Philadelphia Chromosome Positive Burkitt Type Acute Lymphoblastic Leukaemia

Mckinley, R.; Scott, C. Anthony; Yip, Moh-Ying; Kwan, Yiu Lam; Lam‐Po‐Tang, P.R.L.

doi:10.1111/j.1365-2141.1986.tb04101.x

Cited by 7 publications

(2 citation statements)

References 5 publications

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“…We found a translocation t(9;22) in a mature B‐cell or Burkitt cell leukaemia defined by cytomorphology and immunophenotyping. In contrast to the only other case reported to date (Mckinley et al , 1986), we were not able todetect any of the characteristic translocations t(8;14)(q24;q32) or the variants t(2;8)(p11;q24) or t(8;22) (q24;q11) on metaphases. Additionally, FISH with a probe for t(8;14)(q24;q32) was negative and no splits of c‐myc were detectable.…”

Section: Discussioncontrasting

confidence: 99%

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Philadelphia chromosome‐positive mature B‐cell (Burkitt cell) leukaemia

et al. 2002

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Summary. Philadelphia chromosome-positive (Ph + ) acute leukaemia usually shows lymphoblastic morphology and a B-precursor phenotype. The bone marrow aspirate of a 9-year-old boy showed a L3 blast cell morphology in 90% of cells; immunophenotyping revealed a mature B-blast population. The translocation t(9;22) (q34;q11) was seen in 45 out of 50 metaphases, and expression of the corresponding bcr1/abl fusion transcripts, but no IgH/myc co-localization or splitting of c-myc, was demonstrated. Chemotherapy according to the Berlin-Frankfurt-Munster non-Hodgkin's lymphoma (NHL-BFM 95) protocol with maintenance according to the BFM acute lymphoblastic leukaemia (ALL-BFM 90) protocol resulted in continuing complete remission of 54 months. The occurrence of Ph + Burkitt's leukaemia might reflect multiple-step cancer development.

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Section: Discussioncontrasting

confidence: 99%

“…The presence of a Philadelphia chromosome in a mature B‐cell leukaemia has rarely been observed (Mc Kinley et al , 1986). Its occurrence is not only a therapeutic challenge but it also gives room to speculations about multi‐step leukaemogenesis.…”

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Philadelphia chromosome‐positive mature B‐cell (Burkitt cell) leukaemia

et al. 2002

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Chromosomal abnormalities in adult non‐endemic burkitt's lymphoma and leukemia: 22 new reports and a review of 148 cases from the literature

Kornblau

Goodacre

Cabanillas

1991

Hematological Oncology

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Tumour cell karyotypes from patients with Burkitt lymphoma (BL) or Burkitt's type leukemia (ALL3) were studied for correlation with survival, bone marrow and cerebral spinal fluid involvement (CSF), human immunodeficiency virus (HIV) serology, and for recurrent cytogenetic abnormalities. The records of 22 patients with BL from our institution and of 148 cases of BL and ALL3 reported in the literature with karyotypes were evaluated for clinical and cytological features. Overall survival was only 28 per cent and 88 per cent of deaths occurred within the first nine months after diagnosis. Those who survived at least 18 months were unlikely to relapse. Age and gender did not significantly affect survival. Patients presenting with advanced Ann Arbor stage, bone marrow or CSF involvement had lower survival rates. The association of translocations involving chromosome band 8q24 with this disease is confirmed. Sixty-two per cent of karyotypes had t(8;14)(q24;q32) translocations; the recognized variant translocations t(8;22)(q24;q11) and t(2;8)(p12;q24) affected 12 per cent and 9 per cent respectively. Seventeen per cent had abnormal karyotypes but no classic translocation. Patients with variant translocations had the poorest survival rates, and those with the classic t(8;14)(q24;q32) did the best. Despite a small sample size, the variant translocation t(8;22)(q24;q11) appeared to occur at an increased frequency in the patients with AIDS. In the entire group, recurrent involvement of chromosome regions 1q2, 6q11-14 and 17p1 suggests that alteration of genes at these loci, B Cell Growth Factor (BCGF) at 1q2 and p53 on 17p, may contribute to the development and progression of this tumour. Similarly, the frequent trisomies of chromosomes 7, 8, 12 and 18 may indicate an effect on tumour cell growth due to increased gene dosage. Trisomy 12 was found in eight tumours, five from patients with AIDS, suggesting that chromosome 12 has a site or gene whose allelic dosage is selected for in AIDS related lymphoma cells. Cytogenetic studies of adult Burkitt lymphoma and leukemia suggest several likely loci for gene alterations that in conjunction with myc translocations can lead to tumorigenesis.

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