V. Zagonel

CD13 Expression in B-Cell Chronic Lymphocytic Leukemia is Associated with the Pattern of Bone Marrow Infiltration

The ectopic expression of the cell surface peptidase CD13 (aminopeptidase N) and of three other myelomonocytic antigens i.e. CD33, CD14 and CD15 was analyzed by flow cytometry in neoplastic lymphocytes from 81 consecutive patients with B-cell chronic lymphocytic leukemia (B-CLL). CD13 and CD14 antigens were detected on lymphocytes from 30% and 60% of patients respectively whilst a smaller percentage of samples was found positive for CD15 (5%) and CD33 (12%). The presence of CD13 and CD33 antigens on neoplastic B cells showed a statistically significant association with the two most important clinicopathologic prognostic factors in B-CLL: the clinical stage (CD13, p < 0.01; CD33, p < 0.05—Rai and Binet staging systems) and the pattern of bone marrow infiltration (CD13, p < 0.001; CD33, p = 0.02). A multiple logistic regression analysis showed that the increased risk of CD13 positive patients (13.7 fold higher than in CD13 negative cases; p = 0.001) of presenting a diffuse pattern of bone marrow infiltratio...

Lung cancer in the elderly

In western countries, the elderly constitute the most rapidly growing section of the population and the group at highest risk for developing cancers (I). It has been hypothesized that, by the turn of the century, approximately one-fifth of the population in industrialized countries will comprise individuals aged 65 years or more (1). The extent to which cancer affects the elderly population is well illustrated by the fact that 59% of all cancers diagnosed from 1973 to 1981 among males in the USA, and 52% among females, occurred in the age group of 65 years and over (2). The older patient with cancer poses particular management problems which need to be addressed by clinical oncologists. We summarize here current clinical and therapeutic issues related to the management of lung cancer in the elderly.

Report of an unusual small lymphocytic B‐cell lymphoma selectively involving the B‐zone of lymph node

Selective involvement of the B‐cell compartment of lymph node by B‐cell malignant lymphomas is an occasional finding related to early phases of lymph node infiltration. The authors have observed a unique case of diffuse small lymphocytic lymphoma that consisted of immunohistologically and genotypically proven B‐clonal population exhibiting a repetitive pattern of infiltration in three lymph node samples obtained from the patient during a 9‐year period. This pattern consisted of a selective and complete replacement of the B‐areas with disappearance of follicles and widening of the medullary cords, an expanded T‐zone showing features consistent with dermatopathic lymphadenitis and well‐preserved sinuses. Clinically, multiple involved sites at presentation (lymph nodes, spleen, skin, bone marrow, and peripheral blood) and during the 9‐year follow‐up (testis) were detected, and the disease was associated with a relative indolent course like other low‐grade lymphomas. The phenotypic profile of lymphoma cells studied by immunoperoxidase method, and by single‐labeling and double‐labeling flow cytometric analyses (SIg+, K+, LN2+, MB1+, MB2+, HLA‐DR+, CD 9+, CD19+, CD20+, CD 21+, CD 22+, CD 24+, Leu 8+, CD 5–, CD 10–, CD 11b–, CD 11c–, CD 25–, CD 38–, PCA‐1–, FMC‐7–, CD 23–) was consistent with a B‐cell proliferation at an intermediate stage of differentiation but distinct from other well‐defined B‐cell neoplasms. Whether such unique B‐zone pattern was due to an intrinsic property of this lymphoma or it is to be related to the coexisting reactive T‐zone expansion remains controversial.

Expression of myeloid associated antigens in chronic lymphocytic leukaemia.

I have read with interest the recent article entitled ‘An in vitro direct chemiluminescence assay for assessment of plateletbound antibody in thrombocytopenic patients’ (Kazemi et al. 1991). The authors, without looking at our study (Ozsoylu et al, 1977). stated that ‘the interaction between phagocytes and autologous autosensitized platelets was not measured’. In our study it was looked for in vivo but could not be found (~zsoylu et al, 1977). I would also l i e to bring to the authors attention that by using the method described by Handel & Stossel (1974) we were able to detect antiplatelet antibodies (APA) in all 103 patients with acute idiopathic thrombocytopenic purpura (ITP) and 46 patients with chronic ITP. These antibodies could also be found during remission in all children who had had acute (100 cases) and chronic (32 cases) ITP, although the level was markedly lower than that during the thrombocytopenic period. Moreover, a rise in the APA level was seen during relapse in four chronic and two acute ITP patients. A decrease of APA was also shown by two out of four children who had re-entered remission after relapsed chronic ITP (c)zsoylu et aI, 1991). APA were not found in any of 126 control sera obtained from 67 haematologically normal individuals and 59 thrombocytopenic patients of whom 28 had acute leukaemia. 10 acquired aplastic anaemia, 10 Fanconi’s anaemia and 11 sepsis with thrombocytopenia ((lzsoylu et al. 1991). The persistence of APA during remission in cases of acute and chronic ITP, previously reported by us ((lzsoylu et al, 1976), explains the shorter survival of platelets in these children. Although the results of Kazemi et al (1991) are somewhat supportive of our findings it could be concluded that the method of Handin & Stossel (1974) is more appropriate for the detection of APA in ITP cases in relapse or in remission even though the two methods are very similar in principle.