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K H Robèrt

Publications and source records attributed to K H Robèrt.

43 records · Page 3Linked to original sources

Mitogen-induced differentiation of human CLL lymphocytes to antibody-secreting cells.

Peripheral blood lymphocytes from nine patients with chronic lymphatic leukaemia (CLL) have been stimulated by photohaemagglutinin, pokeweed mitogen and Epstein-Barr virus. Our results provide proof that the leukaemic B cells in CLL are capable of responding to mitogenic signals by producing and secreting antibodies, transforming into blast cells, and, probably, increasing their rate of DNA synthesis.

Antibody Specificity↗

Covariances of mitogenic responses in leukaemic blood lymphocytes: a functional marker system for the human B lymphocyte differentiation.

Various polyclonal activating substances have been shown to stimulate human chronic lymphatic leukaemic (CLL) cells to undergo blast transformation, to divide and to secrete monoclonal immunglobulin. CLL cells from different patients show distinct response patterns to these ligands. We have statistically analysed these response patterns and found that responses to certain ligands demonstrate covariance; that is, a high response to one ligand is statistically associated with a high response to another ligand. A factor analysis of these data on the basis of responses of CLL cells from twenty-one patients and from the use of five different ligands in three different concentrations has shown that as few as two factors can account for as much as 63% of the total variance of these responses. On the assumption that these two factors were T-cell dependency of CLL responses and stage of maturity of the responding CLL cell, we have formulated a theory that explains the basis for this functional marker system for CLL cells. It is possible application to the characterization of individual CLL clones has been discussed.

B-Lymphocytes↗

B-cell activation of peripheral blood lymphocytes from patients with chronic lymphatic leukaemia.

The mitogenic response of blood lymphocytes from twelve patients with B-cell CLL and seven healthy controls was investigated. All patients were untreated and had a typical B-cell dominance in their peripheral blood. The patients demonstrated a scattered response pattern with a higher variance than in the control group. We demonstrated examples of stimulation of DNA-synthesis by polyclonal B-cell activators (PBA) as well as inhibition. The variable pattern between the patients might result from a malignant transformation of cells originating from different lymphocyte subpopulations in different patients. Thus PBA studies of lymphocytes from CLL patients might be a valuable tool in characterizing further this clinically variable disease at the cellular level.

B-Lymphocytes↗

B-CLL cell surface markers and mitogen-induced thymidine uptake: a comparison between lymph node cells and peripheral blood lymphocytes in 25 patients.

Lymphocytes from peripheral blood and lymph nodes from 25 patients with B-CLL were analysed by immunofluorescent staining of surface membrane immunoglobulin (SmIg), the B-cell marker B1, and the T-cell markers Leu 1/2/3/4. Tritium-thymidine uptake was measured in mitogen-stimulated 4-day cultures. Differences in these parameters between cells from the two sources in each patient were calculated with the paired T-test. All cell samples showed a clonal B-cell population. More blood lymphocytes than lymph node cells expressed the monoclonal SmIg (mu or gamma, p = 0.04; kappa or lambda, p less than 0.01), and T-cells were more frequent in lymph nodes (p = 0.01), where the T helper/suppressor ratio was higher. Furthermore, lymph node cells showed a higher thymidine uptake in response to the mitogens LPS, PWM, and Cowan (p = 0.01, p = 0.01, and p = 0.004, respectively), but there was no difference in the responses to EBV, DxS, TPA and PHA (p greater than 0.5). The higher response in lymph node cells to some mitogens might in part be explained by differences in the numbers of accessory cells, such as T-helper cells, but also by the existence of leukaemic B-cell subsets with different mitogen response patterns and different distributions within the lymphoid compartments. The characterization of subsets within a malignant cell clone might be of clinical importance.

Adult↗

Inversion of chromosome 14 marks human T-cell chronic lymphocytic leukaemia.

Rare cases of chronic lymphocytic leukaemia (CLL) in man stem from the malignant proliferation of T cells. The disease is usually more aggressive clinically than B-cell-derived CLL. Various haematological tumours are associated with specific chromosome aberrations (for example, refs 1, 2). Only limited numbers of T-cell CLL patients have so far been studied cytogenetically and, whereas chromosome 12 seems particularly to be involved in B-cell CLL, several markers have been found in T-cell tumours. Recently, by stimulating malignant clones with different mitogens, novel chromosome abnormalities have been detected in T-cell CLL. Using the same approach for additional cases of T-cell CLL, we now report that the most consistent chromosome change is an inversion of the long arm of chromosome 14, inv(14)(q11 q32), in four of five patients. Another remarkable chromosome aberration is trisomy for the long arm of chromosome 8, found in three of five patients.

Chromosome Aberrations↗