An identical t(Y;1)(q12;q21) in two patients with myelodysplastic syndromes

Hollings, Peter E.; Giles, Lynette M.; Rosman, Ingrid; Fitzgerald, P. H.

doi:10.1016/0165-4608(88)90275-0

Cited by 20 publications

(8 citation statements)

References 42 publications

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“…59 Nevertheless, 2 0 q -probably affects the pluripotential hematopoietic stem cell, because this abnormality has been found in BFU-E, CFU GM, Epstein-Barr virus immortalized B-cell clones, Tcell clones, and natural killer cell clones from blood and bone marrow samples containing the 20q-. 46 A.J.C.P.^…”

Section: Discussionmentioning

confidence: 99%

“…The 2 0 q -abnormality has been identified in BFU-E, CFU-GM, 46 Epstein-Barr virus transformed Bcell clones, IL-2-dependent T-cell clones, and natural killer cell clones. 4748 Nevertheless, the pathogenetic mechanism by which 20q-alters the hematopoietic stem cells in hematologic disorders remains unknown.…”

Section: From the Department Of Laboratory Medicine And Pathology DImentioning

confidence: 99%

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Hematologic Disorders Associated With Deletions of Chromosome 20q:A Clinicopathologic Study of 107 Patients

et al. 1996

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Section: Discussionmentioning

confidence: 99%

Section: From the Department Of Laboratory Medicine And Pathology DImentioning

confidence: 99%

Hematologic Disorders Associated With Deletions of Chromosome 20q:A Clinicopathologic Study of 107 Patients

et al. 1996

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“…The der(Y)t(Y;1) abnormality has, to our knowledge, been previously reported in 9 cases, all of whom had MDS or CMPD either with or without transition [15, 16, 17, 18, 19, 20, 21]. Seven of 10 reported cases (including the present case) were associated with MDS; e.g.…”

Section: Discussionmentioning

confidence: 80%

Spectral Karyotyping Refined the Identification of a der(Y)t(Y;1)(q11.1 or .2;q12) in the Blast Cells of a Patient with Atypical Chronic Myeloid Leukemia

Ohsaka

Hisa

2002

Acta Haematol

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We report a case of atypical chronic myeloid leukemia who showed leukocytosis with immature granulocytes and dysplastic features but no monocytosis or basophilia. Cytogenetic analysis by conventional G-banding showed an abnormal clone, which was interpreted as 46,X,-Y,+der(?)t(?;1)(?;q?1), and no Philadelphia chromosome. Reverse transcription-polymerase chain reaction did not show either major or minor BCR-ABL chimeric mRNA. Spectral karyotyping (SKY) and fluorescence in situ hybridization (FISH) refined the karyotype to 46,X,der(Y)t(Y;1)(q11.1 or .2;q12). The der(Y)t(Y;1) abnormality was reported previously in 9 cases and associated with myelodysplastic syndrome or chronic myeloproliferative disorders. SKY in combination with the standard banding method and FISH may be useful for exploring undefined chromosome abnormalities in hematological disorders.

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“…In 3/4 polycythemia vera patients the aberration correlated with transition into myelodysplasia; in one patient no data on transition were provided [7], In 2/3 MDS patients the disease evolved into AML [3,5]. One patient with CMMol was lost to follow-up [2], Recently, correlations between specific secondary karyotypic abnor malities and previous (chemo)therapy regimens have been described [9]. FISH analysis revealed that the breakpoint in chromosome 1 maps in band q l 2, thereby revising its previously reported location (q21).…”

Section: Discussionmentioning

confidence: 99%

“…One special case history of a patient with Fanconi anemia was described [4], In this patient the transient appearance of a clone with the chro mosomal aberration was found, not correlating with a dis tinct phase of the disease. The other three patients all had myelodysplasia: one CMMol with no blasts (this patient was lost to follow-up [2]; one patient with an RAEB, who evolved into AML 4 months after diagnosis [3]; and a third patients with an RA who was known to have neutro-and thrombocytopenia as well as monocytosis for 14 years, and evolved into AML, FAB M2 and died 2 months later der(y)t(Y;l)(ql2;ql2), +9 in PV 85 [5]. Remarkably, the 47,X,der(Y)t(Y;l)(ql2;ql2),+9 aberra tion was found in nearly all cases during transition of the disease.…”

Section: Discussionmentioning

confidence: 99%

Derivative (y)t(Y;1)(q12;q12),+9 in a patient with polycythemia vera during transition into myelodysplasia

Raymakers¹,

Stellink²,

Kessel³

1996

Cancer Genetics and Cytogenetics

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Cytogenetic analysis of bone marrow cells of a 63-year-old male Caucasian patient with polycythemia vera [PV) who developed anemia, thrombocytopenia, and increased granulocytic imma turity revealed a 47,X,der(Y) t(Y;l)(ql2;ql2),+9 karyotype. The breakpoint in chromosome 1 appeared to map to ql2 and not to q21, as has been described in previous reports without FISH confirmation. In the 4 years before this transition the patient was polycythemic and, accordingly; treated with phlebot omy and three short courses of busulfan, The cytogenetic picture observed has been described before in seven patients: three with PV, three with myelodysplasia, and one with Fan coni anemia. In 5/7 cases, like in our patient, the abnormality was observed during transition of the disease into either myelodys plasia or AML.

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An identical t(Y;1)(q12;q21) in two patients with myelodysplastic syndromes

Cited by 20 publications

References 42 publications

Hematologic Disorders Associated With Deletions of Chromosome 20q:A Clinicopathologic Study of 107 Patients

Hematologic Disorders Associated With Deletions of Chromosome 20q:A Clinicopathologic Study of 107 Patients

Spectral Karyotyping Refined the Identification of a der(Y)t(Y;1)(q11.1 or .2;q12) in the Blast Cells of a Patient with Atypical Chronic Myeloid Leukemia

Derivative (y)t(Y;1)(q12;q12),+9 in a patient with polycythemia vera during transition into myelodysplasia

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