Nonrandom additional chromosome changes in acute nonlymphocytic leukemia with inv(16)(p13q22)

Maseki, Nobuo; Kaneko, Yasuhiko; Sakurai, Masaharu

doi:10.1016/0165-4608(87)90065-3

Cited by 10 publications

(3 citation statements)

References 28 publications

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“…Trisomy 22 is a common additional chromosomal abnormalities in AML with inv(16)/t(16;16) [27]. In patients with AML and trisomy 22 as the sole karyotype abnormality, cytogenetically cryptic inv(16) (p13q22) is always present, based on small case series reports [28,29].…”

Section: Discussionmentioning

confidence: 99%

“…Approximately one-third of AML with inv(16) cases have additional karyotypic abnormalities (for example, trisomy 22, trisomy 8, or partial deletion of 7q), occurring concurrently with inv (16) or arising during clonal evolution [27][28][29]. There is only one reported case of AML with inv (16), which occurred in a patient with long-standing history of CLL [25].…”

Section: Introductionmentioning

confidence: 99%

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Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: Molecular evidence of two separate diseases

Murata-Collins²,

Wang

et al. 2006

American J Hematol

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Acute myeloid leukemia (AML) occurring concurrently with or after untreated chronic lymphocytic leukemia (CLL) is rare. We report a case of a 59-year-old man who was evaluated for anemia, thrombocytopenia, and leukocytosis with circulating blasts. On the basis of the morphology and immunophenotyping results, a preliminary diagnosis of chronic myelomonocytic leukemia with concurrent CLL was considered. Subsequently, cytogenetic analysis of the leukemic blood specimen revealed inv(16)(p13.1q22) with secondary trisomy 22 in a sideline clone. Fluorescence in situ hybridization confirmed the CBFb rearrangement associated with inv(16) in myeloblasts and myelomonocytic cells, but not in CLL cells. Therefore, a final diagnosis of AML with inv(16) with concurrent CLL was made. After standard chemotherapy for AML, the patient achieved complete remission for both his AML and CLL. The unique aspects of this case include concomitant AML and CLL, which do not share clonality, complex cytogenetic abnormalities with trisomy 22 as a secondary abnormality associated with inv(16), and achievement of remission for both AML and CLL by AML chemotherapy regimen. This case also represents one of the rare instances where a diagnosis of AML can be established even when the blast percentage in the marrow and blood is less than 20%. Am. J. Hematol. 81:963-968, 2006. V V C 2006 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: Molecular evidence of two separate diseases

Murata-Collins²,

Wang

et al. 2006

American J Hematol

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“…Although polymerase chain reaction (PCR) analysis is necessary to demonstrate the expression of CEBP-beta/MYH11 transcripts in the cases of FISH-positive AML, we could not perform it due to the lack of leukemic cell material. Trisomy 22 is a rare abnormality in AML, being first recognized in the myelomonocytic subtype [8,18]. In fact, trisomy 22 was considered a non-random secondary chromosomal abnormality associated with inv(16) in patients with AML [8,9].…”

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confidence: 99%

Trisomy 22 as the Sole Abnormality is an Important Marker for the Diagnosis of Acute Myeloid Leukemia with Inversion 16

Xu¹,

Zhou²,

Fan³

et al. 2008

Onkologie

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Background: The inversion of chromosome 16 (inv(16) (p13q22)) and the related t(16;16)(p13;q22) are chromosomal aberrations observed in approximately 10% of de novo acute myeloid leukemia (AML), mostly classified as M4Eo subtype, and associated with a relatively favorable outcome. However, it is a cryptic rearrangement and often difficult to recognize in conventional cytogenetics (CC). Trisomy 22 is an uncommon karyotypic aberration in AML and is often associated with inv(16)(p13q22). The aim of this study was to explore the value of trisomy 22 in the diagnosis of AML with inv(16). Patients and Meth-ods: Dual-color interphase fluorescence in situ hybridization (FISH) was performed in 19 AML cases with trisomy 22 abnormality shown by R-banding CC. The probe was a two-color break-apart probe for CBFβon the centromeric side and the telomeric side. Results: R-banding CC did not reveal inv(16) in any of the 19 AML with trisomy 22, but FISH analysis showed inv(16) in 11 cases and del(16)(q22) in 1 case. Among the 11 cases with inv(16), 9 showed trisomy 22 as the sole abnormality, 1 was complicated by trisomy 8, and 1 was del(16)(q22). Conclusion: This study further confirmed that trisomy 22 as the sole abnormality can be regarded as an important marker for inv(16) in AML.

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Mapping of the humanGSPT1 gene, a human homolog of the yeastGST1 gene, to chromosomal band 16p13.1

Ozawa¹,

Murakami²,

Eki³

et al. 1992

Somat Cell Mol Genet

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The GSPT1 gene, a human homolog of the yeast GST1 gene (formerly named GST1-Hs), was mapped on human chromosome 16p13.1 by a combination of nonradioactive in situ hybridization and Giemsa staining. Southern blot hybridization with a panel of human-rodent somatic cells confirmed the location of the GSPT1 gene on chromosome 16 and also showed the existence of a homologous gene on the X chromosome. A breakpoint for nonrandom chromosome rearrangements has been found in the region of GSPT1 in patients with acute nonlymphocytic leukemia.

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Nonrandom additional chromosome changes in acute nonlymphocytic leukemia with inv(16)(p13q22)

Cited by 10 publications

References 28 publications

Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: Molecular evidence of two separate diseases

Concurrent acute myeloid leukemia with inv(16)(p13.1q22) and chronic lymphocytic leukemia: Molecular evidence of two separate diseases

Trisomy 22 as the Sole Abnormality is an Important Marker for the Diagnosis of Acute Myeloid Leukemia with Inversion 16

Mapping of the humanGSPT1 gene, a human homolog of the yeastGST1 gene, to chromosomal band 16p13.1

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