001 Dec 15;15(24):3286-95 [11751634.001]

[Cites] Curr Opin Genet Dev. 2002 Apr;12(2):198-209 [11893494.001]

[Cites] Nature. 2002 Sep 26;419(6905):407-11 [12353038.001]

[Cites] Cell. 2002 Oct 4;111(1):91-103 [12372303.001]

[Cites] Cell. 2002 Oct 4;111(1):105-15 [12372304.001]

[Cites] Cell. 2002 Oct 4;111(1):117-27 [12372305.001]

[Cites] Mol Cell. 2002 Nov;10(5):1107-17 [12453418.001]

[Cites] Mol Cell. 2002 Nov;10(5):1119-28 [12453419.001]

[Cites] Mol Cell Biol. 2003 Jan;23(1):140-9 [12482968.001]

[Cites] Nature. 2003 Feb 6;421(6923):652-6 [12540855.001]

[Cites] Nat Struct Biol. 2003 Mar;10(3):187-96 [12567185.001]

[Cites] Cell. 2003 Mar 7;112(5):711-23 [12628190.001]

[Cites] Mol Cell. 2003 Mar;11(3):709-19 [12667453.001]

[Cites] Genes Dev. 2003 Apr 1;17(7):896-911 [12670868.001]

[Cites] Nat Struct Biol. 2003 Jul;10(7):545-52 [12819771.001]

[Cites] Mol Cell. 2003 Jul;12(1):177-85 [12887903.001]

[Cites] Mol Cell. 2003 Nov;12(5):1325-32 [14636589.001]

[Cites] Mol Cell. 2003 Dec;12(6):1591-8 [14690610.001]

[Cites] Mol Cell. 2004 Feb 27;13(4):587-97 [14992727.001]

[Cites] PLoS Biol. 2004 Jul;2(7):E171 [15252442.001]

[Cites] Mol Cell Biol. 1993 Oct;13(10):6357-66 [8413234.001]

[Cites] EMBO J. 1994 Aug 15;13(16):3822-31 [7915232.001]

[Cites] Mech Dev. 1995 Aug;52(2-3):209-23 [8541210.001]

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

[Cites] Anal Biochem. 1996 Jun 1;237(2):260-73 [8660575.001]

[Cites] Mol Biol Cell. 1997 Dec;8(12):2421-36 [9398665.001]

[Cites] Protein Expr Purif. 1999 Feb;15(1):34-9 [10024467.001]

[Cites] Nature. 2005 Jan 27;433(7024):434-8 [15647753.001]

[Cites] J Biol Chem. 2005 Feb 18;280(7):5563-70 [15590646.001]

[Cites] Cell. 2005 Jun 17;121(6):873-85 [15960975.001]

[Cites] Genes Dev. 2005 Jun 15;19(12):1444-54 [15933069.001]

[Cites] Genes Dev. 2005 Jun 15;19(12):1455-65 [15933070.001]

[Cites] Biophys J. 2005 Jul;89(1):619-34 [15863475.001]

[Cites] Genome Biol. 2005;6(8):227 [16086857.001]

[Cites] Mol Cell. 2009 Jan 30;33(2):181-91 [19187761.001]

[Cites] Biochemistry. 2000 Nov 14;39(45):13633-40 [11076501.001]

[Cites] Cell. 2005 Aug 26;122(4):517-27 [16122420.001]

[Cites] Plant Cell. 2005 Sep;17(9):2439-53 [16100335.001]

[Cites] Mol Cell. 2005 Sep 16;19(6):849-56 [16168379.001]

[Cites] PLoS Biol. 2005 Oct;3(10):e328 [16122352.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14765-70 [16199523.001]

[Cites] J Biol Chem. 2005 Dec 16;280(50):41725-31 [16253997.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Apr 25;103(17):6629-34 [16618927.001]

[Cites] J Mol Biol. 2006 May 26;359(1):86-96 [16603186.001]

[Cites] Nature. 2006 Jul 6;442(7098):96-9 [16728974.001]

[Cites] Nature. 2006 Jul 6;442(7098):86-90 [16728976.001]

[Cites] Nat Struct Mol Biol. 2006 Aug;13(8):713-9 [16878130.001]

[Cites] Nat Struct Mol Biol. 2006 Sep;13(9):852-4 [16892064.001]

[Cites] Nat Genet. 2007 Mar;39(3):311-8 [17277777.001]

[Cites] Biochemistry. 2007 Mar 27;46(12):3905-15 [17338551.001]

[Cites] Mutat Res. 2007 May 1;618(1-2):102-15 [17374386.001]

[Cites] J Biol Chem. 2007 May 4;282(18):13419-28 [17355966.001]

[Cites] J Biol Chem. 2007 Jul 13;282(28):20395-406 [17500065.001]

[Cites] Curr Opin Genet Dev. 2008 Apr;18(2):159-68 [18281209.001]

[Cites] J Biol Chem. 2008 Nov 21;283(47):32162-75 [18829457.001]

[Cites] J Biol Chem. 2008 Nov 21;283(47):32158-61 [18829459.001]

[Cites] Anal Chem. 2000 Jul 15;72(14):3311-9 [10939405.001]

(PMID = 19556245.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA140522

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

[Publication-country] United States

[Chemical-registry-number] 0 / ASH2L protein, human; 0 / DNA-Binding Proteins; 0 / DPY30 protein, human; 0 / Histones; 0 / MLL protein, human; 0 / Multiprotein Complexes; 0 / Nuclear Proteins; 0 / RBP5 protein, human; 0 / Retinol-Binding Proteins, Cellular; 0 / Transcription Factors; 0 / WDR5 protein, human; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; K3Z4F929H6 / Lysine

[Other-IDs] NLM/ PMC2782018

   

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

Proteolysis of alpha- and beta2-adaptins, as well as the accessory clathrin adaptors epsin 1, adaptor protein 180, and the clathrin assembly lymphoid myeloid leukemia protein, was detected in brain tissues after experimentally induced ischemia and in cases of human Alzheimer disease.

[MeSH-major] Adaptor Protein Complex alpha Subunits / metabolism. Adaptor Protein Complex beta Subunits / metabolism. Alzheimer Disease / metabolism. Brain / metabolism. Calpain / metabolism. Clathrin / metabolism. Endocytosis. Neurons / metabolism

[MeSH-minor] Adaptor Proteins, Vesicular Transport. Animals. Brain Ischemia / genetics. Brain Ischemia / metabolism. Brain Ischemia / pathology. Calcium / metabolism. Cell Line. Cell Membrane / genetics. Cell Membrane / metabolism. Cell Membrane / pathology. Female. Glutamic Acid / metabolism. Humans. Hydrolysis. Male. Membrane Lipids / genetics. Membrane Lipids / metabolism. Monomeric Clathrin Assembly Proteins / genetics. Monomeric Clathrin Assembly Proteins / metabolism. Rats. Rats, Sprague-Dawley. Rats, Wistar

MedlinePlus Health Information. consumer health - Alzheimer's Disease.

Hazardous Substances Data Bank. GLUTAMIC ACID HYDROCHLORIDE .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Physiol Rev. 1999 Oct;79(4):1431-568 [10508238.001]

[Cites] Neurology. 1999 Apr 12;52(6):1158-65 [10214737.001]

[Cites] Mol Cell. 2005 May 27;18(5):519-31 [15916959.001]

[Cites] Neuron. 2005 Aug 18;47(4):487-94 [16102532.001]

[Cites] Neuron. 2005 Sep 15;47(6):845-57 [16157279.001]

[Cites] Nat Immunol. 2005 Oct;6(10):1020-8 [16170319.001]

[Cites] Neurobiol Dis. 2005 Dec;20(3):785-98 [16006135.001]

[Cites] Neuroscience. 2006 May 12;139(2):577-95 [16504408.001]

[Cites] J Neuropathol Exp Neurol. 2006 Mar;65(3):278-88 [16651889.001]

[Cites] FEBS J. 2006 Aug;273(15):3437-43 [16884489.001]

[Cites] J Biol Chem. 2006 Sep 22;281(38):28079-89 [16864575.001]

[Cites] PLoS Biol. 2006 Sep;4(9):e262 [16903783.001]

[Cites] Neuroscience. 1999;94(2):389-94 [10579202.001]

[Cites] Hum Gene Ther. 2000 Jan 1;11(1):179-90 [10646649.001]

[Cites] Neurosci Lett. 2000 Jun 2;286(2):149-53 [10825658.001]

[Cites] EMBO J. 2000 Aug 15;19(16):4216-27 [10944104.001]

[Cites] Annu Rev Biochem. 2000;69:699-727 [10966473.001]

[Cites] Exp Cell Res. 2000 Nov 25;261(1):260-70 [11082296.001]

[Cites] Neuroreport. 2000 Dec 18;11(18):4007-11 [11192619.001]

[Cites] Exp Neurol. 2001 Jul;170(1):27-35 [11421581.001]

[Cites] Exp Mol Med. 2001 Dec 31;33(4):245-50 [11795487.001]

[Cites] J Neurosci. 2002 Jun 15;22(12):4842-9 [12077181.001]

[Cites] J Cell Biol. 2002 Jun 24;157(7):1197-209 [12070131.001]

[Cites] Cell. 2002 May 17;109(4):523-35 [12086608.001]

[Cites] J Neurosci. 2003 May 15;23(10):4081-91 [12764095.001]

[Cites] Physiol Rev. 2003 Jul;83(3):731-801 [12843408.001]

[Cites] J Cell Biol. 2003 Sep 1;162(5):909-18 [12952941.001]

[Cites] Neuropharmacology. 2003 Nov;45(6):729-37 [14529712.001]

[Cites] Mol Cell Biol. 2004 Mar;24(6):2499-512 [14993287.001]

[Cites] Trends Cell Biol. 2004 Apr;14(4):167-74 [15066634.001]

[Cites] J Biol Chem. 2004 May 14;279(20):20775-85 [14988399.001]

[Cites] Eur J Biochem. 1995 May 15;230(1):25-31 [7601107.001]

[Cites] J Neurotrauma. 1997 Mar;14(3):121-34 [9104930.001]

[Cites] Mol Cell Biol. 1997 May;17(5):2806-15 [9111352.001]

[Cites] Neurosci Lett. 1998 May 29;248(2):109-12 [9654354.001]

[Cites] Stroke. 1998 Jul;29(7):1454-60; discussion 1461 [9660403.001]

[Cites] J Cell Physiol. 1999 Mar;178(3):311-9 [9989777.001]

[Cites] Mol Biol Cell. 2006 Dec;17(12):5298-308 [17035630.001]

[Cites] Neuron. 2007 Feb 1;53(3):399-412 [17270736.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Feb 20;104(8):2991-6 [17289840.001]

[Cites] J Physiol. 2007 Apr 1;580(Pt 1):241-54 [17234699.001]

[Cites] Mol Ther. 2007 May;15(5):903-11 [17375066.001]

[Cites] EMBO J. 2007 Jun 20;26(12):2981-90 [17541403.001]

[Cites] J Neurochem. 2007 Aug;102(3):789-800 [17437546.001]

[Cites] Nature. 2007 Aug 23;448(7156):883-8 [17713526.001]

[Cites] Prog Neurobiol. 2000 Oct;62(3):273-95 [10840150.001]

[Cites] EMBO J. 2004 Nov 10;23(22):4371-83 [15496985.001]

(PMID = 19240038.001).

[ISSN] 0021-9258

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

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

[Publication-country] United States

[Chemical-registry-number] 0 / Adaptor Protein Complex alpha Subunits; 0 / Adaptor Protein Complex beta Subunits; 0 / Adaptor Proteins, Vesicular Transport; 0 / Clathrin; 0 / Membrane Lipids; 0 / Monomeric Clathrin Assembly Proteins; 0 / PICALM protein, human; 0 / Picalm protein, rat; 0 / epsin; 3KX376GY7L / Glutamic Acid; EC 3.4.22.- / Calpain; SY7Q814VUP / Calcium

[Other-IDs] NLM/ PMC2673311

   

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

[Title] [Clinical study on prognosis of acute leukemia subtypes Ly + AML and My + ALL].

The purpose of this study was to investigate the prognosis of acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL), lymphoid antigen-positive acute myeloid leukemia (Ly + AML), myeloid antigen-positive acute leukemia (My + ALL) and biphenotypic acute leukemia (BAL).

Immunophenotyping was performed on medullary specimens of 197 acute leukemia (AL) patients by using three-color flow cytometry analysis and CD45/SSC gating.

The results showed that in Ly + AML, CD7 was the most common (53.8%) as compared to other lymphoid markers, however, in My + ALL CD13 was the most common (47.2%) as compared to other myeloid markers.

It is concluded that since Ly + AML has lymphoid markers, and the prognosis of Ly + AML is worse than AML, the clinical therapy for Ly + AML should contain both AML and ALL.

Though My + ALL had myeloid markers, no significant difference was found between My + ALL and ALL, it might be supposed that their therapy could be the same.

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

(PMID = 17493361.001).

[ISSN] 1009-2137

[Journal-full-title] Zhongguo shi yan xue ye xue za zhi

[ISO-abbreviation] Zhongguo Shi Yan Xue Ye Xue Za Zhi

[Language] CHI

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD34; 0 / Antigens, CD7; EC 3.4.11.2 / Antigens, CD13