Chromosomal translocation is the hallmark of leukaemias and acute lymphoblastic leukaemia (ALL) in particular. DNA damage arises from endogenous and exogenous genotoxic factors and lack of complete fidelity in DNA-repair leads to chromosomal translocations (Greaves and Wiemels 2003; Zhang et al. 2010). Chromosomal breakpoints tend to occur at transcriptionally active DNA sites and the fusiongene transcripts generally involve genes which frequently encode cell cycle regulators, transcription factors, signal transduction molecules, receptors or immunoglobulin and TCR molecules (Rabbits 1994; Ferrando and Look 2000). The commonly detected chromosomal translocations and fusion genes in B-lineage ALL (B-ALL) are mBCR-ABL, E2A-PBX1, TEL-AML1 andMLL-AF4. Due to the chromosomal translocations and subsequent expression of fusion gene transcripts, the normal functions of the genes are altered. Although cytogenetic analysis is a standard procedure to detect chromosomal translocations it has revealed a substantial number of false negative results and an inability to detect some translocations like TEL-AML1 and MLL-AF4 (Shurtleff et al. 1995). Reverse transcriptase-PCR (RT-PCR) and real-time PCR detection of fusion gene transcripts is not only sensitive and specific but also requires smaller number of tumour cells (Van Dongen et al. 1999; Liang et al. 2010). For the detection of chromosomal translocations, the fusion