Cytogenetic analysis of hematologic malignancies in Hong Kong

Li, Chan; Kwong, Yok Lam; Liu, H.W.; Chan, T. K.; Todd, D.; Ching, L. M.

doi:10.1016/0165-4608(92)90255-7

Cited by 32 publications

(7 citation statements)

References 14 publications

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“…We found that the Ph chromosome was detected in 4% of childhood ALL and 23% of adult ALL by cytogenetic analysis, and BCR-ABL fusion genes/transcripts were demonstrated in 5% of unselected childhood ALL and 27% of adult ALL by molecular methods. The incidences are comparable to those reported in literature [4][5][6][7][8][9][10][11]20,23,38,39]. In addition, three patients who were negative for Ph chromosome were BCR-ABL-positive in molecular studies.…”

Section: Discussionsupporting

confidence: 85%

Additional chromosomal abnormalities and variability of BCR breakpoints in Philadelphia chromosome/BCR‐ABL‐positive acute lymphoblastic leukemia in Taiwan

Tang

Lee

et al. 2002

American J Hematol

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From 1986 to 1998, 26 (23%) of 114 adult acute lymphoblastic leukemia (ALL) patients and 11 (4%) of 328 pediatric patients were found to have Philadelphia (Ph) chromosome. In the 30 patients with available data at diagnosis, 18 (60%) had extra-chromosomal abnormalities. They included 1q duplication (5/18, 28%), supernumerary Ph chromosome (4/18, 22%), 9p abnormalities (3/18, 17%), 7q deletion/monosomy 7 (3/18, 17%), trisomy 19 (1/18, 6%), and trisomy 8 (1/18, 6%). Excluding those with specific cytogenetic changes, only one patient had hyperdiploid karyotype with more than 50 chromosomes. The incidence of 1q duplication was higher and that of hyperdiploidy was lower in this study than has been previously reported. There was no prognostic implication of these additional cyto-

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Section: Discussionsupporting

confidence: 85%

Additional chromosomal abnormalities and variability of BCR breakpoints in Philadelphia chromosome/BCR‐ABL‐positive acute lymphoblastic leukemia in Taiwan

Tang

Lee

et al. 2002

American J Hematol

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“…Morphologic, cytochemical and immunophenotypic diagnoses of APL (AML-M3) were performed according to standard French-American-British (FAB) criteria. Cytogenetic studies were performed on Giemsa-banded metaphases obtained through short-term synchronized and unsynchronized cultures of bone marrow cells supplemented by direct harvest, according to standard protocols previously published (3). Details of the karyotypes were reported in accordance with the International System for Human Cytogenetic Nomenclature (ISCN2005) (4).…”

Section: Methodsmentioning

confidence: 99%

Diagnostic utility of dual fusion PML/RARα translocation DNA probe (D-FISH) in acute promyelocytic leukemia

Wan¹,

So²,

Hui³

et al. 2007

Oncol Rep

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Translocation(15;17) leading to the formation of fusion gene PML/RAR• is the diagnostic hallmark of acute promyelocytic leukemia (APL). Interphase fluorescence in situ hybridization (FISH) is one of the diagnostic tools employed for the detection of PML/RAR• rearrangement. Using a dual color dual fusion (D-FISH) PML/RAR• translocation DNA probe which hybridises both to PML/RAR• and RAR•/PML fusion genes, we characterised the FISH pattern of 52 APL patients at diagnosis and correlated the findings with conventional cytogenetics and RT-PCR analysis. The diagnostic sensitivity of the probe for PML/RAR• was 100%. Seven patients had atypical D-FISH patterns; two had a masked PML/RAR• fusion signal caused by the insertion of PML into RAR• on 17q; 3 had an extra copy of PML/RAR• in the form of isochromosome der(17)(q10)t(15;17) and one had duplication of the normal RAR• gene with an ider(17q) masquerading as i(17)(q10). There was also one case of t(7;17;15) with a typical D-FISH pattern and in which metaphase FISH suggested an unusual 4-point break. In summary, PML/RAR• D-FISH is a highly sensitive method for confirming diagnosis of APL. However D-FISH cannot be solely relied on for the diagnosis of APL owing to atypical patterns which are infrequently observed in cases with additional 17q structural abnormalities, gene insertion and gene duplication.

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“…A cell suspension of the tumor was made and cultured for preparation of metaphases for cytogenetic studies essentially as described [3]. G-banding was performed and 3 metaphases were analysed.…”

Section: Case Reportmentioning

confidence: 99%

Malignant peripheral neuroectodermal tumor in an infant with neurofibromatosis type 1

Chan

Nicholls

Lee

et al. 1996

Med. Pediatr. Oncol.

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A case of multifocal malignant peripheral neuroectodermal tumor (PNET) arising from a plexiform neurofibroma in a 4‐month‐old Chinese boy with neurofibromatosis type 1 (NF‐1) is described. Cytogenetic culture demonstrated hypotriploid karyotype with an abnormal clone characterized by 59–60, XY, +2, +3, +6, +8, +8, +12, +i(13)(q10), +der(14)t(1;14)(q21;q32), +16, +19, +20, +mar[cp3] with no apparent abnormality of chromosome 17. The child was treated with combination chemotherapy comprising ifosphamide, vincristine and doxorubicin. Despite initial partial response the child finally died of tumor progression and pulmonary metastases 8 months after diagnosis. We believe this is the first reported case of PNET in a child with NF‐1 and may support an association between these two disorders of neural crest origin. © 1996 Wiley‐Liss, Inc.

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Cytogenetic analysis of hematologic malignancies in Hong Kong

Cited by 32 publications

References 14 publications

Additional chromosomal abnormalities and variability of BCR breakpoints in Philadelphia chromosome/BCR‐ABL‐positive acute lymphoblastic leukemia in Taiwan

Additional chromosomal abnormalities and variability of BCR breakpoints in Philadelphia chromosome/BCR‐ABL‐positive acute lymphoblastic leukemia in Taiwan

Diagnostic utility of dual fusion PML/RARα translocation DNA probe (D-FISH) in acute promyelocytic leukemia

Malignant peripheral neuroectodermal tumor in an infant with neurofibromatosis type 1

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