Cellular phenotypes of normal and leukemic hemopoietic cells determined by analysis with selected antibody combinations.

Individual leukemic cells and the corresponding rare normal cell types in nonleukemic bone marrow were analyzed with various combinations of antisera (labeled with different fluorochromes: TRITC and FITC). Double staining for membrane Ia-like molecules (TRITC) and nuclear terminal transferase (FITC) was a very useful combination that distinguished common non-T, non-B ALL (Ia+,TdT+) and thymic ALL (Ia-,TdT+) from the rare cases of B ALL (Ia+,TdT-) and from AML (frequently Ia+, TdT-; in some cases Ia-, TdT-). Additional antisera (such as anti-ALL, anti-HuTLA, anti-immunoglobulin reagents, etc.

Remission induction with adenosine-deaminase inhibitor 2'-deoxycoformycin in Thy-lymphoblastic leukaemia.

Two patients with relapsed acute lymphoblastic leukaemia of thymic phenotype (Thy-ALL) resistant to all conventional chemotherapy achieved complete remission when treated with 2'-deoxycoformycin, a selectively lymphocytotoxic compound that acts by inhibition of the enzyme adenosine deaminase. These observations show that malignant thymocytes are dependent on adenosine-deaminase activity and suggest that it may be possible to use deoxycoformycin in other patients with Thy-ALL to induce remission or to kill Thy-ALL blasts in bone marrow harvested before autologous bone-marrow transplantation, leaving normal haemopoietic stem cells intact.

Subpopulations of normal and leukemic human thymocytes: an analysis with the use of monoclonal antibodies.

Combinations of antibodies to membrane antigens and to terminal deoxynucleotidyl transferase (TdT) were used to study human thymocyte and bone marrow subpopulations and leukemia cells. Cortical thymocytes were TdT+ and expressed T-cell antigens (HuTLA+), a thymocyte-specific antigen (HTA-1+), and a leukocyte antigen (HLe-l++) but lacked detectable HLA-A,B,C and la (HLA-D) antigens. In contrast, medullary thymocytes were TdT-, HuTLA+, HTA-1-, HLe-l++.

Mixed lymphoblastic-myelomonoblastic leukemia in treated Hodgkin's disease.

In a case of acute leukemia occurring 5.5 yr after diagnosis of Hodgkin's disease, a mixture of lymphoid and myelomonocytoid blasts was identified by morphological, cytochemical, and immunologic methods. The majority of blasts were characterised as lymphoid by their strong expression of nuclear terminal transferase (TdT) enzyme.

Terminal transferase enzyme assay and immunological membrane markers in the diagnosis of leukaemia: a multiparameter analysis of 300 cases.

Multiparameter analyses have been carried out with recently developed enzyme and membrane markers in 300 patients with various leukaemias including ALL, AML, but excluding Ph1 positive leukaemias. TdT enzyme levels were particularly valuable in the differential diagnosis of adult acute lymphoid and myeloid leukaemias. The levels were raised in 108 (94%) of the 115 patients who were considered to be non-T, non-B ALL on membrane marker and morphological analysis; all seven cases giving negative TdT results in this group were young children.

Terminal transferase-positive human bone marrow cells exhibit the antigenic phenotype of common acute lymphoblastic leukemia.

Combined immunologic assays for TdT enzyme and membrane markers show that TdT+ cells in nonleukemic human bone marrow carry ALL-associated and Ia-like antigens but no thymocyte markers or surface Ig. These cells could be precursors involved in acute lymphoblastic leukemia of the "common" or non-T, non-B type and in lymphoid blast crisis of Ph' positive chronic myeloid leukemia. A few TdT+, Ia+ cells express cytoplasmic IgM, indicating that some pre-B cells may be TdT positive.

The successful treatment of primary amyloidosis with intermittent chemotherapy.

A patient with primary amyloidosis is described with extensive vital organ involvement including infiltration of the liver, kidney and myocardium. Treatment with intermittent melphalan and prednisone resulted in improved hepatic and renal function, a reduction in liver size and arrested amyloid deposition in the myocardium. These observations suggest that chemotherapy can halt tissue amyloid deposition, and improve the prognosis of primary amyloidosis.