[Change in cell line in relapses of acute lymphoid leukemia: frequency, morphologic, phenotypic and cytogenetic characteristics and clinical course].
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Biomedical subjects
Publications and source records attributed to M T Ferro.
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High resolution chromosome analysis was performed on bone marrow cells from four patients with acute promyelocytic leukemia and t(15;17), and in lymphocytes from two unrelated, phenotypically normal persons with an apparently identical constitutional translocation. Scrutiny of prophase-prometaphase chromosomes localized the breakpoints in all six cases to subbands 15q22.3 and 17q11.2. Molecular genetic studies have localized the oncogene c-erbA to chromosome #17 between the breakpoints of the constitutional and the acquired anomaly. The present results, therefore, map c-erbA to subband 17q11.2.
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We have observed three patients with t(4;11)(q21;q23) among the 50 cases of ALL studied. Two were classified as L1 and the third as L3. We comment on the relationship between the morphologic classification of leukemias and the association with a t(4;11).
Three patients presenting with acute leukemic disorder and chromosome 3 rearrangement involving bands q21;q26 are reported, and the literature on chromosome 3q abnormalities is reviewed. All reported patients carrying a paracentric 3q inversion or a translocation 3;3 with breakpoints in q21;q26 had a myelodysplastic or acute leukemic disorder with a normal or elevated platelet count and lack of response to cytotoxic drug therapy. They showed an associated incidence of -7 or 7q- anomalies higher than de novo acute leukemia and appear to constitute a definite subgroup of the leukemic disorders with very poor prognosis. The majority of patients showing other chromosome 3 long arm rearrangements showed evidence of leukemic process, were in blastic crisis, or had been exposed to chemotherapy, exhibiting also a higher incidence of associated -5 or -7 cytogenetic abnormalities than is observed in patients not exposed to toxic agents.
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A number of chromosomes other than chromosome No. 8 participate in formation of the 14q+ marker in lymphoproliferative disorders. Among them is chromosome No. 11 which appears to be important because its break points are constant; it is also possibly significant because of its participation in cytogenetic alterations in B-cell disorders.
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A child was brought to us with multiple anomalies. On examination we found an interstitial deletion in the long arms of chromosome 1. We studied genetic and chromosome markers, comparing our clinical and cytogenetic findings with other reported cases of chromosome 1 interstitial deletion.
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