Surface Markers and Prognostic Factors in Acute Lymphoblastic Leukemia

Abstract

We investigated the surface markers on lymphoblasts from 37 patients with acute lymphoblastic leukemia. Spontaneous rosette formation with sheep erythrocytes (E rosettes) identified T cells and the presence of surface immunoglobulin identified B cells. Eight patients had T-marker lymphoblasts; 28 had no markers (null lymphoblasts), and one patient had B-marker lymphoblasts. The eight patients with T-marker acute lymphoblastic leukemia had massive leukemic infiltration, frequently a mediastinal mass, and a poor prognosis. The T-marker lymphoblasts had a weak or negative periodic acid-Schiff reaction and a very low antigenic stimulation to allogeneic lymphocytes. The association of T-marker lymphoblasts and some of the conventional poor-risk factors appears to be reliable in predicting a poor prognosis.

T lymphoblastic leukaemia and the central nervous system

“…Prophylactic therapy to the CNS, as currently used, is ineffective in most patients with T ALL. While it might be observed that systemic therapy is equally ineffective (Tsukimoto, 1976) …”

“…IT HAS BEEN recognized for some time that the T-cell variety of lymphoblastic leukaemia (T ALL) carries a worse prognosis than non-T disease (Tsukimoto et al, 1976;Reid et al, 1977) and it has also been suggested to be frequently associated with meningeal (CNS) infiltration (Catovsky et al, 1974;Sallan et al, 1980). However, the inextricable association between T ALL and high white counts, a well known adverse prognostic feature in any ALL, begs the question whether it is the cellular characteristics of T lymphoblasts or merely their numbers that possibly predispose them to infiltrate the CNS.…”

Correlation of adenosine deaminase activity with cell surface markers in acute lymphoblastic leukemia.

“…Such encouraging results make it important to establish the prognosis for individual patients at the onset of treatment, particularly if it becomes possible to identify patients in a poor-prognostic category for whom different and more intensive therapy may be indicated (1). It has been shown that 20-25% of ALL patients have T-cell surface markers, and that these patients respond less well to therapy than the larger proportion of patients with null-cell ALL (21). Because the presence of high levels of ADA correlates with T-cell leukemia, determination of ADA activity in the lymphoblast cells of newly diagnosed ALL patients offers a simple and rapid technique to identify patients with a less favorable^,.rgnosis.…”

Walter Hubert Lecture, delivered 1 April 1980 to the 21st AGM of the BACR Malignant lymphomas as tumours of the immune system

“…The malignant cells have in particular the surface, cytochemical and biochemical features of immature thymocytes (Kaplan et al, 1974;Gatien et al, 1975;Coccia et al, 1976;Jaffe et al, 1976;Stein et al, 1976;Donlon et al, 1977;Stein & Muller-Hermelink, 1977;Kersey et al, 1978;Kung et al, 1978;Lukes et al, 1978a, b;Bollum, 1979;Long et al, 1979). The marked propensity for progression to leukaemia establishes a continuum between these tumours and a subset of acute lymphoblastic leukaemia (ALL), i.e., the 25% of cases of ALL with T-cell markers (Kersey et al, 1973;Sen & Borella, 1975;Tsukimoto et al, 1976 (Catovsky et al, 1974). In our series of lymphoblastic lymphomas, cases which did not form E rosettes tended to manifest AP activity as a diffuse multigranular reaction.…”