Malignant B-cell intra-clonal diversification: Following the yarn in the labyrinth

Leukemia and Lymphoma

Volumn 52, Issue 11, 2011, Pages 2050-2056

  Nadav Dagan, Liat ^a   Katz, Ben Zion ^b,c  

^a UNIVERSITY OF MIAMI MILLER SCHOOL OF MEDICINE   (United States)

^b TEL AVIV SOURASKY MEDICAL CENTER   (Israel)

^c TEL AVIV UNIVERSITY   (Israel)

Author keywords

B cell; Cell population; Genes

Indexed keywords

IMMUNOGLOBULIN;

ACUTE LYMPHOBLASTIC LEUKEMIA; B CELL MALIGNANCY; B LYMPHOCYTE; BONE MARROW; BURKITT LYMPHOMA; CLONAL VARIATION; COPY NUMBER VARIATION; FOLLICULAR LYMPHOMA; GENE REARRANGEMENT; GENE SEQUENCE; GENETIC VARIABILITY; HEMATOLOGIC MALIGNANCY; HUMAN; IMMUNOGLOBULIN GENE; LARGE CELL LYMPHOMA; MULTIPLE MYELOMA; NONHUMAN; PRIORITY JOURNAL; REVIEW; SOMATIC HYPERMUTATION; TUMOR MICROENVIRONMENT;

EID: 80054972574     PISSN: 10428194     EISSN: 10292403     Source Type: Journal    
DOI: 10.3109/10428194.2011.587564     Document Type: Review

References (55)

1. Lyons JG, Lobo E, Martorana AM, Myerscough MR. Clonal diversity in carcinomas: its implications for tumour progression and the contribution made to it by epithelial-mesenchymal transitions. Clin Exp Metastasis 2008;25:665-677.
2. Heng HH, Bremer SW, Stevens JB, Ye KJ, Liu G, Ye CJ. Genetic and epigenetic heterogeneity in cancer: a genome-centric perspective. J Cell Physiol 2009;220:538-547.
3. Cobaleda C, Jochum W, Busslinger M. Conversion of mature B cells into T cells by dedifferentiation to uncommitted progenitors. Nature 2007;449:473-477.
4. Robbiani DF, Bothmer A, Callen E, et al. AID is required for the chromosomal breaks in c-myc that lead to c-myc/IgH translocations. Cell 2008;135:1028-1038.
5. Alt FW, Yancopoulos GD, Blackwell TK, et al. Ordered rearrangement of immunoglobulin heavy chain variable region segments. EMBO J 1984;3:1209-1219.
6. Kosmas C, Stamatopoulos K, Papadaki T, et al. Somatic hypermutation of immunoglobulin variable region genes: focus on follicular lymphoma and multiple myeloma. Immunol Rev 1998;162:281-292.
7. Bateman CM, Colman SM, Chaplin T, et al. Acquisition of genomewide copy number alterations in monozygotic twins with acute lymphoblastic leukemia. Blood 2010;115:3553-3558.
8. Mullighan CG, Phillips LA, Su X, et al. Genomic analysis of the clonal origins of relapsed acute lymphoblastic leukemia. Science 2008;322:1377-1380.
9. Davis RE, Ngo VN, Lenz G, et al. Chronic active B-cell-receptor signalling in diffuse large B-cell lymphoma. Nature 2010;463:88-92.
10. Lenz G, Wright GW, Emre NC, et al. Molecular subtypes of diffuse large B-cell lymphoma arise by distinct genetic pathways. Proc Natl Acad Sci USA 2008;105:13520-13525.
11. Lenz G, Wright G, Dave SS, et al. Stromal gene signatures in large-B-cell lymphomas. N Engl J Med 2008;359:2313-2323.
12. Neuberger MS, Milstein C. Somatic hypermutation. Curr Opin Immunol 1995;7:248-254.
13. Stavnezer J. Antibody class switching. Adv Immunol 1996;61: 79-146.
14. King LB, Norvell A, Monroe JG. Antigen receptor-induced signal transduction imbalances associated with the negative selection of immature B cells. J Immunol 1999;162:2655-2662.
15. Martinez-Climent JA, Fontan L, Gascoyne RD, Siebert R, Prosper F. Lymphoma stem cells: enough evidence to support their existence? Haematologica 2010;95:293-302.
16. Szereday Z, Csernus B, Nagy M, Laszlo T, Warnke RA, Matolcsy A. Somatic mutation of the 5 'noncoding region of the BCL-6 gene is associated with intraclonal diversity and clonal selection in histological transformation of follicular lymphoma. Am J Pathol 2000;156: 1017-1024.
17. Carlotti E, Wrench D, Matthews J, et al. Transformation of follicular lymphoma to diffuse large B-cell lymphoma may occur by divergent evolution from a common progenitor cell or by direct evolution from the follicular lymphoma clone. Blood 2009;113:3553-3557.
18. Hart J, Turner AR, Larratt L, et al. Transmission of a follicular lymphoma by allogeneic bone marrow transplantation-evidence to support the existence of lymphoma progenitor cells. Br J Haematol 2007;136:166-167.
19. Takai A, Toyoshima T, Uemura M, et al. A novel mouse model of hepatocarcinogenesis triggered by AID causing deleterious p53 mutations. Oncogene 2009;28:469-478.
20. Marusawa H. Aberrant AID expression and human cancer development. Int J Biochem Cell Biol 2008;40:1399-1402.
21. Mottok A, Hansmann ML, Brauninger A. Activation induced cytidine deaminase expression in lymphocyte predominant Hodgkin lymphoma. J Clin Pathol 2005;58:1002-1004.
22. Brauninger A, Yang W, Wacker HH, Rajewsky K, Kuppers R, Hansmann ML. B-cell development in progressively transformed germinal centers: similarities and differences compared with classical germinal centers and lymphocyte-predominant Hodgkin disease. Blood 2001;97:714-719.
23. Khuda SE, Loo WM, Janz S, Van Ness B, Erickson LD. Deregulation of c-Myc confers distinct survival requirements for memory B cells, plasma cells, and their progenitors. J Immunol 2008;181:7537-7549.
24. Ruzinova MB, Caron T, Rodig SJ. Altered subcellular localization of c-Myc protein identifies aggressive B-cell lymphomas harboring a c-MYC translocation. Am J Surg Pathol 2010;34:882-891.
25. Grogan TM, Durie BG, Lomen C, et al. Delineation of a novel pre-B cell component in plasma cell myeloma: immunochemical, immunophenotypic, genotypic, cytologic, cell culture, and kinetic features. Blood 1987;70:932-942.
26. Vescio RA, Cao J, Hong CH, et al. Myeloma Ig heavy chain V region sequences reveal prior antigenic selection and marked somatic mutation but no intraclonal diversity. J Immunol 1995;155:2487-2497.
27. Berek C. The development of B cells and the B-cell repertoire in the microenvironment of the germinal center. Immunol Rev 1992;126: 5-19.
28. Billadeau D, Ahmann G, Greipp P, Van Ness B. The bone marrow of multiple myeloma patients contains B cell populations at different stages of differentiation that are clonally related to the malignant plasma cell. J Exp Med 1993;178:1023-1031.
29. Bakkus MH, Van Riet I, Van Camp B, Th ielemans K. Evidence that the clonogenic cell in multiple myeloma originates from a pre-switched but somatically mutated B cell. Br J Haematol 1994;87:68-74.
30. Palumbo A, Battaglio S, AstolfiM, Frieri R, Boccadoro M, Pileri A. Multiple independent immunoglobulin class-switch recombinations occurring within the same clone in myeloma. Br J Haematol 1992; 82:676-680.
31. Bakkus MH, Asosingh K, Vanderkerken K, et al. Myeloma isotypeswitch variants in the murine 5T myeloma model: evidence that myeloma IgM and IgA expressing subclones can originate from the IgG expressing tumour. Leukemia 2001;15:1127-1132.
32. Bakkus MH, Schots R, Gomez La Fuente PB, et al. Clonally related IgA-and IgE-secreting plasma cells in a myeloma patient. Eur J Haematol 2000;65:348-355.
33. Szczepek AJ, Seeberger K, Wizniak J, Mant MJ, Belch AR, Pilarski LM. A high frequency of circulating B cells share clonotypic Ig heavy-chain VDJ rearrangements with auto-logous bone marrow plasma cells in multiple myeloma, as measured by single-cell and in situ reverse transcriptase-polymerase chain reaction. Blood 1998;92:2844-2855.
34. Berenson JR, Vescio RA, Hong CH, et al. Multiple myeloma clones are derived from a cell late in B lymphoid development. Curr Top Microbiol Immunol 1995;194:25-33.
35. Rasmussen T, Kastrup J, Knudsen LM, Johnsen HE. High numbers of clonal CD19-cells in the peripheral blood of a patient with multiple myeloma. Br J Haematol 1999;105:265-267.
36. Mellstedt H, Hammarstrom S, Holm G. Monoclonal lymphocyte population in human plasma cell myeloma. Clin Exp Immunol 1974;17:371-384.
37. Bergsagel PL, Smith AM, Szczepek A, Mant MJ, Belch AR, Pilarski LM. In multiple myeloma, clonotypic B lymphocytes are detectable among CD19+peripheral blood cells expressing CD38, CD56, and monotypic Ig light chain. Blood 1995;85:436-447.
38. Zojer N, Schuster-Kolbe J, Assmann I, et al. Chromosomal aberrations are shared by malignant plasma cells and a small fraction of circulating CD19+cells in patients with myeloma and monoclonal gammopathy of undetermined significance. Br J Haematol 2002;117:852-859.
39. Reiman T, Seeberger K, Taylor BJ, et al. Persistent preswitch clonotypic myeloma cells correlate with decreased survival: evidence for isotype switching within the myeloma clone. Blood 2001;98: 2791-2799.
40. Bergui L, Schena M, Gaidano G, Riva M, Caligaris-Cappio F. Interleukin 3 and interleukin 6 synergistically promote the proliferation and differentiation of malignant plasma cell precursors in multiple myeloma. J Exp Med 1989;170:613-618.
41. Matsui W, HuffCA, Wang Q, et al. Characterization of clonogenic multiple myeloma cells. Blood 2004;103:2332-2336.
42. Matsui W, Wang Q, Barber JP, et al. Clonogenic multiple myeloma progenitors, stem cell properties, and drug resistance. Cancer Res 2008;68:190-197.
43. Taylor BJ, Kriangkum J, Pittman JA, et al. Analysis of clonotypic switch junctions reveals multiple myeloma originates from a single class switch event with ongoing mutation in the isotype-switched progeny. Blood 2008;112:1894-1903.
44. Mitsiades CS, Mitsiades NS, Munshi NC, Richardson PG, Anderson KC. The role of the bone microenvironment in the pathophysiology and therapeutic management of multiple myeloma: interplay of growth factors, their receptors and stromal interactions. Eur J Cancer 2006;42:1564-1573.
45. Herishanu Y, Perez-Galan P, Liu D, et al. The lymph node microenvironment promotes B-cell receptor signaling, NF-kappaB activation, and tumor proliferation in chronic lym-phocytic leukemia. Blood 2011;117:563-574.
46. Zhu D, Orchard J, Oscier DG, Wright DH, Stevenson FK. V(H) gene analysis of splenic marginal zone lymphomas reveals diversity in mutational status and initiation of somatic mutation in vivo. Blood 2002;100:2659-2661.
47. Hecht M, von Metzler I, Sack K, Kaiser M, Sezer O. Interactions of myeloma cells with osteoclasts promote tumour expansion and bone degradation through activation of a complex signalling network and upregulation of cathepsin K, matrix metalloproteinases (MMPs) and urokinase plasmi-nogen activator (uPA). Exp Cell Res 2008;314:1082-1093.
48. Chauhan D, Singh AV, Brahmandam M, et al. Functional interaction of plasmacytoid dendritic cells with multiple myeloma cells: a therapeutic target. Cancer Cell 2009;16: 309-323.
49. Nadav L, Katz BZ, Baron S, Cohen N, Naparstek E, Geiger B. The generation and regulation of functional diversity of malignant plasma cells. Cancer Res 2006;66:8608-8616.
50. Nadav L, Katz BZ, Baron S, et al. Diverse niches within multiple myeloma bone marrow aspirates affect plasma cell enumeration. Br J Haematol 2006;133:530-532.
51. Nadav-Dagan L, Shay T, Dezorella N, et al. Adhesive interactions regulate transcriptional diversity in malignant B cells. Mol Cancer Res 2010;8:482-493.
52. Nadav L, Kalchenko V, Barak MM, Naparstek E, Geiger B, Katz BZ. Tumorigenic potential and disease manifestations of malignant B-cell variants differing in their fibronectin adhesiveness. Exp Hematol 2008;36:1524-1534.
53. Quiroga MP, Balakrishnan K, Kurtova AV, et al. B-cell antigen receptor signaling enhances chronic lymphocytic leukemia cell migration and survival: specific targeting with a novel spleen tyrosine kinase inhibitor, R406. Blood 2009;114:1029-1037.
54. Burger JA. Chemokines and chemokine receptors in chronic lymphocytic leukemia (CLL): from understanding the basics towards therapeutic targeting. Semin Cancer Biol 2010;20:424-430.
55. Katz BZ. Adhesion molecules-the lifelines of multiple myeloma cells. Semin Cancer Biol 2010;20:186-195.