Detection of karyotypic abnormalities in most patients with acute nonlymphocytic leukemia by adding ethidium bromide to short-term cultures

Misawa, Shinichi; Yashige, H; Horiike, Shigeo; Nishigaki, H; Okuda, Tsukasa; Yokota, Shouhei; Tsuda, S; Edagawa, J.; Imanishi, Hitoshi; Takino, Tatsuro; Inazawa, Johji; Abe, Tatsuo; Nakanishi, Satoshi; Nakagawa, Masao; Kobayashi, Hiroshi; Maekawa, Taira; Fujii, Hiroshi; Akaogi, Teruaki; Hayashi, Hideo; Fujiyama, Yoshihide; Kohsaki, M

doi:10.1016/0145-2126(88)90004-5

Cited by 25 publications

(6 citation statements)

References 21 publications

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“…Trisomy 11 has been previously described in one patient with myelodysplasia (Swansbury and Lawler, 1980) and in one mosaic case of APL which had the karyotype 46,XX,t(9;? ),t( 15; 17) (q22;q12)/47, XX, + 11 (Misawa et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Myelodysplastic syndrome transforming to acute promyelocytic‐like leukemia with trisomy and rearrangement of chromosome II

Najfeld¹,

Chen

Scalise³

et al. 1994

Genes Chromosomes & Cancer

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Variants of the t(15;17)(q22;q12-q21) chromosomal rearrangement associated with acute promyelocytic leukemia (APL) have been previously described and they frequently involve either chromosome 15 and/or 17. Previously we reported a rare variant t(11;17). We now describe two patients with myelodysplastic syndrome (MDS) that transformed to APL-like leukemia. Both had trisomy 11 at the diagnosis of APL-like leukemia. Following treatment for APL, patient 1 reverted to MDS and showed a normal karyotype. When leukemia recurred, his bone marrow karyotype was 47,XY,t(4;11), +11,der(22)t(1;22). Both patients were treated with all-trans retinoic acid (ATRA) for APL for 5 weeks, but failed to respond. The karyotype of patient 1 after ATRA treatment was 46,XY,t(4;11); the trisomy 11 had been lost and the bone marrow was replaced with immature myeloblasts without promyelocytes. In patient 2, the karyotype remained the same as at diagnosis, i.e., 47,X,-Y,dir ins(4;7),del(5), +6,del(7), +8, + 11,-18. Molecular analysis by reverse transcriptase PCR analysis showed the presence of wild type retinoic acid receptor alpha (RARA) and the absence of the PML-RARA chimeric gene associated with t(15;17). Additional analysis of PLZF, a new zinc finger gene associated with t(11;17), also showed the absence of this hybrid gene. These data support the concept that APL is a heterogeneous disorder and that variants with chromosome 11 rearrangement exist that do not respond to ATRA.

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Section: Discussionmentioning

confidence: 99%

Myelodysplastic syndrome transforming to acute promyelocytic‐like leukemia with trisomy and rearrangement of chromosome II

Najfeld¹,

Chen

Scalise³

et al. 1994

Genes Chromosomes & Cancer

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“…It has been grouped with complex karyotypes as being associated with poor outcome, 22 and grouped with other MLL+ve 11q23 abnormalities and poor outcome. 8,23 However, Fenaux et al 24 had no relapses among the patients with t(9;11) in their series, and they suggested that the outlook might be less severe than had been thought, an inference which has been subsequently supported for AML patients, both children 3,25 and adults.…”

Section: Figurementioning

confidence: 99%

Hematological malignancies with t(9;11)(p21–22;q23) – a laboratory and clinical study of 125 cases

et al. 1998

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This paper reports clinical and cytogenetic data from 125 cases with t(9;11)(p21-22;q32) which were accepted for a European Union Concerted Action Workshop on 11q23. This chromosome abnormality is known to occur predominantly in acute myeloid leukemia (AML) FAB type M5a and less often in AML M4; in this series it was also found to occur, uncommonly, in other AML FAB types, in childhood acute lymphoblastic leukemia (ALL) (nine cases), in relatively young patients with myelodysplastic syndrome (MDS) (five cases), acute biphenotypic leukemia (two cases), and acute undifferentiated leukemia (one case). All age groups were represented but 50% of the patients were aged less than 15 years. The t(9;11) was the sole abnormality in 57 cases with AML; trisomy 8 was the most common additional abnormality (23 cases, including seven with further abnormalities), and 28 cases had other additional abnormalities. Among the t(9;11)+ve patients with AML, the white cell count (WBC) and age group were significant predictors of event-free survival; central nervous system (CNS) involvement or karyotype class (sole, with trisomy 8, or with other), also contributed to prognosis although our data could not show these to be independent factors. The best outcome was for patients aged 1-9 years, with low WBC, and with absence of CNS disease or presence of trisomy 8. For patients aged less than 15 years, the event-free survival for ALL patients was not significantly worse than that of AML patients.

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“…Although the association of inv( 16) with M4 patients having significant eosinophilia has been established, its occurrence in other FAB categories such as M1, M2, M4, and M6 has also been found by others (Le Beau et al, 1983;Larson et al, 1984;Yunis, 1984;Woods et al, 1985;Stamberg, 1987;Misawa et a/., 1988).…”

Section: Other Recurrent Anomaliesmentioning

confidence: 88%

Specific chromosomal changes in patients with acute nonlymphocytic leukemia from India

Kadam

Merchant

Advani

et al. 1991

Hematological Oncology

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SUMMARYWe analysed forty consecutive patients with acute nonlymphocytic leukemia (ANLL) using methotrexate cell synchronization and 24 h-unstimulated cultures of bone marrow cells to determine the incidence of chromosomal aberrations and the association of specific anomalies with FAB morphological subtypes, in an Indian population. All patients demonstrated an abnormal karyotypic pattern. The specific chromosomal changes viz., t(9;22), t(8;21), t(15;17), t/del(l lq), 12p-were found in M1(3/5), M2(8/15), M3(8/8), M4(1/1) M5(2/4) and M2Ba(l/l) (M2 with Basophilia) patients. Abnormalities of I l q were also noted in two M2 patients showing monocytic involvement. A translocation involving chromosomes 6 and 9 was seen in one patient with M 1 and two patients with M2. An inv( 16) was observed in MI (one case), M2 (two cases) and M6 (one case). A del(16) was noted in an M4 case. Although t(9;22) is frequently associated with M1 patients, it was also detected in M2 (two patients) and M4 (one patient). Among all the FAB specific anomalies described above, t(8;21) and t( 15;17) were observed only in M2 and M3 patients, respectively. Interestingly, one M2 patient had two independent clones, one with t(8;21) and t(9;ll). Deletion or translocation involving 1 lq was found in a Ph positive M4 patient. New structural rearrangements such as t(1;7) (q32;q36) in association with t(8;21), and t(14;22) (q32;qll) in association with del(1 l)(q23) were detected in a M2 and a M5 patient, respectively. In conclusion, our studies have revealed that the incidence of FAB specific abnormalities viz., t(8;2 1); t(15;17), t(9;22), t/del(llq) and also other recurrent anomalies viz., -7/7q-, + 8 is much higher in our patients, as compared with other countries. This difference may be attributed to the influence of differential environmental exposure to unknown carcinogenic agents.

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Detection of karyotypic abnormalities in most patients with acute nonlymphocytic leukemia by adding ethidium bromide to short-term cultures

Cited by 25 publications

References 21 publications

Myelodysplastic syndrome transforming to acute promyelocytic‐like leukemia with trisomy and rearrangement of chromosome II

Myelodysplastic syndrome transforming to acute promyelocytic‐like leukemia with trisomy and rearrangement of chromosome II

Hematological malignancies with t(9;11)(p21–22;q23) – a laboratory and clinical study of 125 cases

Specific chromosomal changes in patients with acute nonlymphocytic leukemia from India

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