Multiple myeloma (MM) mainly

5 cases presented with multiple myeloma (3 males and 2 females aged 43 to 73 years) (Mugneret et al., 1995; Smadja et al., 2001; Kaufmann et al., 2003; Mohamed et al., 2007) and there was one 76-years old male with acute myeloid leukemia (AML) (Oshimura et al., 1976) and 1 female with mantle cell lymphoma (Knuutila et al., 1994) ) (Table 1).

	Sex/Age	Disease	Karyotype
1	M/76	AML	43,X,-Y,-1,t(1;8)(p22;q24),-11,der(11)t(11;13)(q23-25;q12-14),-13,-16,-17,add(17) (p11),+22,der(22)t(1;22)(q11;p11-12)x2,+mar
2	F	Mantle cell lymphoma LN	42-45,X,add(X)(q22),der(1)t(1;6)(p32;q15),t(2;3)(q37;q21),del(5)(q13q22),del(6)(q15), +7,del(10)(q24),-13,t(14;18)(q32;q21),-15,-17,der(22)t(13;22)(q12-14;q11-13),+4 -5mar,inc/46,X,add(X),der(1),t(1;8)(p21;q24),t(3;19) (q28;p13),del(5),del(6),+7,del(10), -13,t(14;18),-15,+der(19)t(3;19),der(22)
3	M/70	MM	45,X,-Y/44,XY,+1,der(1;16)(q10;p10),+der(1;21)(q10;p10),t(1;8)(p21;q24),-13, -14
4	M	MM	54,X,-Y,del(1)(p21p22),+der(1)t(1;8)(p13;q12),t(1;8)(?p22;q24),+3,t(4;16) (q13;p10), +5,+add(5)(p15),+7,-8,der(8;16)(q11;q11),+9,+11,+15,+19,+21
5	M	MM	43,X,-Y,del(1)(p21),t(1;8)(p21;q24),add(4)(p16),add(8)(p10),-13,-22
6	F/43	MM	48-49,X,-X,der(1;9)(q10;p10),t(1;8)(p21;q24),+3,add(5)(q35),-16,+18,+19,+21
7	F/61	MM	49,X,-X,t(1;8)(p22;q24),+5,del(14)(q22),+15,+15,add(22)(q11),+mar

Abbreviations: M, male; F, female; AML, acute myeloid leukemia; LN, lymph node; MM, multiple myeloma.
1. Oshimura et al., 1976; 2. Knuutila et al., 1994; 3. Mugneret et al., 1995; 4. Smadja et al., 2001; 5. Kaufmann et al., 2003; 6-7. Mohamed et al., 2007.

Additional anomalies Complex karyotypes showing either hypodiploid or hyperdiploid karyotypes; associated with t(14;18)(q32;q21) and -13 in the mantle cell lymphoma case (Knuutila et al., 1994) and monosomy 13 in AML (Oshimura et al., 1976) and in 2 MM patients (Mugneret et al., 1995; Kaufmann et al., 2003).

The chromosomal translocation t(1;8)(p21-22;q24) is a rare anomaly, that has been described mainly in multiple myeloma patients. It involves the MYC loci at 8q24, however MYC rearrangement and/or its overexpression was studied only in sporadic cases (Mugneret et al., 1995). It is also possible, that breakpoints may be located in the vicinity of MYC locus, at least in some patients with dispersed 1p21-22 breakpoints, therefore the molecular consequences of this rearrangement are likely be heterogeneous and probably disease specific. In all the described cases, the t(1;8)(p21-22;q24) was part of complex karyotypes, indicating that it developed concurrently with other genetic alterations and likely to be a late progression event important in disease progression.