Cytokine Profiles of Multiple Myeloma and Waldenström Macroglobulinemia
Authors:
L. Sedlaříková 1,2; K. Sadílková 1; L. Kubiczková 1,2; R. Hájek 1,2; S. Ševčíková 1,2
Authors place of work:
Babákova myelomová skupina, Ústav patologické fyziologie, LF MU, Brno
1; Oddělení klinické hematologie, FN Brno
2
Published in the journal:
Klin Onkol 2014; 27(1): 18-23
Category:
Review
Summary
Multiple myeloma (MM) and Waldenström macroglobulinemia (WM) are malignant disorders of B lymphocytes. These diseases are characterized by monoclonal immunoglobulin production and bone marrow infiltration, which further lead to disease manifestation mainly via osteolytic lesions and disruption of hematopoiesis. The bone marrow microenvironment plays a crucial role in pathogenesis of both of these diseases, as it is well known that interaction between malignant cells and bone marrow cells facilitates both survival and growth of these tumor cells. The interactions are mediated by several different factors, including cytokines. Their production leads to tumor cell growth, proliferation and survival contributing to pathogenesis of MM and WM. In this review, we focus on function of the most important cytokines in both these diseases.
Key words:
multiple myeloma − Waldenström macroglobulinemia – cytokines − bone marrow microenvironment
This study was supported by scientific programs of the Ministry of Education, Youth and Sports MSM0021622434, by grant of Integral Grant Agency of the Czech ministry of Health NT14575 and NT12130 and by internal grant MUNI/11//InGA17/2012. Further it was supported by project of the Ministry of Health for conceptual development of research organization 65269705 (UH Brno).
The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study.
The Editorial Board declares that the manuscript met the ICMJE “uniform requirements” for biomedical papers.
Submitted:
5. 9. 2013
Accepted:
7. 11. 2013
Zdroje
1. Hájek R, Krejčí M, Pour L et al. Multiple myeloma. Klin Onkol 2011; 24 (Suppl 1): S10– S13.
2. Adam Z, Smardová J, Scudla V. Waldenströmova makroglobulinemie: klinické projevy a diferenciální diagnostika a prognóza nemoci. Vnitr Lek 2007; 53(12): 1325– 1337.
3. Balakumaran A, Robey PG, Fedarko N et al. Bone marrow microenvironment in myelomagenesis: its potential role in early diagnosis. Expert Rev Mol Diagn 2010; 10(4): 465– 480.
4. Haas HS, Schauenstein K. Neuroimmunomodulation via limbic structures – the neuroanatomy of psychoimmunology. Prog Neurobiol 1997; 51(2): 195– 222.
5. Negus RP, Balkwill FR. Cytokines in tumour growth, migration and metastasis. World J Urol 1996; 14(3): 157– 165.
6. Naugler WE, Karin M. The wolf in sheep‘s clothing: the role of interleukin‑6 in immunity, inflammation and cancer. Trends Mol Med 2008; 14(3): 109– 119.
7. Mitsiades CS, Mitsiades N, Munshi NC et al. Focus on multiple myeloma. Cancer Cell 2004; 6(5): 439– 444.
8. Chng, WJ, Schop RF, Price‑ Troska T et al. Gene‑ expression profiling of Waldenström macroglobulinemia reveals a phenotype more similar to chronic lymphocytic leukemia than multiple myeloma. Blood 2006; 108(8): 2755– 2763.
9. Uchiyama H, Barut BA, Mohrbacher AF et al. Adhesion of human myeloma‑ derived cell lines to bone marrow stromal cells stimulates interleukin‑6 secretion. Blood 1993; 82(12): 3712– 3720.
10. Dankbar B, Padró T, Leo R et al. Vascular endothelial growth factor and interleukin‑6 in paracrine tumor‑ stromal cell interactions in multiple myeloma. Blood 2000; 95(8): 2630– 2636.
11. Jourdan M, Mahtouk K, Veyrune JL et al. Delineation of the roles of paracrine and autocrine interleukin‑6 (IL‑6) in myeloma cell lines in survival versus cell cycle. A possible model for the cooperation of myeloma cell growth factors. Eur Cytokine Netw 2005; 16(1): 57– 64.
12. Abildgaard N, Glerup H, Rungby J et al. Biochemical markers of bone metabolism reflect osteoclastic and osteoblastic activity in multiple myeloma. Eur J Haematol 2000; 64(2): 121.
13. Hatzimichael EC, Christou L, Bai M et al. Serum levels of IL‑6 and its soluble receptor (sIL‑6R) in Waldenström‘s macroglobulinemia. Eur J Haematol 2001; 66(1): 1– 6.
14. Blanchard F, Duplomb L, Baud’huin M et al. The dual role of IL‑6‑type cytokines on bone remodeling and bone tumors. Cytokine Growth Factor Rev 2009; 20(1): 19– 28.
15. Elsawa SF, Novak AJ, Ziesmer SC et al. Comprehensive analysis of tumor microenvironment cytokines in Waldenstrom macroglobulinemia identifies CCL5 as a novel modulator of IL‑6 activity. Blood 2011; 118(20): 5540– 5549.
16. Boyce BF, Xing L. The RANKL/ RANK/ OPG pathway. Curr Osteoporos Rep 2007; 5(3): 98– 104.
17. Corso A, Dovio A, Rusconi C et al. Osteoprotegerin serum levels in multiple myeloma and MGUS patients compared with age‑ and sex‑ matched healthy controls. Leukemia 2004; 18(9): 1555– 1557.
18. Terpos E, Szydlo R, Apperley JF et al. Soluble receptor activator of nuclear factor kappaB ligand‑ osteoprotegerin ratio predicts survival in multiple myeloma: proposal for a novel prognostic index. Blood 2003; 102(3): 1064– 1069.
19. Marcelli C, Chappard D, Rossi JF et al. Histologic evidence of an abnormal bone remodeling in B‑ cell malignancies other than multiple myeloma. Cancer 1988; 62(6): 1163– 1170.
20. Terpos E, Anagnostopoulos A, Kastritis E et al. Abnormal bone remodelling and increased levels of macrophage inflammatory protein‑1 alpha (MIP‑1alpha) in Waldenström macroglobulinaemia. Br J Haematol 2006; 133(3): 301– 304.
21. Terpos E, Tasidou A, Eleftherakis‑ Papaiakovou E et al. Expression of CCL3 by neoplastic cells in patients with Waldenström‘s macroglobulinemia: an immunohistochemical study in bone marrow biopsies of 67 patients. Clin Lymphoma Myeloma Leuk 2011; 11(1): 115– 117.
22. Miñano FJ, Sancibrian M, Vizcaino M at al. Macrophage inflammatory protein‑1: unique action on the hypothalamus to evoke fever. Brain Res Bull 1990; 24(6): 849– 852.
23. Kukita T, Nomiyama H, Ohmoto Y et al. Macrophage inflammatory protein‑1α (LD78) expressed in human bone marrow: its role in regulation of hematopoiesis and osteoclast recruitment. Lab Invest 1997; 76(3): 399– 406.
24. Uneda S, Hata H, Matsuno F et al. Macrophage inflammatory protein‑1 alpha is produced by human multiple myeloma (MM) cells and its expression correlates with bone lesions in patients with MM. Br J Haematol 2003; 120(1): 53– 55.
25. Michigami T, Shimizu N, Williams PJ et al. Cell‑ cell contact between marrow stromal cells and myeloma cells via VCAM‑1 and α4β1- integrin enhances production of osteoclast‑ stimulating activity. Blood 2000; 96(5): 1953– 1960.
26. Vallet S, Pozzi S, Patel K et al. A novel role for CCL3 (MIP‑1α) in myeloma‑induced bone disease via osteocalcin downregulation and inhibition of osteoblast function. Leukemia 2011; 25(7): 1174– 1181. doi: 10.1038/ leu.2011.43.
27. Lentzsch S, Gries M, Janz M et al. Macrophage inflammatory protein 1‑alpha (MIP‑1 alpha) triggers migration and signaling cascades mediating survival and proliferation in multiple myeloma (MM) cells. Blood 2003; 101(9): 3568– 3573.
28. Neufeld G, Cohen T, Gengrinovitch S et al. Vascular endothelial growth factor (VEGF) and its receptors. FASEB J1999; 13(1): 9– 22.
29. Okada F, Rak JW, Croix BS et al. Impact of oncogenes in tumor angiogenesis: mutant K‑ ras upregulation of vascular endothelial growth factor/ vascular permeability factor is necessary, but not sufficient for tumorigenicity of human colorectal carcinoma cells. Proc Natl Acad Sci USA 1998; 95(7): 3609– 3614.
30. Kumar S, Witzig TE, Timm M et al. Expression of VEGF and its receptors by myeloma cells. Leukemia 2003; 17(10): 2025– 2031.
31. Rajkumar SV, Mesa RA, Fonseca R et al. Bone marrow angiogenesis in 400 patients with monoclonal gammopathy of undetermined significance, multiple myeloma, and primary amyloidosis. Clin Cancer Res 2002; 8(7): 2210– 2216.
32. Podar K, Tai YT, Davies FE et al. Vascular endothelial growth factor triggers signaling cascades mediating multiple myeloma cell growth and migration. Blood 2001; 98(2): 428– 435.
33. Marković O, Marisavljević D, Čemerikić V et al. Expression of VEGF and microvessel density in patients with multiple myeloma: clinical and prognostic significance. Med Oncol 2008; 25(4): 451– 457.
34. Podar K, Anderson K. The pathophysiologic role of VEGF in hematologic malignancies: therapeutic implication. Blood 2005; 105(4): 1383– 1395.
35. Nakagawa M, Kaneda T, Arakawa T et al. Vascular endothelial growth factor (VEGF) directly 51 enhances osteoclastic bone resorption and survival of mature osteoclasts. FEBS Lett 2000; 473(2): 161– 164.
36. Anagnostopoulos A, Eleftherakis‑ Papaiakovou V, Kastritis E et al. Serum concentrations of angiogenic cytokines in Waldenstrom macroglobulinaemia: the ratio of angiopoietin‑1 to angiopoietin‑2 and angiogenin correlate with disease severity. Br J Haematol 2007; 137(6): 560– 568.
37. Kumar S, Witzig TE, Timm M et al. Bone marrow angiogenic ability and expression of angiogenic cytokines in myeloma: evidence favoring loss of marrow angiogenesis inhibitory aktivity with disease progression. Blood 2004; 104(4): 1159– 1165.
38. Rinderknecht E, Humbel RE. The amino acid sequence of human insulin like growth factor I and its structural homology, with proinsulin. J Biol Chem 1978; 253(8): 2769– 2776.
39. Menu E, van Valckenborgh E, van Camp B et al. The role of the insulin‑like growth factor 1 receptor axis in multiple myeloma. Arch Physiol Biochem 2009; 115(2): 49– 57.
40. Qiang YW, Yao L, Tosato G et al. Insulin‑like growth factor I induces migration and invasion of human multiple myeloma cells. Blood 2004; 103(1): 301– 308.
41. Standal T, Borset M, Lenhoff S et al. Serum insulin-like growth factor is not elevated in patients with multiple myeloma but is still a prognostic factor. Blood 2002; 100(12): 3925– 3929.
42. Leleu X, Jia X, Runnels J et al. The Akt pathway regulates survival and homing in Waldenstrom macroglobulinemia. Blood 2007; 110(13): 4417– 4426.
43. Schneider P, MacKay F, Steiner V et al. BAFF, a novel ligand of the tumor necrosis factor family, stimulates B cell growth. J Exp Med 1999; 189(11): 1747– 1756.
44. Mackay F, Schneider P, Rennert P et al. BAFF AND APRIL: a tutorial on B cell survival. Annu Rev Immunol 2003; 21: 231– 264.
45. Xu G, Shen XJ, Pu J et al. BLyS expression and JNK activation may form a feedback loop to promote survival and proliferation of multiple myeloma cells. Cytokine 2012; 60(2): 505– 513.
46. Gross JA, Johnston J, Mudri S et al. TACI and BCMA are receptors for a TNF homologue implicated in B‑ cell autoimmune disease. Nature 2000; 404(6781): 995– 999.
47. Thompson JS, Bixler SA, Qian F et al. BAFF‑ R, a newly identified TNF receptor that specifically interacts with BAFF. Science 2001; 293(5537): 2108– 2111.
48. Hahne M, Kataoka T, Schröter et al. APRIL, a new ligand of the tumor necrosis factor family, stimulans tumor cell growth. J Exp Med 1998; 188(6): 1185– 1190.
49. Novak AJ, Darce JR, Arendt BK et al. Expression of BCMA, TACI, and BAFF‑ R in multiple myeloma: a mechanism for growth and survival. Blood 2004; 103(2): 689– 694.
50. Hideshima T, Anderson KC. Molecular mechanisms of novel therapeutic approaches for multiple myeloma. Nat Rev Cancer 2002; 2(12): 927– 937.
51. Elsawa SF, Novak AJ, Grote DM et al. B‑lymphocyte stimulator (BlyS) stimulates immunoglobulin production and malignant B‑ cell growth in Waldenström macroglobulinemia. Blood 2006; 107: 2882– 2888.
52. Cohen S, Shachar I. Cytokines as regulators of proliferation and survival of healthy and malignant peripheral B cells. Cytokine 2012; 60(1): 13– 22. doi: 10.1016/ j.cyto.2012.06.019.
53. Derksen PW, de Gorter DJ, Meijer HP et al. The hepatocyte growth factor/ Met pathway controls proliferation and apoptosis in multiple myeloma. Leukemia 2003; 17(4): 764– 774.
54. Mahtouk K, Tjin EP, Spaargaren M et al. The HGF/ MET pathway as target for the treatment of multiple myeloma and B‑ cell lymphomas. Biochim Biophys Acta 2010; 1806(2): 208– 219. doi: 10.1016/ j.bbcan.2010.07.006.
55. Hov H, Holt RU, Rø TB et al. A selective c‑ met inhibitor blocks an autocrine hepatocyte growth factor growth loop in ANBL‑ 6 cells and prevents migration and adhesion of myeloma cells. Clin Cancer Res 2004; 10(19): 6686– 6694.
56. Du W, Hattori Y, Yamada T et al. NK4, an antagonist of hepatocyte growth factor (HGF), inhibits growth of multiple myeloma cells: molecular targeting of angiogenic growth factor. Blood 2007; 109(7): 3042– 3049.
57. Seidel C, Børset M, Turesson I et al. Elevated serum concentrations of hepatocyte growth factor in patients with multiple myeloma. The Nordic Myeloma Study Group. Blood 1998; 91(3): 806– 812.
58. Alexandrakis MG, Passam FH, Sfiridaki A et al. Elevated serum concentration of hepatocyte growth factor in patients with multiple myeloma: correlation with markers of disease activity. Am J Hematol 2003; 72(4): 229– 233.
59. Hov H, Tian E, Holien T et al. c‑ Met signaling promotes IL‑6‑induced myeloma cell proliferation. Eur J Haematol 2009; 82(4): 277– 287. doi: 10.1111/ j.1600– 0609.2009.01212.
60. Standal T, Abildgaard N, Fagerli UM et al. HGF inhibits BMP‑induced osteoblastogenesis: possible implications for the bone disease of multiple myeloma. Blood 2007; 109(7): 3024– 3030.
61. Holt RU, Baykov V, Rø TB et al. Human myeloma cells adhere to fibronectin in response to hepatocyte growth factor. Haematologica 2005; 90(4): 479– 488.
62. Minarik J, Pika T, Bacovsky J et al. Prognostic value of hepatocyte growth factor, syndecan‑ 1, and osteopontin in multiple myeloma and monoclonal gammopathy of undetermined significance. ScientificWorldJournal 2012; 2012: 356128. doi: 10.1100/ 2012/ 356128.
63. Scudla V, Budíková M, Petrová P et al. Analýza sérových hladin vybraných bio logických ukazatelů u monoklonální gamapatie nejistého významu a mnohočetného myelomu. Klin Onkol 2010; 23(3): 171– 181.
64. Pour L, Svachova H, Adam Z et al. Levels of angiogenic factors in patients with multiple myeloma correlate with treatment response. Ann Hematol 2010; 89(4): 385– 389. doi: 10.1007/ s00277– 009– 0834– 3.
65. Pour L, Svachova H, Adam Z et al. Pretreatment hepatocyte growth factor and thrombospondin‑1 levels predict response to high‑dose chemotherapy for multiple myeloma. Neoplasma 2010; 57(1): 29– 34.
66. Pour L, Svachova H, Adam Z et al. Treatment response to bortezomib in multiple myeloma correlates with plasma hepatocyte growth factor concentration and bone marrow thrombospondin concentration. Eur J Haematol 2010; 84(4): 332– 336. doi: 10.1111/ j.1600– 0609.2009.01396.x.
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