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Biomedical subjects

K F Wong

Publications and source records attributed to K F Wong.

At least 19 recordsLinked to original sources
PubMed1995

Translocational rearrangements of 11q23 in acute monoblastic leukemia.

We report the rearrangements of 11q23 in the form of t(6;11)(q27;q23) and t(11;16)(q23;q24) in three cases of acute monoblastic leukemia. The former translocation had only previously been reported in five cases of acute myeloid leukemia, while the latter is hitherto undescribed. In addition to describing a new chromosomal locus 16q24, which may participate in translocational exchanges with 11q23, this report also confirms the close association between 11q23 rearrangement and the involvement of the monocytic lineage in acute myeloid leukemia.

Adult↗
PubMed1995

Biclonal acute monoblastic leukemia showing del(7q) and trisomies 9 and 22.

Cytogenetic biclonality is a rare phenomenon in acute myeloid leukemia. We report a case of acute monoblastic leukemia with biclonal cytogenetic abnormalities, showing an abnormal clone with an unusual occurrence of trisomy 9 and trisomy 22, in addition to a second clone with deletion of the long arm of chromosome 7 as the only abnormality. The significance of these findings in leukemogenesis is discussed.

Adult↗
PubMed1995

Aggressive pleomorphic CD2+, CD3-, CD56+ lymphoma with t(5;9)(q31;q34) abnormality.

CD56-positive lymphoma is a recently described entity which is characterized by predominantly extranodal involvement and an aggressive clinical course. We report one such case with involvement of the bone marrow and spinal cord at presentation, and associated with reactive hemophagocytic syndrome. The lymphoma cells had a highly pleomorphic appearance which is uncommon in CD56-positive lymphoma. Cytogenetic studies revealed a t(5;9)(q31;q34) abnormality. Analysis of more cases is required to determine if this is a recurring chromosomal translocation characteristic of the group of aggressive CD56-positive lymphoma.

Antigens, CD↗
PubMed1995

Use of the polymerase chain reaction in the detection of AML1/ETO fusion transcript in t(8;21).

BACKGROUND: t(8;21)(q22;q22), found in acute myeloid leukemia (AML) and occasionally in myelodysplasia (MDS), results in the fusion of the AML1 gene on 22q22 to the ETO gene on 8q22, generating a chimeric AML1/ETO transcript, which is a molecular marker of the translocation. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR), with two pairs of nested AML1 and ETO primers, was used to amplify the AML1/ETO fusion transcript. The Kasumi-1 cell line was used as a positive control. RESULTS: RT-PCR has a sensitivity of 0.0001% (10(-6)), corresponding to detection of 0.5 picograms of leukemic RNA in the presence of 0.5 micrograms of normal RNA. Using this approach, patients with t(8;21) (three patients with de novo AML, one with therapy-related AML, and one patient with myelodysplasia) yielded the same 222 base pair PCR product, suggesting that the breakpoints occurred at the same AML1 and ETO introns as previously reported. Three patients were still PCR-positive when in complete remission after chemotherapy and two experienced relapse. However, in another three patients with t(8;21) who were in remission for 2 months, 2 years, and 3 1/2 years, respectively, PCR was negative. CONCLUSION: RT-PCR is a sensitive method of detection of t(8;21), and is useful in the monitoring of minimal residual leukemia. As the junction of AML1/ETO appears to be constant, RT-PCR may offer a quick and accurate diagnosis of t(8;21).

Adult↗
PubMed1995

Inversion 14q in acute lymphoblastic leukemia of B-lineage.

Many types of leukemia are associated with specific chromosomal rearrangements. Inversion 14(q11q32) has been reported to be specifically associated with post-thymic T-cell malignancies, including T-chronic lymphocytic leukemia. T-prolymphocytic leukemia, and adult T-cell leukemia/lymphoma. We have previously reported its occurrence in T-cell acute lymphoblastic leukemia. Recently, we encountered a case of acute lymphoblastic leukemia with inv(14)(q11q32), which surprisingly showed a B-cell immunophenotype (CD10+CD19+HLA-DR+Ig mu-).

Adult↗
PubMed1995

B-cell small lymphocytic lymphoma with circulating granular prolymphocytes and a novel trisomy 15 anomaly.

A 53-year-old man presented with cervical lymphadenopathy and massive splenomegaly. Peripheral blood examination showed many prolymphocytes with cytoplasmic azurophilic granules, giving an initial impression of large granular lymphocytosis. The lymph node biopsy and immunohistochemical study findings, however, were more compatible with a diagnosis of B-cell small lymphocytic lymphoma. The circulating prolymphocytes showed restricted kappa light chain expression similar to the lymphoid infiltrate in the lymph node. Karyotypic analysis revealed trisomy 15, a chromosomal abnormality that has rarely been described in small lymphocytic lymphoma or chronic lymphocytic leukemia.

Bone Marrow↗
PubMed1995

der(1;15)(q10;10): a nonrandom chromosomal abnormality of myeloid neoplasia.

The occurrence of an unusual karyotypic abnormality der(1;15)(q10;q10) is reported in three patients, one with acute megakaryoblastic leukemia and two with myelodysplastic syndrome. A literature review shows that this cytogenetic abnormality is a rare but nonrandom change in myeloid neoplasia/neoplasia.

Aged↗
PubMed1995

Concomitant partial tetrasomy 3q and trisomy 18 in Waldenström macroglobulinemia.

We report a 54-year-old female patient with Waldenström macroglobulinemia who shows concomitant partial tetrasomy 3q in the form of an additional isochromosome 3q, and trisomy 18. To our knowledge, isochromosome 3q has not been reported in chronic lymphoproliferative disorders. A review of the literature on karyotypic aberrations in Waldenström macroglobulinemia suggests that additional copies of the long arm of chromosome 3 and chromosome 18 may play a possible role in the pathogenesis of a subset of this disorder.

Aneuploidy↗
PubMed1995

Hyperdiploid acute myeloid leukemia. Relationship between blast size and karyotype demonstrated by fluorescence in situ hybridization.

Hyperdiploidy is a rare finding in acute myeloid leukemia (AML), and the cases described so far showed characteristic large and bizarre blasts. We further demonstrate this morphologic/karyotypic relationship in a case of hyperdiploid AML by fluorescence in situ hybridization. Together with previous observations, we propose that in myeloid leukemias, increase in DNA content is accompanied by a corresponding increase in blast size. If large and bizarre blasts are shown on morphologic analysis, polyploid metaphases on cytogenetic preparations should also be analyzed, as they may be derived from these cells.

Aged↗
PubMed1995

Large granular lymphocyte leukemia. A study of nine cases in a Chinese population.

Large granular lymphocyte (LGL) leukemia is a neoplastic disorder of lymphocytes that is characterized by the presence of prominent cytoplasmic granules, and involves the proliferation of at least two distinct cell types, T cells and natural killer (NK) cells. The authors report the clinical and pathologic features of 9 Chinese patients with LGL leukemia, who represented 14% of 64 cases of chronic lymphoproliferative disorders diagnosed at their centers in 3 years. Three different groups could be defined on immunophenotypic and clinical grounds. The first group of 4 cases were CD2+CD3+CD4-CD8+. With the exception of a pediatric case, these cases ran an indolent course that was similar to the T-cell LGL leukemia most common in Western patients. However, thrombocytopenia and pure red cell aplasia were more common in the patients in this study, which was similar to the experience in Japanese patients. The second group of two cases were CD2+CD3+CD4+CD8-, and appeared to have worse outcomes than the first group. The third group of 3 cases were CD2+CD3-CD4-CD8-CD56+. Although phenotypically similar to the NK-cell LGL leukemia reported in Western patients, these cases were clinically more aggressive than their Western counterparts. This study is the first to report comprehensively the different types of LGL leukemias in Chinese patients, and provides useful information on the similarities and similarities and differences of these disorders as compared to those cases in the West.

Adult↗
PubMed1995

Pure red cell aplasia associated with thymic lymphoid hyperplasia and secondary erythropoietin resistance.

Systemic disorders, often immune in nature, can sometimes be associated with the presence of thymic pathology. Thymic enlargement due to lymphoid hyperplasia or thymoma is a common occurrence in patients with myasthenia gravis. In patients with pure red cell aplasia, at least 10% to 15% of patients are found to have thymoma, usually of spindle cell or medullary type. Pure red cell aplasia with demonstrable thymic enlargement due to lymphoid follicular hyperplasia is distinctly unusual, and has not been previously reported. The authors report such a case developing in a patient with end-stage renal failure maintained on hemodialysis and erythropoietin therapy. Because the red cell aplasia resolved after thymectomy, the disease process was considered etiologically related to the reactive lymphoid hyperplasia.

Adult↗
PubMed1995

Hemolytic transfusion reaction due to Rh antibodies detectable only by manual polybrene and polyethylene glycol technique.

The authors report two cases of severe hemolytic transfusion reaction (HTR) attributable to Rh antibodies, which were not detectable by the saline indirect antiglobulin test (SIAT), low ionic strength saline solution technique (LISS), or two-stage enzyme (Enz) indirect antiglobulin test (IAT), but were readily detectable by the manual polybrene technique (MPT), MPT-IAT, and polyethylene glycol (PEG) IAT. With rare exceptions, Rh antibodies can usually be easily detected by the SIAT or Enz-IAT, and seldom cause intravascular HTR. The two cases in this report illustrate the value of the MPT and PEG-IAT in the detection of clinically significant Rh antibodies that would not otherwise be detectable by conventional methods.

Adult↗
PubMed1995

Hepatosplenic gamma delta T-cell lymphoma. A distinctive aggressive lymphoma type.

The T-cell receptor (TCR) expressed on the surface of most T-lymphocytes is of alpha beta type, and only a minority bear the gamma delta-TCR. Similarly, postthymic T-cell lymphomas rarely express gamma delta-TCR. Hepatosplenic gamma delta T-cell lymphoma is an uncommon entity that has so far not been widely recognized. We report one such case that has been comprehensively studied by multiple modalities and showed the unique occurrence of leukemic picture at presentation. The 39-year-old man presented with fever, marked weight loss, and massive splenomegaly. Peripheral blood showed thrombocytopenia and a white cell count of 5.8 x 10(9)/l, with 66% medium-sized lymphoid cells that had a round or folded nucleus, condensed chromatin and a moderate amount of pale blue cytoplasm. Splenectomy was performed and histologic examination of the spleen, bone marrow, liver, and abdominal lymph nodes demonstrated lymphoma infiltration with a predominantly sinusoidal pattern. Immunohistochemical studies of the lymphoma cells showed a T-cell phenotype: CD2+ CD3+ CD5+ CD7+ gamma delta-TCR+ alpha beta-TCR- CD56+ CD4- CD8- CD16- CD57-. Cytogenetic studies showed complex clonal chromosomal abnormalities of 44,X, -Y, -11, -22, + mar in 3/16 cells. Rearrangement of the TCR gamma chain gene was demonstrated by polymerase chain reaction; the TCR beta chain gene was partially chain reaction; the TCR beta chain gene was partially rearranged. The patient did not respond to single agent chemotherapy, but achieved clinical remission with combination chemotherapy. Based on the available data in the literature, hepatosplenic gamma delta T-cell lymphoma exhibits distinctive clinicopathologic features, and probably represents the neoplastic counterpart of splenic gamma delta T-lymphocytes. This disease is associated with a poor prognosis and usually relapses despite initial response to chemotherapy.

Adult↗