Acute lymphocytic leukaemia (ALL) and acute promyelocytic leukemia (APL)

Only 2 ALL cases reported: a 49-years old male with T-cell ALL (Cho et al., 2009) and a 10-years old male diagnosed with B-ALL (Kaleem et al., 2000). In addition, a t(1;5)(p32;q31) was detected as an additional anomaly in a 29-years old female patient diagnosed with acute promyelocyte leukemia (Zamecnikova, unpublished case).

Yet poorly known; the pediatric case with B-precursor phenotype achieved complete remission after induction chemotherapy and remains in complete continuous remission for 24 months (Kaleem et al., 2000). Induction chemotherapy failed to induce remission in the adult patient with T-ALL and 5 months later the patient died due to renal failure and metabolic acidosis (Cho et al., 2009). In the APL case, induction was started with ATRA based therapy resulting in complete remission and she remains in complete remission for 14+ months.

May be overlooked in suboptimal preparations.

LSI CSF1R (SpectrumOrange/D5S23, D5S721 SpectrumGreen, and Vysis LSI 1p36 (SpectrumOrange) / LSI 1q25 (SpectrumGreen) probes.

Secondary anomaly in addition to t(8;14)(q11.2;q32) in a pediatic B-ALL patient (Kaleem et al., 2000), associated with del(6q) in a sideline in the T-ALL case (Cho et al., 2009) and found in association witht(15;17)(q24;q21) in the APL case.

Because of its rarity, the role of t(1;5)(p32;q31) in disease pathogenesis as well as its clinical significance is unclear. Unlike in the T-ALL case described by François et al., 1998, neither TAL1 translocation nor its aberrant expression was detected FISH and by immunohistochemical staining in the other T-ALL patient (Cho et al., 2009). Therefore it is likely that some other genes located at 1p32 such as BLYM, EPS15, CDKN2C, and JUN may be involved in leukemogenesis (Cho et al., 2009). In the remaining 2 cases, t(1;5)(p32;q31) was found in addition to t(8;14)(q11.2;q32) and to t(15;17)(q24;q21) likely representing a secondary event in these cases.