Canterbury DHB



The most frequent cytogenetic abnormalities in precursor B-cell ALL, with their underlying DNA rearrangements, are shown in the following table. For further information, see Iacobucci, I. and C. G. Mullighan (2017). "Genetic Basis of Acute Lymphoblastic Leukemia." Journal of Clinical Oncology 35(9): 975-983.

Table 1 – Cytogenetic and DNA changes in precursor B-cell ALL

t (9;22) (q34; q11.2)


t (4;11) (q21; q23)


t (12;21) (p13;q22)


t (1;19) (q23; p13.3)




Hyperdiploid >50


Unfavourable cytogenetic findings include:

The t(12;21) TEL/AML1 rearrangement present in 20-25% of childhood ALL carries a favourable prognosis.

In precursor T-cell ALL, cytogenetic changes are seen in about 30% of patients. Currently, these do not have any known impact on prognosis or disease management.

In Burkitt-like leukaemias, almost all patients will have a translocation that results in juxtaposing the MYC gene with an immunoglobulin (IG) gene. The MYC gene is located on the long arm of chromosome 8 (8q24) and is commonly involved in a translocation with one of the following IG loci:

The translocated MYC gene is controlled by IG gene promoters which results in over-expression of MYC. This is believed to continuously drive the tumour cells through the cell cycle.

About this Canterbury DHB document (8844):

Document Owner:

Peter Ganly (see Who's Who)

Last Reviewed:

December 2021

Next Review:

December 2024


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Topic Code: 8844