Helvise Morse

REMISSION OF RELAPSED LEUKÆMIA DURING A GRAFT-VERSUS-HOST REACTION A "GRAFT-VERSUS-LEUKÆMIA REACTION" IN MAN?

Abstract Acute lymphoblastic leukaemia in two boys relapsed after engraftment of marrow from siblings identical at HLA A, B, and D loci but went into remission during subsequent graft-versus-host reactions without specific anti-leukaemia therapy. Later leukaemic relapse was primarily in extramedullary sites, with little or no involvement of bone-marrow, liver, or spleen Cytogenetic studies in both cases showed that the relapsed leukaemic blasts were those of the recipients while marrow cells and blood lymphocytes detected during marrow remission originated from the female donors. Blood lymphocytes from one of the recipients killed 51 Cr-labelled autologous lymphoblasts. The prolonged bone-marrow remission in the face of active and even massive extramedullary leukaemia suggests a graft-versus-leukaemia reaction in these two patients.

Acute nonlymphoblastic leukemia in childhood. High incidence of clonal abnormalities and nonrandom changes

Cytogenetic studies have been done on a group of childhood patients over a period of 3 1/2 years in which time Giemsa trypsin banding was applied to all specimens. Fifteen of the 107 patients (14%) were diagnosed as having acute nonlymphoblastic leukemia (ANLL). Twelve of the 15 had chromosomal abnormalities. The most common was an involvement of the #7 chromosome which occurred in five patients. Three patients had trisomy 19. No correlation could be found between the disease subgroup and the karyotypic aberration in patients with anomalies involving a common chromosome.

4;11 translocation in acute lymphoblastic leukemia: a specific syndrome.

Abstract Three patients with acute lymphoblastic leukemia (ALL) having t(4;11) (q21;q23) are described. Their clinical characteristics are compared with ten other published cases all involving similar histories and poor prognoses.

Chromosome mapping of biological pathways by fluorescence-activated cell sorting and cell fusion: human interferon gamma receptor as a model system

Human chromosome 6 encodes both the interferon gamma receptor as well as the class I major histocompatability complex antigens, HLA-A, -B, and -C. However, the presence of chromosome 6 in somatic cell hybrids is insufficient to confer sensitivity to human interferon gamma (Hu-IFN-γ) as assayed by class I HLA induction; it is necessary for both human chromosomes 6 and 21 to reside in the hybrid to generate a response to Hu-IFN-γ. Treatment of such a hamster-human hybrid, Q72-18, with Hu-IFN-γ induces the class I HLA antigens. Q72-18 cells selected by fluorescence-activated cell sorting for the loss of class I HLA induction also lost human chromosome 21. Fusions of such cells to a hybrid that contains only human chromosome 21 reconstitutes HLA antigen induction by Hu-IFN-γ. Furthermore, fusions of hybrids containing a translocated human chromosome 6q and the HLA-B7 gene to a line containing only human chromosome 21 or a translocated 21q also reconstitutes HLA-B7 mRNA and antigen induction by Hu-IFN-γ. Thus the segregation of cells on the basis of a biological effect by fluorescence-activated cell sorting and reconstitution by hybrid fusion provides a strategy by which some biological pathways can be mapped at a chromosomal level.

Karyotyping of bone-marrow cells in hematologic diseases

SummaryCultures of bone-marrow cells incubated for 5 h at 4° had cells in metaphase with elongated chromosomes which were easily Giemsa banded. Colcemid was not necessary for metaphase arrest at this temperature. This technique made possible routine karyotyping of patients with leukemia and other hematological diseases in which the detection of aberrations was otherwise difficult.

Cytogenetic studies of chronic myelocytic leukemia in children and adolescents.

In a 3 1/2 year cytogenetic study of 107 leukemia patients diagnosed in childhood and adolescence, 8 presented with chronic myelogenous leukemia (CML). Seven of the 8 had chromosomal abnormalities. Six had the Ph1 chromosome; 5 had the usual 9;22 translocation. Two patients had involvement with chromosome 15; one had a 9;15 translocation in Ph1 positive cells during remission while a second had a 1;15 translocation during blastic crisis. The 2 patients who did not have a Ph1 chromosome survived 13 and 30 months, respectively, considerably less time than the 4+ year survival in most of those with Ph1 positive CML.

Multiple keukemic clones in acute leukemia of childhood

SummaryTwo abnormal karyotypes representing clonal populations have been demonstrated in three patients in the early stage of acute leukemia. The karyotypes were apparently unrelated in one patient, while in the other two, a relationship was conjectured. Both clones were present before therapy in two patients. Although a clone resistant to therapy was associated with relapse in one case, in two cases a clone has persisted in the lymphocyte culture during drug treatment with the patients in remission.

Cytogenetic studies in an acute leukemia patient following cerebellar astrocytoma.

SummaryAcute, monomyelogenous leukemia (AMML) was diagnosed in a patient with a derived 13;14 translocation and prior treatment for a cerebellar astrocytoma. A bone marrow aspirate at the time of diagnosis of leukemia showed abnormalities of chromosome 11, 12 and 16 in addition to the constitutional aberration. The patients mother carried the same 13;14 translocation, as did 2 siblings, a maternal uncle, and four of his six children. The father had a reciprocal translocation between numbers 1 and 19 which was incidental to the present study.

9;22;15 complex translocation in Ph1 chromosome positive CML revealed by Giemsa-11 procedure in apparent lymphoid cells of blastic crisis

A Ph1 chromosome positive chronic myeloid leukemia patient whose chronic phase lasted 7.5 years experienced a blastic transformation originating in the spleen. The spleen was infiltrated with undifferentiated blast cells that on cytogenetic analysis had a hyperdiploid karyotype and were Ph1 chromosome positive. The blast cells were negative for PAS, peroxidase. Sudan black and esterase stains. They were non-T, non-B with TdT activity. Remission was achieved in response to prednisone, vincristine, and adriamycin. Ph1 positive cells were present with cells responding to PHA stimulation throughout the course of the disease. A Giemsa-11 staining procedure male possible the ascertainment of a No. 9 translocation chromosome in blastic crisis cells that had also been present in Ph1 chromosome positive cells early in the disease. The presence of this translocation initially in myeloid cells and subsequently in apparent lymphoid cell types suggests the origin of this patients leukemia as a pluripotential stem cell.