Search

A 51-year-old male patient was diagnosed with Burkitt lymphoma 3 months after cardiac transplantation. The bone marrow karyotype was very complex, and to better define the complex karyotype we used the in situ suppression hybridization technique. Previously we interpreted this karyotype to be: 48,XY,t(2;8)(p11;q24), +der(2)t(2;8)(p11;q24),del(2)(q23), +7, +der(8)t(2;8)(p11;q24), +12, -13, -18, by G banding techniques, with a duplication of the t(2;8) derivatives. After in situ hybridization we changed to a: 48,XY,t(2;8)(p11;q24),t(2;18)(q23;q22), +7, +der(8)t(2;8)(p11;q24), +12, -13, which implies duplication of only one t(2;8) derivative.

A patient diagnosed with chronic myeloid leukemia was studied periodically during his illness. The result showed the presence of a Philadelphia (Ph) chromosome by a 9;22 translocation as a single abnormality to the time of blastic crisis. At that time, the chromosome studies showed a clonal evolution. Furthermore, a second derivated line was added to the Ph line. This new anomaly consisted of a 8;21 translocation, considered as specific of M2 type acute nonlymphoblastic leukemia of French-American-British classification.

We report three cases of ANLL and one case of ALL in which we found chromosome abnormalities not previously described. The first patient had a (9;11;16)(p22;q23;p13) translocation in the relapse after bone marrow transplantation. In the second case, a secondary leukemia following a Wilms' tumor, there was a single chromosome anomaly, an inversion of chromosome 13. The third case also presented an isochromosome 13q. In the fourth patient we observed a translocation between two achrocentric chromosomes, as in the third patient, but not of the Robertsonian type: t(21;21)(q22.1;q22.5).

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.

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).

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.