Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

MeSH Review:

Leukemia, Promyelocytic, Acute

Asou, N. et al., Boss, M.A. et al., Gianní, M. et al., Ledbetter, D.H. et al., Bocchia, M. et al., et al.

Koyama, Shibakura, Ohsawa, Kamiyama, Hirosawa, P. Demmer, Westervelt, Brown, Adkins, Khoury, Curtin, Hurd, Luger, Ma, Ley, DiPersio, Lo Coco, Diverio, Avvisati, Petti, Meloni, Pogliani, Biondi, Rossi, Carlo-Stella, Selleri, Martino, Specchia, Mandelli, Douer, Estey, Santillana, Bennett, Lopez-Bernstein, Boehm, Williams, Park, Chumakov, Vuong, Chih, Gombart, Miller, Koeffler,

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Leukemia, Promyelocytic, Acute

We show that in both acute promyelocytic leukemia and breast cancer cells the retinoic acid (RA) and interferon signaling pathways converge on the promoter of the tumoricidal death ligand TRAIL [1].
Arsenic trioxide has been shown to be effective in treating acute promyelocytic leukemia (APL), with minimal overall toxicity reported to date [2].
A novel intravenous liposomal formulation of all-trans retinoic acid (ATRA) was evaluated in 69 patients with acute promyelocytic leukemia (APL): 32 new diagnoses, 35 relapses, and 2 oral ATRA failures [3].
The role of heparin in the treatment of the disseminated intravascular coagulation (DIC) associated with acute promyelocytic leukemia (APL) remains unclear [4].
The ability of a series of synthetic peptides corresponding to the junctional sequences of chronic myelogenous leukemia (CML)-derived bcr-abl and acute promyelocytic leukemia (APL)-derived PML-RAR alpha fusion proteins to bind to purified class I molecules was studied [5].

High impact information on Leukemia, Promyelocytic, Acute

In line with this, both RNAi against NFI-A and ectopic expression of miR-223 in acute promyelocytic leukemia (APL) cells enhance differentiation, whereas miR-223 knockdown inhibits the differentiation response to RA [6].
The fusion protein PML-RARalpha, generated by the t(15;17)(q22;q11.2) translocation associated with acute promyelocytic leukemia (APL), initiates APL when expressed in the early myeloid compartment of transgenic mice [7].
The PML gene, involved in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL), encodes a protein which localizes to the PML-nuclear body, a subnuclear macromolecular structure [8].
BACKGROUND: Two reports from China have suggested that arsenic trioxide can induce complete remissions in patients with acute promyelocytic leukemia (APL) [9].
The promyelocytic leukemia-retinoic acid receptor alpha (PML-RARalpha) protein of acute promyelocytic leukemia (APL) is oncogenic in vivo [10].

Chemical compound and disease context of Leukemia, Promyelocytic, Acute

Rearrangements and aberrant expression of the retinoic acid receptor alpha gene in acute promyelocytic leukemias [11].
BACKGROUND: All-trans-retinoic acid (all-trans RA) induces complete remission in most patients with acute promyelocytic leukemia (APL) [12].
We show that it was rapidly induced in the acute promyelocytic leukemia (APL) cell line NB4 during granulocytic differentiation after exposure to retinoic acid (RA) [13].
We recently found that retinoids, which are vitamin A derivatives, exert anticoagulant effects by upregulating thrombomodulin (TM) and downregulating tissue factor (TF) expression in acute promyelocytic leukemia cells and monoblastic leukemia cells [14].
Arsenic compounds have recently been shown to induce high rates of complete remission in patients with acute promyelocytic leukemia (APL) [15].

Biological context of Leukemia, Promyelocytic, Acute

We investigated the effect of the acute promyelocytic leukemia (APL) specific PML/RARalpha fusion protein on the sensitivity to TNF-alpha-mediated apoptosis [16].
We have previously shown that transgenic mice expressing PML-RARalpha (PR) and RARalpha-PML frequently develop acute promyelocytic leukemia (APL) in association with a large (>20 Mb) interstitial deletion of chromosome 2 that includes PU [17].
The gene cluster including ErbA1 is known to be flanked by the constitutional 15;17 translocation breakpoint in hybrid SP3 and by the acute promyelocytic leukemia (APL) breakpoint, which provides the following gene and breakpoint order: cen-SP3-(D17S33,CRYB1)-NF1-(CSF3,ERBA1, ERBB2)-APL-tel [18].
The cell surface antigenic phenotype of HL-60, a human acute promyelocytic leukemia cell line, has been analyzed before and after maturation induction with dimethylsulfoxide (DMSO) using a panel of markers including a "library" of monoclonal antibodies and "conventional" antisera in conjunction with the fluorescene-activated cell sorter [19].
Analysis of a variant translocation t(11;17) in a case of acute promyelocytic leukemia (APL) led to discovery of a novel zinc finger gene, PLZF, fused to the retinoic acid receptor-alpha (RAR alpha) gene [20].

Anatomical context of Leukemia, Promyelocytic, Acute

Treatment of acute promyelocytic leukemia (APL) blasts with cyclic adenosine monophosphate (cAMP) analogs, in combination with all-trans retinoic acid (ATRA), results in the upregulation of the expression of leukocyte alkaline phosphatase (LAP), a marker for the differentiation of the granulocyte [21].
The hierarchical level of stem cell involvement in acute promyelocytic leukemia (APL) characterized by the pathognomonic PML-RARA fusion gene is unknown [22].
Several lines of investigation suggest that granulocyte colony-stimulating factor (G-CSF) augments all-trans retinoic acid (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL) [23].
Transgenic mice expressing PML-RARalpha in early myeloid cells under control of human cathepsin G regulatory sequences all develop a myeloproliferative syndrome, but only 15% to 20% develop acute promyelocytic leukemia (APL) after a latent period of 6 to 14 months [24].
Previously we demonstrated that this region of FN mediated binding of FN to HL-60 cells (acute promyelocytic leukemia cell line) by direct interaction independently of RGD and CS1 [H. Fujita et al., (1995) Exp. Cell Res. 217, 484-488] [25].

Gene context of Leukemia, Promyelocytic, Acute

A unique mRNA produced in leukemic cells from a t(15;17) acute promyelocytic leukemia (APL) patient encodes a fusion protein between the retinoic acid receptor alpha (RAR alpha) and a myeloid gene product called PML [26].
Acute promyelocytic leukemia (APL) is typified by the t(15;17), generating the PML-RAR alpha fusion and predicting a beneficial response to retinoids [27].
The prognostic significance of FLT3 mutations in acute promyelocytic leukemia (APL) is not firmly established and is of particular interest given the opportunities for targeted therapies using FLT3 inhibitors [28].
Here, we report that annexin II, a surface phospholipid-binding protein and one of the proposed causes of the hemorrhagic complications of acute promyelocytic leukemia (APL), is also implicated in t(17;19)+ ALL [29].
The promyelocytic leukemia (PML) gene, a tumor suppressor inactivated in acute promyelocytic leukemia (APL), regulates apoptosis induced by DNA damage [30].

Analytical, diagnostic and therapeutic context of Leukemia, Promyelocytic, Acute

All transretinoic acid (ATRA) followed by daunorubicin (DNR)-AraC chemotherapy (CT) has improved the outcome of acute promyelocytic leukemia (APL) by comparison to CT alone [31].
For the acute promyelocytic leukemia cell line NB4, C/EBP epsilon was the only C/EBP family member that was easily detected by RT-PCR [32].
Fourteen patients with PML/RARalpha-positive acute promyelocytic leukemia (APL) were given salvage therapy at the time of first molecular relapse [33].
Signal transducer and activator of transcription (STAT) 5b-retinoic acid receptor (RAR) alpha is the fifth fusion protein identified in acute promyelocytic leukemia (APL) [34].
PURPOSE: We conducted a multicenter study of differentiation therapy with all-trans retinoic acid (ATRA) followed by intensive chemotherapy in patients with newly diagnosed acute promyelocytic leukemia (APL) and analyzed the prognostic factors for predicting complete remission (CR), event-free survival (EFS), and disease-free survival (DFS) [35].
Targeting of the oligomerization of PML-RARalpha through coiled-coil-domain (PCC) peptides leads to an inhibition of the leukemic phenotype and is accompanied by protein degradation that efficiently destroys the oncogenicity of the fusion protein [36].

References

Tumor suppressor IRF-1 mediates retinoid and interferon anticancer signaling to death ligand TRAIL. Clarke, N., Jimenez-Lara, A.M., Voltz, E., Gronemeyer, H. EMBO J. (2004) [Pubmed]
Sudden death among patients with acute promyelocytic leukemia treated with arsenic trioxide. Westervelt, P., Brown, R.A., Adkins, D.R., Khoury, H., Curtin, P., Hurd, D., Luger, S.M., Ma, M.K., Ley, T.J., DiPersio, J.F. Blood (2001) [Pubmed]
Treatment of newly diagnosed and relapsed acute promyelocytic leukemia with intravenous liposomal all-trans retinoic acid. Douer, D., Estey, E., Santillana, S., Bennett, J.M., Lopez-Bernstein, G., Boehm, K., Williams, T. Blood (2001) [Pubmed]
Is heparin administration necessary during induction chemotherapy for patients with acute promyelocytic leukemia? Goldberg, M.A., Ginsburg, D., Mayer, R.J., Stone, R.M., Maguire, M., Rosenthal, D.S., Antin, J.H. Blood (1987) [Pubmed]
Specific binding of leukemia oncogene fusion protein peptides to HLA class I molecules. Bocchia, M., Wentworth, P.A., Southwood, S., Sidney, J., McGraw, K., Scheinberg, D.A., Sette, A. Blood (1995) [Pubmed]
A minicircuitry comprised of microRNA-223 and transcription factors NFI-A and C/EBPalpha regulates human granulopoiesis. Fazi, F., Rosa, A., Fatica, A., Gelmetti, V., De Marchis, M.L., Nervi, C., Bozzoni, I. Cell (2005) [Pubmed]
Neutrophil elastase cleaves PML-RARalpha and is important for the development of acute promyelocytic leukemia in mice. Lane, A.A., Ley, T.J. Cell (2003) [Pubmed]
The role of PML in tumor suppression. Salomoni, P., Pandolfi, P.P. Cell (2002) [Pubmed]
Complete remission after treatment of acute promyelocytic leukemia with arsenic trioxide. Soignet, S.L., Maslak, P., Wang, Z.G., Jhanwar, S., Calleja, E., Dardashti, L.J., Corso, D., DeBlasio, A., Gabrilove, J., Scheinberg, D.A., Pandolfi, P.P., Warrell, R.P. N. Engl. J. Med. (1998) [Pubmed]
In vivo analysis of the role of aberrant histone deacetylase recruitment and RAR{alpha} blockade in the pathogenesis of acute promyelocytic leukemia. Matsushita, H., Scaglioni, P.P., Bhaumik, M., Rego, E.M., Cai, L.F., Majid, S.M., Miyachi, H., Kakizuka, A., Miller, W.H., Pandolfi, P.P. J. Exp. Med. (2006) [Pubmed]
Rearrangements and aberrant expression of the retinoic acid receptor alpha gene in acute promyelocytic leukemias. Longo, L., Pandolfi, P.P., Biondi, A., Rambaldi, A., Mencarelli, A., Lo Coco, F., Diverio, D., Pegoraro, L., Avanzi, G., Tabilio, A. J. Exp. Med. (1990) [Pubmed]
Constitutive variability in the pharmacokinetics of the natural retinoid, all-trans-retinoic acid, and its modulation by ketoconazole. Rigas, J.R., Francis, P.A., Muindi, J.R., Kris, M.G., Huselton, C., DeGrazia, F., Orazem, J.P., Young, C.W., Warrell, R.P. J. Natl. Cancer Inst. (1993) [Pubmed]
CCAAT/enhancer binding protein epsilon is a potential retinoid target gene in acute promyelocytic leukemia treatment. Park, D.J., Chumakov, A.M., Vuong, P.T., Chih, D.Y., Gombart, A.F., Miller, W.H., Koeffler, H.P. J. Clin. Invest. (1999) [Pubmed]
Anticoagulant effects of 1alpha,25-dihydroxyvitamin D3 on human myelogenous leukemia cells and monocytes. Koyama, T., Shibakura, M., Ohsawa, M., Kamiyama, R., Hirosawa, S. Blood (1998) [Pubmed]
Phenylarsine oxide blocks interleukin-1beta-induced activation of the nuclear transcription factor NF-kappaB, inhibits proliferation, and induces apoptosis of acute myelogenous leukemia cells. Estrov, Z., Manna, S.K., Harris, D., Van, Q., Estey, E.H., Kantarjian, H.M., Talpaz, M., Aggarwal, B.B. Blood (1999) [Pubmed]
The PML/RARalpha fusion protein inhibits tumor necrosis factor-alpha-induced apoptosis in U937 cells and acute promyelocytic leukemia blasts. Testa, U., Grignani, F., Samoggia, P., Zanetti, C., Riccioni, R., Lo Coco, F., Diverio, D., Felli, N., Passerini, C.G., Grell, M., Pelicci, P.G., Peschle, C. J. Clin. Invest. (1998) [Pubmed]
Reduced PU.1 expression causes myeloid progenitor expansion and increased leukemia penetrance in mice expressing PML-RARalpha. Walter, M.J., Park, J.S., Ries, R.E., Lau, S.K., McLellan, M., Jaeger, S., Wilson, R.K., Mardis, E.R., Ley, T.J. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
Precise localization of NF1 to 17q11.2 by balanced translocation. Ledbetter, D.H., Rich, D.C., O'Connell, P., Leppert, M., Carey, J.C. Am. J. Hum. Genet. (1989) [Pubmed]
Differentiation-linked expression of cell surface markers on HL-60 leukemic cells. Boss, M.A., Delia, D., Robinson, J.B., Greaves, M.F. Blood (1980) [Pubmed]
Clinical and molecular characterization of a rare syndrome of acute promyelocytic leukemia associated with translocation (11;17). Licht, J.D., Chomienne, C., Goy, A., Chen, A., Scott, A.A., Head, D.R., Michaux, J.L., Wu, Y., DeBlasio, A., Miller, W.H. Blood (1995) [Pubmed]
All-trans retinoic acid and cyclic adenosine monophosphate cooperate in the expression of leukocyte alkaline phosphatase in acute promyelocytic leukemia cells. Gianní, M., Terao, M., Norio, P., Barbui, T., Rambaldi, A., Garattini, E. Blood (1995) [Pubmed]
Highly purified primitive hematopoietic stem cells are PML-RARA negative and generate nonclonal progenitors in acute promyelocytic leukemia. Turhan, A.G., Lemoine, F.M., Debert, C., Bonnet, M.L., Baillou, C., Picard, F., Macintyre, E.A., Varet, B. Blood (1995) [Pubmed]
G-CSF signaling can differentiate promyelocytes expressing a defective retinoic acid receptor: evidence for divergent pathways regulating neutrophil differentiation. Maun, N.A., Gaines, P., Khanna-Gupta, A., Zibello, T., Enriquez, L., Goldberg, L., Berliner, N. Blood (2004) [Pubmed]
High-penetrance mouse model of acute promyelocytic leukemia with very low levels of PML-RARalpha expression. Westervelt, P., Lane, A.A., Pollock, J.L., Oldfather, K., Holt, M.S., Zimonjic, D.B., Popescu, N.C., DiPersio, J.F., Ley, T.J. Blood (2003) [Pubmed]
The novel recognition site in the C-terminal heparin-binding domain of fibronectin by integrin alpha 4 beta 1 receptor on HL-60 cells. Mohri, H., Katoh, K., Iwamatsu, A., Okubo, T. Exp. Cell Res. (1996) [Pubmed]
Chromosomal translocation t(15;17) in human acute promyelocytic leukemia fuses RAR alpha with a novel putative transcription factor, PML. Kakizuka, A., Miller, W.H., Umesono, K., Warrell, R.P., Frankel, S.R., Murty, V.V., Dmitrovsky, E., Evans, R.M. Cell (1991) [Pubmed]
Characterization of acute promyelocytic leukemia cases lacking the classic t(15;17): results of the European Working Party. Groupe Français de Cytogénétique Hématologique, Groupe de Français d'Hematologie Cellulaire, UK Cancer Cytogenetics Group and BIOMED 1 European Community-Concerted Action "Molecular Cytogenetic Diagnosis in Haematological Malignancies". Grimwade, D., Biondi, A., Mozziconacci, M.J., Hagemeijer, A., Berger, R., Neat, M., Howe, K., Dastugue, N., Jansen, J., Radford-Weiss, I., Lo Coco, F., Lessard, M., Hernandez, J.M., Delabesse, E., Head, D., Liso, V., Sainty, D., Flandrin, G., Solomon, E., Birg, F., Lafage-Pochitaloff, M. Blood (2000) [Pubmed]
Relationship between FLT3 mutation status, biologic characteristics, and response to targeted therapy in acute promyelocytic leukemia. Gale, R.E., Hills, R., Pizzey, A.R., Kottaridis, P.D., Swirsky, D., Gilkes, A.F., Nugent, E., Mills, K.I., Wheatley, K., Solomon, E., Burnett, A.K., Linch, D.C., Grimwade, D. Blood (2005) [Pubmed]
Regulation of annexin II by cytokine-initiated signaling pathways and E2A-HLF oncoprotein. Matsunaga, T., Inaba, T., Matsui, H., Okuya, M., Miyajima, A., Inukai, T., Funabiki, T., Endo, M., Look, A.T., Kurosawa, H. Blood (2004) [Pubmed]
The promyelocytic leukemia protein PML regulates c-Jun function in response to DNA damage. Salomoni, P., Bernardi, R., Bergmann, S., Changou, A., Tuttle, S., Pandolfi, P.P. Blood (2005) [Pubmed]
A randomized comparison of all transretinoic acid (ATRA) followed by chemotherapy and ATRA plus chemotherapy and the role of maintenance therapy in newly diagnosed acute promyelocytic leukemia. The European APL Group. Fenaux, P., Chastang, C., Chevret, S., Sanz, M., Dombret, H., Archimbaud, E., Fey, M., Rayon, C., Huguet, F., Sotto, J.J., Gardin, C., Makhoul, P.C., Travade, P., Solary, E., Fegueux, N., Bordessoule, D., Miguel, J.S., Link, H., Desablens, B., Stamatoullas, A., Deconinck, E., Maloisel, F., Castaigne, S., Preudhomme, C., Degos, L. Blood (1999) [Pubmed]
A novel, myeloid transcription factor, C/EBP epsilon, is upregulated during granulocytic, but not monocytic, differentiation. Morosetti, R., Park, D.J., Chumakov, A.M., Grillier, I., Shiohara, M., Gombart, A.F., Nakamaki, T., Weinberg, K., Koeffler, H.P. Blood (1997) [Pubmed]
Therapy of molecular relapse in acute promyelocytic leukemia. Lo Coco, F., Diverio, D., Avvisati, G., Petti, M.C., Meloni, G., Pogliani, E.M., Biondi, A., Rossi, G., Carlo-Stella, C., Selleri, C., Martino, B., Specchia, G., Mandelli, F. Blood (1999) [Pubmed]
Interactions of STAT5b-RARalpha, a novel acute promyelocytic leukemia fusion protein, with retinoic acid receptor and STAT3 signaling pathways. Dong, S., Tweardy, D.J. Blood (2002) [Pubmed]
Analysis of prognostic factors in newly diagnosed acute promyelocytic leukemia treated with all-trans retinoic acid and chemotherapy. Japan Adult Leukemia Study Group. Asou, N., Adachi, K., Tamura, J., Kanamaru, A., Kageyama, S., Hiraoka, A., Omoto, E., Akiyama, H., Tsubaki, K., Saito, K., Kuriyama, K., Oh, H., Kitano, K., Miyawaki, S., Takeyama, K., Yamada, O., Nishikawa, K., Takahashi, M., Matsuda, S., Ohtake, S., Suzushima, H., Emi, N., Ohno, R. J. Clin. Oncol. (1998) [Pubmed]
Targeting the Acute Promyelocytic Leukemia-Associated Fusion Proteins PML/RARα and PLZF/RARα with Interfering Peptides. Beez, S., Demmer, P., Puccetti, E. PLoS. One. (2012) [Pubmed]

Contributions to this collaborative article are from individual authors of WikiGenes or mined by the WikiGenes Data Mining Engine from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.