Full-text resources of PSJD and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl

PL EN


Preferences help
enabled [disable] Abstract
Number of results

Journal

2014 | 9 | 2 | 204-209

Article title

Significance of GRP78 expression in acute myeloid leukemias

Content

Title variants

Languages of publication

EN

Abstracts

EN
The GRP78 (glucose-regulated protein 78) is a major endoplasmic reticulum (ER) chaperone facilitating proper folding of the newly synthesized proteins. By the interaction with caspases, GRP78 has antiapoptotic properties allowing cells to survive under stress condition. GRP78 expression and its association with tumor proliferation, metastasis and resistance to chemotherapy were observed in solid tumors. There are limited data on the expression and impact of this protein on the clinical course and treatment response in acute myeloid leukemia (AML). The aim of this study was to evaluate the expression of GRP78 mRNA in patients with de novo AML. These results were compared to healthy controls, blast phenotype, molecular and cytogenetic status and clinical features of AML. 101 non-M3 AML patients and 26 healthy individuals were included in this study. The expression of GRP78 mRNA in bone marrow was analyzed by real-time quantitative polymerase chain reaction (RQ-PCR). We demonstrated increased GRP78 mRNA expression in AML patients compared to healthy controls, although this difference was statistically significant only in CD34+ leukemias. There was also no significant correlation between GRP78 mRNA expression and complete remission rate, relapse-free survival and overall survival. These results indicate that GRP78 expression is increased in CD34+ leukemias and has no prognostic impact on clinical outcome in AML.

Publisher

Journal

Year

Volume

9

Issue

2

Pages

204-209

Physical description

Dates

published
1 - 4 - 2014
online
13 - 2 - 2014

Contributors

  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland
author
  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland
  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland
  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland
  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland
author
  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland
  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland
  • Department of Hematology, Blood Neoplasms and Bone Marrow Transplantation, Wroclaw Medical University, Pasteura 4 Street, 50-367, Wroclaw, Poland

References

  • [1] Christ O, Feuring-Buske M, Hiddemann W et al. Pathobiology of acute myeloid leukemia. Med Clin. 2007; 102:290–295
  • [2] Schroder M, Kauffman RJ. ER stress and the unfolded protein response. Mutat Res 2005; 569:29–63 http://dx.doi.org/10.1016/j.mrfmmm.2004.06.056[Crossref]
  • [3] Ron D, Walter P. Signal integration in the endoplasmic reticulum unfolded protein response. Nat Rev Mol Cell Biol. 2007; 8:519–529 http://dx.doi.org/10.1038/nrm2199[WoS][Crossref]
  • [4] Fu Y, Lee AS. Glucose regulated proteins in cancer progression, drug resistance and immunotherapy. Cancer Biol Ther. 2006; 5:741–744 http://dx.doi.org/10.4161/cbt.5.7.2970[Crossref]
  • [5] Bennett JM, Catovsky D, Daniel MT et al. Proposals for the classification of the acute leukaemias. A report of the French-American-British (FAB) cooperative group. Ann Intern Med. 1985;103:620–625 http://dx.doi.org/10.7326/0003-4819-103-4-620[Crossref]
  • [6] Döhner H, Estey EH, Amadori S et al. Diagnosis and management of acute myeloid leukemia in adults: recommendations from an international expert panel, on behalf of the European Leukemia Net. Blood. 2010; 115: 453–474 http://dx.doi.org/10.1182/blood-2009-07-235358[Crossref]
  • [7] Hołowiecki J, Grosicki S, Robak T et al. Polish Adult Leukemia Group (PALG). Addition of cladribine to daunorubicin and cytarabine increases complete remission rate after a single course of induction treatment in acute myeloid leukemia. Multicenter, phase III Study. Leukemia. 2004; 18:989–997 [Crossref]
  • [8] Hołowiecki J, Grosicki S, Kyrcz-Krzemien S et al. Daunorubicin, cytarabine and fludarabine (DAF) for remission induction in relapsed or refractory acute myeloid leukemia. Evaluation of safety, tolerance and early outcome-Polish Adult Leukemia Group (PALG) pilot study. Ann Hematol. 2008; 81:361–367 http://dx.doi.org/10.1007/s00277-007-0421-4[Crossref]
  • [9] Hołowiecki J, Grosicki S, Robak T et al. Daunorubicin, Cytarabine, and 2CdA (DAC-7) for remission indiction in “de novo” Adult Acute Myeloid Leukemia Patients. Acta Haematol Pol. 2001; 2002:839–847
  • [10] Yates J, Glidewell O, Wiernik P et al. Cytosine arabinoside with daunorubicin or adriamycin for therapy of acute myelocytic leukemia: a CALGB study. Blood. 1982; 60:454–462
  • [11] Wrzesień-Kus A, Robak T, Jamroziak K et al. The treatment of acute myeloid leukemia with mitoxantrone, etoposide and low-dose cytarabine in elderly patients - a report of Polish Acute Leukemia Group (PALG) phase II study. Neoplasma. 2002; 49:405–411
  • [12] Byrd JC, Mrózek K, Dodge RK et al. Cancer and Leukemia Group B(CALGB 8461). Pretreatment cytogenetic abnormalities are predictive of induction success, cumulative incidence of relapse, and overall survival in adult patients with de novo acute myeloid leukemia: results from Cancer and Leukemia Group B (CALGB 8461). Blood. 2002; 100: 4325–4336 http://dx.doi.org/10.1182/blood-2002-03-0772[Crossref]
  • [13] Castaigne S, Chevret S, Archimbaud E et al. Randomized comparison of double induction and timed-sequential induction to a “ 3+7” induction in adults with AML; long term analysis of the Acute Leukemia French Association (ALFA) 9000 study. Blood. 2004; 104: 2467–2474 http://dx.doi.org/10.1182/blood-2003-10-3561[Crossref]
  • [14] Jurisic V, Srdic-Rajic T, Konjevic G et al. TNF-α induced apoptosis is accompanied with rapid CD30 and slower CD45 shedding from K-562 cells. J Membr Biol. 2011; 239:115–122 http://dx.doi.org/10.1007/s00232-010-9309-7[WoS][Crossref]
  • [15] Xing X, Lai M, Wang Y et al. Overexpression of glucose-regulated protein 78 in colon cancer. Clin Chim Acta. 2006; 364:308–315. http://dx.doi.org/10.1016/j.cca.2005.07.016[Crossref]
  • [16] Fernandez PM, Tabbara SO, Jacobs LK et al. Overexpression of the glucose-regulated stress gene GRP78 in malignant but not benign human breast lesions. Breast Cancer Res Treat. 2000; 59:15–26 http://dx.doi.org/10.1023/A:1006332011207[Crossref]
  • [17] Arap MA, Lahdenranta J, Mintz PJ et al. Cell surface expression of the stress response chaperone GRP78 enables tumor targeting by circulating ligands. Cancer Cell. 2004; 6:275–284 http://dx.doi.org/10.1016/j.ccr.2004.08.018[Crossref]
  • [18] Uramoto H, Sugio K, Oyama T et al. Expression of endoplasmic reticulum molecular chaperone Grp78 in human lung cancer and its clinical significance. Lung Cancer. 2005; 49: 55–62 http://dx.doi.org/10.1016/j.lungcan.2004.12.011[Crossref]
  • [19] Tanimura A, Yujiri T, Tanaka Y et al. Activation of the unfolded protein response in primary acute myeloid leukemia cells. Int J Hematol. 2011; 94:300–302 http://dx.doi.org/10.1007/s12185-011-0918-4[Crossref]
  • [20] Valk PJ, Verhaak RG, Beijen MA et al. Prognostically useful gene-expression profiles in acute myeloid leukemia. N Engl J Med. 2004; 350:1617–1628 http://dx.doi.org/10.1056/NEJMoa040465[Crossref]
  • [21] Schardt JA, Weber A, Eyholzer M et al. Activation of the unfolded protein response is associated with favorable prognosis in acute myeloid leukemia. Clin Cancer Res. 2009; 15:3834–3841 http://dx.doi.org/10.1158/1078-0432.CCR-08-2870[Crossref]
  • [22] Khan MM, Nomura T, Chiba T et al. The fusion oncoprotein PML-RARalpha induces endoplasmic reticulum (ER)-associated degradation of N-CoR and ER stress. J Biol Chem. 2004; 279:11814–11824 http://dx.doi.org/10.1074/jbc.M312121200[Crossref]
  • [23] Jordan CT. The leukemic stem cell. Best Pract Res Clin Haematol 2007; 20:13–18 http://dx.doi.org/10.1016/j.beha.2006.10.005[Crossref]
  • [24] Ota J, Yamashita Y, Okawa K et al. Proteomic analysis of hematopoietic stem cell-like fractions in leukemic disorders. Oncogene. 2003; 22:5720–5728 http://dx.doi.org/10.1038/sj.onc.1206855[Crossref]
  • [25] Bagratuni T, Wu P, Gonzalez de Castro D et al. XBP1s levels are implicated in the biology and outcome of myeloma mediating different clinical outcomes to thalidomide-based treatments. Blood. 2010; 116:250–253 http://dx.doi.org/10.1182/blood-2010-01-263236[WoS][Crossref]
  • [26] Bhojwani D, Kang H, Moskowitz NP et al. Biologic pathways associated with relapse in childhood acute lymphoblastic leukemia: a Children’s Oncology Group study. Blood. 2006; 108:711–717 http://dx.doi.org/10.1182/blood-2006-02-002824[Crossref]
  • [27] Schardt JA, Mueller BU, Pabst T et al. Activation of unfolded protein response in human acute myeloid leukemia. Methods Enzymol. 2011; 489:227–243 http://dx.doi.org/10.1016/B978-0-12-385116-1.00013-3[WoS][Crossref]

Document Type

Publication order reference

Identifiers

YADDA identifier

bwmeta1.element.-psjd-doi-10_2478_s11536-013-0200-7
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.