Distinctive immunophenotypic features of t(8;21)(q22;q22) acute myeloblastic leukemia in children [see comments]

Hurwitz, CA; Raimondi, SC; Head, David R.; Krance, Robert A.; Mirro, Joseph; Kalwinsky, David K.; Ayers, GD; Behm, FG

doi:10.1182/blood.v80.12.3182.bloodjournal80123182

Cited by 36 publications

(44 citation statements)

References 27 publications

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“…Furthermore, the percentage of CD56-expressing leukemic cells in these patients was high (mean, 68%; range, 30-89%), a finding in line with a study from northern Taiwan (Hsiao et al, 2002). In a Western series, co-expression of CD19 and CD56 antigens was found only in the t(8;21) group (nine of 16 cases), but not in any of the 48 evaluable cases of de novo AML of other FAB subtypes (P ¼ 0.0009; Hurwitz et al, 1992). In line with their findings, our study showed co-expression of CD19 and CD56 in three of five (60%) AMLs with t(8;21) but not in any other FAB subtypes.…”

Section: Discussionmentioning

confidence: 94%

Aberrant co‐expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan

Chen

Chuang

et al. 2008

Int J Lab Hematology

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Aberrant antigen expression in acute myeloid leukemia (AML) has been extensively studied in the West with limited reports from Taiwan. We carried out this retrospective study to characterize the frequency and significance of aberrant antigen expression of AML in Taiwan. Among 111 cases, 58 (52%) showed aberrant antigen expression, most frequently CD7 (27%) and CD56 (23%). Aberrant CD7 expression was observed in all non-AML-M3 subtypes, most frequently in AML-M7 (4/6, 67%); while CD19 expression was only observed in AML-M2 (5/36, 14%). CD56 expression was most common in AML-M5 (4/8, 50%). The relative frequency of CD19 and CD56 expression in AML with t(8;21) was higher than those with other chromosomal abnormalities or normal karyotype (P = 0.011 and 0.005, respectively). In non-M3 AML, aberrant antigen expression was identified in 56/96 (58%) cases, in contrast to 2/15 (13%) AML-M3 cases (P = 0.001). CD7, CD19 and CD56 expression was not correlated with remission rate. We concluded that aberrant immunophenotype was more frequent in non-M3 leukemias in Taiwan. The relative frequency of CD19 and/or CD56 expression in AML with t(8;21) was significantly higher than those without this translocation and co-expression of these two antigens may serve as the surrogate markers for AML with t(8;21).

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Section: Discussionmentioning

confidence: 94%

Aberrant co‐expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan

Chen

Chuang

et al. 2008

Int J Lab Hematology

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“…The reason why other groups did not recognize the correlation between þ11 and de novo AML of M2 and M1 subtypes may be that they reviewed not only þ11 cases with de novo AML but also patients with secondary AML and MDS (Bilhou-Nabera et al, 1994;Slovak et al, 1995). When we restricted our review of the literature to AML patients with no history of antecedent neoplasia, 80% of them (37/46 FAB classified patients) had M1 or M2 morphology (Yunis et al, 1981;Fitzgerald et al, 1983;Li et al, 1983;Testa et al, 1985;Berger et al, 1987;Ohyashiki et al, 1988;Weh et al, 1988;Keinänen et al, 1989;Nakamura et al, 1989;Tien et al, 1990;Kadam et al, 1991;Cuneo et al, 1992Cuneo et al, , 1994Hurwitz et al, 1992;Marosi et al, 1992;UKCCG, 1992;Fagioli et al, 1993;Suciu et al, 1993;Bilhou-Nabera et al, 1994;Bernard et al, 1995;Slovak et al, 1995;Caligiuri et al, 1996;Satake et al, 1997). Strikingly, more than one half of patients in our series, and 5/16 (31%) previously reported cases (Weh et al, 1988;Tien et al, 1990;Slovak et al, 1995;Caligiuri et al, 1996;Satake et al, 1997), had platelet counts >100 × 10 9 /l.…”

Section: Discussionmentioning

confidence: 99%

“…This is true for isolated trisomy 11 (þ11) despite the fact that þ11 is the third most common sole trisomy in de novo AML, following trisomies of chromosomes 8 and 13 [Cancer and Leukemia Group B (CALGB) cytogenetic data base, C. D. Bloomfield, personal communication, April 1996]. Many cases with þ11 have been reported as part of large series of AML patients with divergent cytogenetic abnormalities and often limited clinical data (Yunis et al, 1981;Fitzgerald et al, 1983;Li et al, 1983;Gustavsson et al, 1984;Testa et al, 1985;Berger et al, 1987;Keinänen et al, 1989;Kadam et al, 1991;Cuneo et al, 1992;Hurwitz et al, 1992;Marosi et al, 1992;UKCCG, 1992) or as case reports (Ohyashiki et al, 1988;Nakamura et al, 1989;Cuneo et al, 1994). The three largest series of de novo AML patients with þ11 detected at diagnosis we know of, were composed of 10 (Caligiuri et al, 1996), seven (Bilhou-Nabera et al, 1994) and six (Slovak et al, 1995) patients.…”

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confidence: 99%

Clinical characteristics of patients with de novo acute myeloid leukaemia and isolated trisomy 11: a Cancer and Leukemia Group B study

et al. 1998

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Isolated trisomy 11 is the third most common sole trisomy in de novo acute myeloid leukaemia (AML). However, only 49 cases have been published, and for only a fraction of these cases has full description of clinical and haematological features been provided. As a result, little is known about the clinical characteristics of de novo AML patients with solitary trisomy 11. We have identified 13 patients (0.9%) with isolated trisomy 11 among a total of 1496 consecutive adult patients successfully karyotyped as part of a prospective Cancer and Leukemia Group B (CALGB) cytogenetic study (CALGB 8461). Nine patients (69%) were over the age of 60 (range 29–73 years). Eight patients (62%) were diagnosed with AML of FAB M2 subtype, three patients (23%) had FAB M1 AML and one patient each had AML of FAB M0 and M7, respectively. Seven patients (54%) had high, >100 × 109/l, platelet counts (median 102 × 109/l; range 17–207 × 109/l). All patients received CALGB induction therapy with standard doses of cytarabine and daunorubicin. Six patients (46%) achieved a complete remission (CR). The median CR duration was 17.5 months (range 8.7–49.8). Only one patient, who underwent bone marrow transplantation in first CR, continues in initial CR. The median survival was 14.3 months (range 0.5–50.7); only one patient survives. We conclude that de novo AML with isolated trisomy 11 is predominantly associated with older age, M2 and M1 FAB subtypes, high platelet count and few long‐term disease‐free survivals, although it is currently unknown whether isolated trisomy 11 constitutes an independent prognostic factor.

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“…Analysis of t(8;21) positive leukaemic blasts has shown characteristic morphological (Berger et al, 1982;Nucifora et al, 1994; tend to be over-represented in the peripheral blood. Immunophenotypic analysis (Hurwitz et al, 1992;Kita et al, 1992Kita et al, , 1994Paietta et al, 1993;Tatsumi et al, 1992) has shown that t(8;21)-positive AMLs frequently express CD19, CD56 and high intensity CD34. In contrast, CD2 and CD7 are rarely expressed and CD33 is characteristically weak.…”

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confidence: 99%

Molecular detection of t(8;21)/AML1‐ETO in AML M1/M2: correlation with cytogenetics, morphology and immunophenotype

et al. 1996

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The t(8;21) identifies a subgroup of acute myeloid leukaemia (AML) with a relatively good prognosis which may merit different treatment. It is associated predominantly, but not exclusively, with AML M2, and corresponds to rearrangements involving the AML1 and ETO genes. AML1-ETO positive, t(8;21) negative cases are well recognized but their incidence is unknown. In order to determine optimal prospective AML1-ETO RT-PCR screening strategies, we analysed 64 unselected AML M1 and M2 cases and correlated the results with other biological parameters. Molecular screening increased the overall detection rate from 8% to 14%. AML1-ETO was found in 3% (1/32) of AML M1 and 25% (8/32) of M2, including three patients without a classic (8;21) but with chromosome 8 abnormalities. It was more common in younger patients. Correlation with morphology enabled development of a scoring system which detected all nine AML1-ETO-positive cases with a false positive rate of 7% (4/55). Although certain AML1-ETO-positive cases demonstrated characteristic immunological features (CD19 and CD34 expression, CD33 negativity), each of these markers was insufficiently specific to permit prediction in an individual case. We conclude that initial routine prospective molecular screening for AML1-ETO in all AMLs, combined with standardized morphological and immunological analysis, is desirable in order to produce improved prognostic stratification and to determine whether screening can ultimately be restricted to appropriate subgroups.

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Distinctive immunophenotypic features of t(8;21)(q22;q22) acute myeloblastic leukemia in children [see comments]

Cited by 36 publications

References 27 publications

Aberrant co‐expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan

Aberrant co‐expression of CD19 and CD56 as surrogate markers of acute myeloid leukemias with t(8;21) in Taiwan

Clinical characteristics of patients with de novo acute myeloid leukaemia and isolated trisomy 11: a Cancer and Leukemia Group B study

Molecular detection of t(8;21)/AML1‐ETO in AML M1/M2: correlation with cytogenetics, morphology and immunophenotype

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