i(X)(p10) occurs in a wide spectrum of hematologic malignancies, in both myeloid and lymphoid disorders, including MDS, CMML, CML, de novo and therapy-related AML, ALL, NHL and Hodgkin lymphoma.
Myelodysplastic syndrome (MDS) was diagnosed in 7 patients (Adeyinka et al., 2007), 2 of them with refractory anaemia with ring sideroblasts (RARS) (Knuutila et al., 1984; Dewald et al., 1989), one patient with refractory anaemia (RA) (Adeyinka et al., 2007) and one with refractory anaemia with excess blasts (RAEB)(Sato et al., 2002).
Chronic myelomonocytic leukaemia (CMML): 3 patients (MacGrogan et al., 2004; Chen et al., 2010; Nacheva et al., 1995).
Chronic myeloid leukemia (CML): 2 patients (Selleri et al., 1989; Barbouti et al., 2002).
Acute myeloid leukemia (AML): there were 8 patients with different variants of AML: 1 AML-M1 (Fitzerald et al., 1983), 1 AML-M2 (Dewald et al., 1989), 1 AML-M4 (Bao et al., 2006), 2 therapy-related AML (Preiss et al., 2010; Adeyinka et al., 2007).
Acute lymphoblastic leukemia (ALL): 3 patients. Two of them with relapse after chemotherapy (Adeyinka et al., 2007) and allo-HSCT (Gindina, own case, table 1, #23), one patient with Down syndrome (Baker et al., 2003).
Hodgkin lymphoma, nodular sclerosis (HL) was diagnosed in 2 patients (Falzetti et al., 2005; Schlegelberger et al., 1994).
Non Hodgkin lymphoma (NHL): 1 patient (Temperani et al., 1995).
Mantle cell lymphoma (MCL): 1 patient (Gindina, own case, table 1, #25).
Cytopenias: 3 patients (Adeyinka et al., 2007), 2 of them with anaemia, one with thrombocytopenia.

i(X)(p10) is observed as the sole abnormality in myeloid malignancies and has been demonstrated in females of advanced age. Nonetheless, this abnormality has been observed seldom in younger patients with AML, ALL, Hodgkin lymphoma, NHL. The median age of female patients is 60 years (range, 3 - 83 years).
Table 1. Reported cases with i(X)(q10).

#	Age, gender	Disease	Karyotype	Author
1	32, F	CML	46,XX,t(9;22)(q34;q11)(8)/47,X,i(X)(p10),t(9;22),+22(8)/48,i(X)(p10)x2,+X,t(9;22),+22(16)	Selleri et al, 1989
2	50, F	CML	46,X,i(X)(p10),t(9;22)(q34;q11),i(17)(q10)(9)/50,idem,+1,+8,+13,+19(2)	Barbouti et al, 2002
3	62, F	RA	46,X,i(X)(p10)(5)/46,XX(15)	Adeyinka et al, 2007
4	76, F	RARS	46,X,i(X)(p10)(22)	Knuutila et al, 1984
5	74, F	RARS	46,X,i(X)(p10)(3)/47,idem,+idic(X)(q13)(2)/47,X,idic(X),+idic(X)(4)/46,XX(10)	Dewald et al, 1989
6	87, F	RAEB	46,X,del(X)(q22q26),+i(X)(p10),t(1;3)(p36;p21),der(6)del(6)(p23p25)del(6)(q1?5q2?5),add(7)(q32),-8, add(9)(p?11),add(11)(q23),t(12;13)(q11;q12),-14,+16,-18,inv(19)(p13q11),+mar(2)/47,idem, +add(14)(q32)(3)/46,idem,der(1)t(1;3)t(1;14)(p32;q32),der(3)t(1;3),der(14)t(1;14)(2)/46,idem, der(1),t(1;3), der(3),der(14),add(17)(p1?3)(2)/46,XX(21)	Sato et al, 2002
7	73, F	MDS	46,X,i(X)(p10),del(5)(q13q33)(6)/46,XX(14)	Adeyinka et al, 2007
8	80, F	MDS	46,X,i(X)(p10)(2)/46,XX(19)	Adeyinka et al, 2007
9	38, F	MDS	46,X,i(X)(p10)(2)/46,XX(18)	Adeyinka et al, 2007
10	?, F	CMML	46,X,i(X)(p10)(20)	MacGrogan et al, 2004
11	?, F	CMML	46,X,i(X)(p10)	Chen et al, 2010
12	75, F	CMML	46,X,i(X)(p10)(3)/46,idem,del(20)(q11q13)(28)	Nacheva et al, 1995
13	74, F	AML	47,X,i(X)(p10)x2(3)/48,idem,+8(21)/49,idem,+20(8)	Hagemeier et al, 1981
14	79, F	AML, M1	47,X,i(Xp10)x2(22)	Fitzgerald et al, 1983
15	83, F	AML, M2	46,X,idic(X)(q13)(3)/47,idem,+idic(X)(2)/46,X,i(X)(p10)(2)46~50,X,i(X)(p10),+8,+2mar(3)/46,XX(4)	Dewald et al, 1989
16	74, F	AML, M4	46,X,i(X)(p10)(5)/46,XX(7)	Bao et al, 2006
17	?, F	AML	46,XX,inv(3)(q21q26)(1)/45,idem,-7(11)/45,idem,i(X)(p10),-1(8)	Lugthart et al, 2010
18	32, F	AML	47~50,XX,+i(X)(p10)x2,+8,+9(cp16)/46,XX(5)	Adeyinka et al, 2007
19	68, F	t-AML, M1	46,XX,del(20)(q11)(5)/45,X,i(X)(p10),-7,del(20)(q11)(20)	Preiss et al, 2010
20	62, F	t-AML	46,X,i(X)(p10)(17)/46,XX(3)	Adeyinka et al, 2007
21	3, F	ALL	48,XX,+i(X)(p10),+21c(12)/47,XX,+21c(10)	Baker et al, 2003
22	17, F	ALL (relapse after CT)	45,X,-X,r(20)(10)/46,X,i(X)(p10),r(20)(7)/46,XX(3)	Adeyinka et al, 2007
23	25, F	Common ALL (relapse after alloHSCT)	49,XX.ish+i(X)(p10),+1,t(1;7)(p13;q11),t(2;3)(p?;q?),der(5)t(5;8)(q?;?),+6,der(6)t(6;9)(p?;?)t(6;9)(q?;?)ins(6;13)(q?;q?q?),der(6)t(6;15)(q?;q?),del(7)(p?), +8,der(8)t(2;8)(?;q?), der(8)t(8;14)(p?;q?),-13,der(15)t(5;15)(?;q?),del(15)(q?),der(20)t(15;20)(?;q?)(17)(24XCyte)	Gindina T (own case)
24	65, F	NHL	47,X,i(X)(p10),add(2p),add(14q),-19,+22,+r(5)/47,idem,del(6q),add(16)(q24)(11)	Temperani et al, 1995
25	58, F	MCL	44,-X,i(X)(p10),del(1)(q31),add(6)(q27),t(11;14)(q13;q32),-13,add(17)(q25),add(21)(p11)(12)/46,XX(8)	Gindina T (own case)
26	18, F	Hodgkin disease, nodular sclerosis	59~83,XXX,-X,i(X)(p10), -1,del(1)(q?),+2,add(2)(q37)x3,+3,del(3)(q26),-6,del(7)(q12q22),del(7)(q35), +8,del(8)(q24),-9,-10,-11,-11,del(11)(q12q13),+12,-13,-13, -14,-15,-16,-17,-17,-18,+20,del(20)(q11q13), add(20)(q13),-21,+4mar(cp6)/46,XX(164)	Falzetti et al, 1999
27	26, F	Hodgkin disease, nodular sclerosis	81-85,XX,-X,i(X)(p10),del(1)(p21),+i(2)(p10)x2,del(3)(q21),del(4)(q?25),i(4)(p10),i(4)(q10),+5,-6,-7,del(7)(q32),i(7)(q10),del(9)(q21q31),der(12)t (3;12)(q21;q22),-13,-13,-15,+16,del(17)(p11),-18,-18,-20,add(20)(q13),-22,-22,-22,i(22)(q10),+mar(8)	Schlegelberger et al. 1994
28	80, F	?	46,X,i(X)(p10)(14)	Adeyinka et al, 2007
29	74, F	?	49,XX,+i(X)(p10),+8,+i(11)(q10)(17)/50,idem,+5(cp2)/46,XX(1)	Adeyinka et al, 2007
30	80, F	?	46,XX,i(17)(q10)(15)/46,X,i(X)(p10),i(17)(q10)(2)/46,XX(3)	Adeyinka et al, 2007
31	84, F	?	46,X,i(X)(p10)(14)/47,X,i(X)(p10),+8(2)/46,XX(2)	Adeyinka et al, 2007
32	49, F	Thrombocytopenia	46,X,i(X)(p10)(11)/46,XX(9)	Adeyinka et al, 2007
33	76, F	Anemia	46,X,i(X)(p10)(6)/46,XX(14)	Adeyinka et al, 2007
34	79, F	Anemia, splenomegaly	46,X,i(X)(p10)(16)/46,XX,t(9;12)(p23;q22)(3)/46,XX(2)	Adeyinka et al, 2007

Survival was 8, 25 months (Dewald et al, 1989, cases # 15, #4) and 11+, 12+ months (Gindina, cases #25, #23 , table 1) in the four cases where information was provided.

There is a problem of distinguishing i(X)(p10) from del(X)(q24) because of the similarity of X p-arm band pattern and X q-arm band pattern extending from the centromere to band Xq24.

CRLF2 BreakApart (CytoCell, UK)

Sole abnormality in 11 patients, mostly in myeloid neoplasms (4 MDS, 3 AML, 2 CMML). Double extra i(X)(p10) was present in 4 patients (Selleri et al., 1989; Adeyinka et al., 2007; Hagemeier et al., 1981; Fitzerald et al., 1983). Additional chromosome anomalies were observed in 2/3 patients. Associated in combination with extra chromosome 8 in 5 females (Barbouti et al., 2002; Hagemeier et al., 1981; Dewald et al., 1989; Adeyinka et al., 2007), idic(X)(q13) in 2 (Dewald et al., 1989), del(20q) in 3 (Nacheva et al., 1995; Preiss et al., 2010; Falzetti et al., 1999), extra chromosome 20in 2 (Hagemeier et al., 1981;), loss of chromosome 7 in 2 (Lugthart et al., 2010; Schlegelberger et al. 1994), del(7q) in 2 (Falzetti et al., 1999; Schlegelberger et al. 1994), ring chromosome in 2 (Adeyinka et al., 2007; Temperani et al, 1995), other isochromosomes in 3 (Barbouti et al., 2002; Schlegelberger et al. 1994, Adeyinka et al., 2007).
In lymphoid malignancies, i(X)(p10) is part of a complex karyotype and seems to be a secondary event.

The pathogenetic importance of i(X)(p10) is underscored by its presence as the sole acquired anomaly. The major consequence of this abnormality is loss of the X q-arm and gain of the X p-arm, this would translate to loss of several genes on Xq and gain of several genes on Xp, that leads to genetic imbalance. I(X)(p10) has been reported in occasional males, indicating that this aberration can arise from active X chromosomes. It is not known whether this anomaly arises randomly from the active or inactive X chromosome in female patients (Adeyinka et al, 2007).

NHL