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Table 2. Summary of CNAs detected by aCGH. Recurrent (R) and unique (U) acquired CNAs are correspondingly highlighted
in first column. Results obtained are presented using standard (gene) abbreviations and such used according to the
international system of cytogenomic nomenclature
Size of
Chromosome
(alteration U or R) Cytobands GRCH37/hg19 imbalance Genes
[Mb]
1 (U) del(1)(p36.31p36.23) chr1:5,958,728-7,238,618 1.27 NPHP4, KCNAB2, CHD5, RPL22, RNF207, ICMT,
HES3, GPR153, ACOT7, HES2, ESPN, MIR4252,
TNFRSF25, PLEKHG5, NOL9, TAS1R1, ZBTB48,
KLHL21, PHF13, THAP3, DNAJC11, CAMTA1
del(1)(q22.2q22.2) chr1:91,620,826-91,739,326 0.2 HFM1
4 (U) del(4)(p16.3p14) chr4:3,072,509-38,882,925 35.8 HTT, C4orf44, RGS12, HGFAC, DOK7, LRPAP1,
LOC100133461, ADRA2C, LOC348926, OTOP1,
TMEM128, LYAR, ZBTB49, D4S234E, STX18,
LOC100507266, MSX1, CYTL1, STK32B, C4orf6,
EVC2, EVC, CRMP1, JAKMIP1, LOC285484,
WFS1, PPP2R2C, MAN2B2, MRFAP1, LOC93622,
S100P, MRFAP1L1, CNO, KIAA0232, TBC1D14,
LOC100129931, CCDC96, TADA2B, GRPEL1,
FLJ36777, SORCS2, PSAPL1, MIR4274, AFAP1
AS1, AFAP1, ABLIM2, SH3TC1, HTRA3, ACOX3,
METTL19, GPR78, CPZ, HMX1, LOC650293,
USP17, USP17L6P, DEFB131, MIR548I2, DRD5, SL-
C2A9, WDR1, MIR3138, ZNF518B, CLNK, MIR572,
HS3ST1, HSP90AB2P, RAB28, LOC285547,
NKX3-2, LOC285548, BOD1L, LOC152742,
CPEB2, C1QTNF7, CC2D2A, FBXL5, FAM200B,
BST1, CD38, FGFBP1, FGFBP2, PROM1, TAPT1,
FLJ39653, LDB2, QDPR, CLRN2, LAP3, MED28,
FAM184B, DCAF16, NCAPG, LCORL, SLIT2,
LOC100505893, MIR218-1, PACRGL, KCNIP4,
NCRNA00099, LOC100505912, GPR125,GBA3,
PPARGC1A, MIR573, DHX15, SOD3, CCDC149,
LGI2, SEPSECS, LOC285540, PI4K2B, ZCCHC4,
ANAPC4, SLC34A2, SEL1L3, C4orf52, RBPJ,
CCKAR, TBC1D19, STIM2, MIR4275, PCDH7,
ARAP2, DTHD1, KIAA1239, C4orf19,RELL1,
PGM2,TBC1D1, PTTG2,FLJ13197, KLF3,TLR10,
TLR1,TLR6, FAM114A1,MIR574
6 (R) amp(6)(q23.3q23.3) chr6:134,245,761-136,118,354 1.87 TBPL1, SLC2A12, HMGA1P7, SGK1, ALDH8A1,
HBS1L, MIR3662, MYB, AHI1, NCRNA00271
9 (R) del(9)(p21.3p21.3) chr9:20,605,923-21,218,606 0.61 MLLT3, KIAA1797, MIR491, PTPLAD2, IFNB1,
IFNW1, IFNA21,IFNA4, IFNA7, IFNA10, IFNA16
del(9)(p21.3p21.3) chr9:21,252,517-23,002,377 1.75 IFNA22P, IFNA5, KLHL9, IFNA6, IFNA13, IFNA2,
IFNA8, IFNA1, LOC554202, IFNE, MIR31, MTAP,
C9orf53, CDKN2A, CDKN2B-AS1, CDKN2B,
DMRTA1
amp(9)(q34.1q34.1) chr9:133,658,293-134,092,544 0.43 ABL1, QRFP, FIBCD1, LAMC3, AIF1L, NUP214
10 (U) del(10)(q25.1q25.2) chr10:111,634,169-112,348,580 0.71 XPNPEP1, ADD3, MXI1, SMNDC1, DUSP5, SMC3
15 (U) amp(15)(q13.3q13.3) chr15:32,098,670-32,539,666 0.44 CHRNA7

CNAs: copy number alterations; aCGH: array-comparative genomic hybridization

potentially benefit from tyrosine kinase inhibitors [16-17] .

Episomes are submicroscopic, circular and large acentric DNA fragments that can replicate autonomously.
One of the common formation-mechanisms for extrachromosomal elements in cancer cells is episome-rep-
lication and unequal segregation during cell division, resulting finally in an increase of copy numbers. Still
they that are invisible in banding cytogenetics; this is because episomes are composed of only several hun-
dred kilobases of amplified oncogenes and/or drug-resistance genes, and thus are too small to be visualized
by light-microscopy [18-20] . Of interest, we detected a variable number of episomes (20-30) in different cells.
However, we suggest that c-MYB is also present on the same episomes [Figure 2]; due to lack of material we
could not confirm this by FISH.

Additionally, recurrent acquired CNAs in different chromosomal regions were also identified besides unique
ones for this case [Table 2]. Taken together, the genomic abnormalities in T-ALL and T-LBL are so similar