i(8)(q10) in ALL

Abstract

Isochromosomes are nonrandom chromosomal anomalies in acute lymphoblastic leukemia (ALL), but relatively few patients ALL and i(8)(q10) have been reported. In the majority of cases, i(8)(q10) was part of complex karyotypes, suggesting that it is a secondary chromosomal abnormality in ALL associated with clonal evolution.

Keywords

Isochromosome; Acute lymphoblastic leukemia; Chromosome gain; Clonal evolution.

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Identity

ICD-Topo	C420,C421,C424
ICD-Morpho	9861/3 AML with mutated NPM1; AML with mutated CEBPA; Acute myeloid leukaemia, NOS
ICD-Morpho	9837/3 T lymphoblastic leukaemia/lymphoma
ICD-Morpho	9808/3 Mixed phenotype acute leukaemia, B/myeloid, NOS 152
Atlas_Id	2052
	Partial karyotypes with isochchromosome i(8)(q10) (A). Fluorescence in situ hybridization with LSI MYC probe hybridizing to 8q24 (Vysis/Abott Molecular, US) showing end-to-end joining of homologous chromosomes 8 at the telomeres (B). It can be hypothesized that telomeric fusion of homologous chromosomes can promote creation of an unstable dicentric chromosome potentially causing an unbalanced translocation product. However, the precise consequences of telomere fusion events and their role in formation of isochromosomes remain unclear.

Clinics and Pathology

Disease	Acute lymphoblastic leukemia
Phenotype / cell stem origin	Associated with B-lineage immunophenotype with exception of 1 chronic myeloid leukaemia (CML) with lymphoid blast crisis of B-cell type who developed a secondary T-cell ALL (Dawson et al., 1999) case and 2 biphenotypic leukemia (Sulak et al.,1990; Saikevich et al., 1991) patients.
Epidemiology	At least 40 reported cases (21 males, 19 females aged 0 to 85 years; median age 17 years) were described. Nearly half the cases were children: 2 female infants (O'Malley et al., 1988; Pui et al., 1991) and 12 pediatric cases aged 0 to 15 years (Pollak & Hagemeijer 1987; Krance et al., 1992; Pui et al., 1992; Rafi et al., 2000; An et al., 2008; Suenobu et al., 2010; Chapiro et al., 2011; Harrison et al., 2014; Olsson et al., 2015; Yasuda et al., 2016; Zhang et al., 2016) or young adults aged 17 to 24 years old ( Mossafa et al., 1994; Tang et al., 1998; Jarosova et al., 2000; Soriani et al., 2011; Harrison et al., 2014; Safavi et al., 2015) (Table 1). 46,idem,t(9;10)(p13;q22) or t(9;10) (p22;q24) 1.Pollak & Hagemeijer 1987; 2.O'Malley et al., 1988; 3.Sulak et al.,1990; 4.Kageyama et al., 1991; 5.Pui et al., 1991; 6.Saikevich et al., 1991; 7.Krance et al., 1992; 8.Pui et al., 1992; 9.Dewald et al., 1993; 10.Tuszynski et al., 1993; 11-13.Mossafa et al., 1994; 14.Pirc-Danoewinata et al., 1995; 15.Martineau et al., 1996; 16-17.Rieder et al., 1996; 18.Pabst et al., 1996; 19.Tang et al., 1998; 20.Dabaja et al., 1999; 21.Dawson et al., 1999; 22.Jarosova et al., 2000; 23.Rafi et al., 2000; 24.Rieder et al., 2003; 25.Strefford et al., 2007; 26-27.An et al., 2008; 28.Coyaud et al., 2010; 29.Kowalczyk et al., 2010; 30.Suenobu et al., 2010; 31.Soriani et al., 2011; 32.Chapiro et al., 2013; 33-36.Harrison et al., 2014; 37.Olsson et al., 2015; 38.Safavi et al., 2015; 39.Yasuda et al., 2016; 40.Zhang et al., 2016. Abbreviations: M, male; F, female.   Sex/Age Karyotype 1 F/7 47,XX,del(7)(p?),i(8)(q10),add(9)(p21),ins(9;9)(p21;q12q22),add(14)(q?) 2 F/0 46,XX,ins(11;4)/46,idem,del(5)(q15q33)/46,idem,del(5),i(8)(q10)/46,idem,t(2;4)(q33;p16),del(5)/47,idem,+8/ 3 M/85 77-87,XY,-X,-Y,del(5)(q23)x2,i(8)(q10)x2,add(22)(q13),inc        Bilineage or biphenotypic leukemia 4 M/53 46,XY,+1,der(1;16)(q10;p10),i(8)(q10),t(9;22),-12,der(15)t(12;15)(q12;p11),i(17)(q10),+21 5 F/0 50,XX,+X,+X,i(8)(q10),+10,-20,+21,i(21)(q10)x2,+mar 6 M/63 43,XY,t(1;9)(q?32;p?24),-2,der(3)t(3;12;17)(p?14;p?11;q?25),-5,i(8)(q10),-12,der(17)t(3;12;17)       Bilineage or biphenotypic leukemia 7 M/13 46,XY,i(8)(q10),t(12;17)(p13;q21) 8 M/10 46,XY,i(7)(q10),t(9;22)(q34;q11)/48,idem,i(8)(q10),+i(8)(q10)x2 9 M 49,XY,+4,+8,i(8)(q10)x2,t(9;22)(q34;q11),+der(22)t(9;22) 10 F 46,XX,t(9;22)(q34;q11)/47,idem,+i(8)(q10)/47,idem,+8,i(8)(q10)x2 11 F/60 46,XX,t(9;22)(q34;q11)/46,idem,i(8)(q10) 12 M/44 46,XY,i(8)(q10),t(9;22)(q34;q11) 13 F/24 46,XX,del(6)(q21q24),i(8)(q10) 14 M 46,XY,t(14;18)(q32;q21)/46,XY,del(3)(p24),i(8)(q10),del(12)(p12) 15 F/42 47,XX,dup(1)(q21q32),add(2)(p11),+7,i(8)(q10),t(8;22)(q24;q11)/47,idem,-dup(1),+trp(1)(q21q32) 16 F/36 53,XX,+4,t(9;22)(q34;q11),i(8)(q10),+18,+19,+der(22)t(9;22)x2 17 M/53 46,XY,t(9;22)(q34;q11)/45,XY,-7,i(8)(q10),ider(9)(q10)t(9;22),der(22)t(9;22) 18 M 48,XY,i(8)(q10),t(9;22)(q34;q11),+2mar 19 F/21 46,XX,i(7)(q10),i(8)(q10),t(9;22) 20 M 47,Y,-X,-5,-7,+13,-14,-15,+5-6mar/84-91,YY,-X,-X,-4,-4,-5,-5,-7,-7,i(8)(q10),-14,-14,-15,del(22)(q13),+8-10mar 21 M/39 46,Y,t(X;11),i(7)(q10),dup(8)(q21q22)/46,idem,i(8)(q10)/45,idem,-Y       T-cell ALL after chemotherapy for CML 22 M/17 45,XY,i(8)(p?),?add(12),-21/45,XY,i(8)(q10),der(12)del(12)(p13)dic(12;21)(p13;p11) 23 F/15 45,X,-X,-6,del(7)(q21),i(8)(q10),-9,add(9),add(12)(q24),t(12;21)(p13;q22),der(13)t(?6;13)(q12;q32),der(22)t(9;22),+1-2mar 24 M/62 46,XY,del(1)(q32),i(8)(q10),-9,-10,der(22)t(9;22)(q34;q11),+2mar 25 F/48 45,X,-X,add(1)(p36),-5,add(6)(q15),i(8)(q10),add(18)(p11)  26 F/14 45,XX,i(8)(q10),dic(9;12)(p11;p11),der(17)t(?X;17)(?q12;?p11) 27 F/13 46,XX,dic(9;20)(p11;q11),+21/46,idem,i(8)(q10)/46,idem,add(15)(p10) 28 M/51 46,XY,i(8)(q10),t(9;22)(q34;q11),der(9)t(8;9)(q1?;p12) 29 M 47,XY,i(8)(q10),+21c 30 F/13 45,XX,t(9;22)(q34;q11),add(10)(q22),-12,der(12)t(12;12)(p13;q13),i(17)(q10)/45,idem,i(8)(q10) 46,X,-X,+1,t(2;16)(p10;q10),+8,-9,t(9;22),add(10),-12,der(12),-13,i(17)(q10),+18,add(19)(p13),del(19)(q?),+21,-22,+mar/47,idem,+8       therapy for neuroblastoma 31 M/17 48,XY,i(8)(q10),+i(8)(q10)x2,t(9;22)(q34;q11)/49,idem,+der(22)t(9;22) 32 M/7 46,XY,t(14;20)(q32;q12)/46,idem,i(8)(q10) 33 F/7 45,XX,dup(1)(q21q32),i(8)(q10),t(9;14)(p22;q11),der(11)t(11;21)(q13;q11)t(21;22)(q22;q11)t(22;22)(q11;q22) 34 M 46,XY,-21,+r/46,idem,inv(11)(p15q13)/46,idem,i(8)(q10) 35 F/19 44,XX,i(8)(q10),-10,add(11)(q23),add(12)(p13),-14,add(14)(q32),add(15)(q25), +16,add(21)(q22),-22,+mar Prognosis As it occurs rarely as a sole anomaly only in sporadic cases in ALL, thus the prognosis is uncertain; patients with favorable primary aberrations and i(8)(q10) may maintain favorable clinical outcome similar to patients with +8; its combination with unfavorable primary anomaly or complex anomalies may lead to the worst prognosis. Cytogenetics Cytogenetics Morphological Sole abnormality in 3 (Kowalczyk et al., 2010; Olsson et al., 2015; Yasuda et al., 2016) and in the stemline, but with other chromosomal changes in 4 patients (Pirc-Danoewinata et al., 1995; Dabaja et al., 1999; Jarosova et al., 2000; Zhang et al., 2016). Double i(8)(q10) was detected in 5 cases (Sulak et al.,1990; Pui et al., 1992; Dewald et al., 1993; Tuszynski et al 1993; Soriani et al., 2011). Complex karyotypes, mainly with occurrence of primary anomalies in the remaining cases. Among them, the most common structural anomaly was t(9;22)(q34;q11) , found in 16 patients (Kageyama et al., 1991; Pui et al., 1992; Dewald et al., 1993; Tuszynski et al., 1993; Mossafa et al., 1994; Rieder et al., 1996; Pabst et al., 1996; Tang et al., 1998; Rafi et al., 2000; Rieder et al., 2003; Coyaud et al., 2010; Suenobu et al., 2010; Soriani et al., 2011; Safavi et al., 2015). Result of the chromosomal anomaly Fusion Protein Oncogenesis Partial chromosome 8q gain resulting from an isochromosome i(8)(q10) is a nonrandom chromosomal anomaly in ALL. It occurs rarely as a sole anomaly and is mainly observed together with primary chromosome aberrations, most frequently with t(9;22)(q34;q11). Therefore, the occurrence of i(8)(q10) in ALL may signal clonal evolution, often associated with disease progression. The consequence of the formation of i(8)(q10) is gain of 8q and loss of 8p, leading to imbalances in gene dosage. As trisomy 8 is among the most common secondary chromosome changes in hematological malignancies, it is likely that gain of 8q, but not the loss of 8p is important in leukemogenesis. In this regard it is interesting to note, that while extra chromosome 8 is a common clonal evolution marker for progression in CML, the occurrence of i(8)(q10) has been only rarely described during CML transformation. 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AZ, Amess JA, Chaplin T, Dorey E, Gibbons B Leukemia 1993 Oct;7(10):1504-8 PMID 8412311   Recurrent DUX4 fusions in B cell acute lymphoblastic leukemia of adolescents and young adults Yasuda T, Tsuzuki S, Kawazu M, Hayakawa F, Kojima S, Ueno T, Imoto N, Kohsaka S, Kunita A, Doi K, Sakura T, Yujiri T, Kondo E, Fujimaki K, Ueda Y, Aoyama Y, Ohtake S, Takita J, Sai E, Taniwaki M, Kurokawa M, Morishita S, Fukayama M, Kiyoi H, Miyazaki Y, Naoe T, Mano H Nat Genet 2016 May;48(5):569-74 PMID 27019113   Jude Children's Research Hospital-Washington University Pediatric Cancer Genome Project Zhang J, McCastlain K, Yoshihara H, Xu B, Chang Y, Churchman ML, Wu G, Li Y, Wei L, Iacobucci I, Liu Y, Qu C, Wen J, Edmonson M, Payne-Turner D, Kaufmann KB, Takayanagi SI, Wienholds E, Waanders E, Ntziachristos P, Bakogianni S, Wang J, Aifantis I, Roberts KG, Ma J, Song G, Easton J, Mulder HL, Chen X, Newman S, Ma X, Rusch M, Gupta P, Boggs K, Vadodaria B, Dalton J, Liu Y, Valentine ML, Ding L, Lu C, Fulton RS, Fulton L, Tabib Y, Ochoa K, Devidas M, Pei D, Cheng C, Yang J, Evans WE, Relling MV, Pui CH, Jeha S, Harvey RC, Chen IL, Willman CL, Marcucci G, Bloomfield CD, Kohlschmidt J, Mrózek K, Paietta E, Tallman MS, Stock W, Foster MC, Racevskis J, Rowe JM, Luger S, Kornblau SM, Shurtleff SA, Raimondi SC, Mardis ER, Wilson RK, Dick JE, Hunger SP, Loh ML, Downing JR, Mullighan CG; St Deregulation of DUX4 and ERG in acute lymphoblastic leukemia Nat Genet PMID 27776115   Citation This paper should be referenced as such : Zamecnikova A i(8)(q10) in ALL; Atlas Genet Cytogenet Oncol Haematol. in press On line version : http://AtlasGeneticsOncology.org/Anomalies/i8q10ALLID2052.html Translocations implicated (Data extracted from papers in the Atlas)   i(8)(q10) External links Mitelman database i(8)(q10) [Case List]    i(8)(q10) [Association List] Mitelman database (CGAP - NCBI) arrayMap Morph ( 9861/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments] arrayMap Morph ( 9837/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments] arrayMap Morph ( 9808/3) - arrayMap (UZH-SIB Zurich)  [auto + random 100 samples .. if exist ]   [tabulated segments]     Disease database i(8)(q10) in ALL REVIEW articles automatic search in PubMed Last year articles automatic search in PubMed All articles automatic search in PubMed © Atlas of Genetics and Cytogenetics in Oncology and Haematology indexed on : Fri Jun 30 11:22:21 CEST 2017 Home   Genes   Leukemias   Solid Tumors   Cancer-Prone   Deep Insight   Case Reports   Journals  Portal   Teaching    For comments and suggestions or contributions, please contact us jlhuret@AtlasGeneticsOncology.org.