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Biomedical subjects

D Catovsky

Publications and source records attributed to D Catovsky.

At least 505 records · Page 28Linked to original sources

The histopathology of prolymphocytic leukaemia with particular reference to the spleen: a comparison with chronic lymphocytic leukaemia.

The histological features of prolymphocytic leukaemia are described in spleen, lymph nodes, liver and bone marrow from nine cases. Eight patients had B-PLL one had T-PLL. These features were compared with those of six cases of B chronic lymphocytic leukaemia (B-CLL) with massive splenomegaly. Both PLL and B-CLL showed enlargement of the white pulp with nodule formation and diffuse infiltration of the red pulp. In both PLL and CLL larger cells were found in the white pulp nodules often concentrated on the periphery producing a bizonal appearance. The extent of involvement of the white pulp was greater in PLL than in uncomplicated CLL. However, this was not so in two cases of B-CLL in prolymphocytoid transformation in which the heavy replacement of the white pulp by large cells without a bizonal arrangement had effaced the red pulp. The cytological differences between PLL and CLL were best appreciated in splenic red pulp. The cells of CLL were small lymphocytes with clumped chromatin, those of PLL were larger with bigger nuclei, often indented in some cases, and distinct nucleoli. The pattern of infiltration in the bone marrow, liver and lymph nodes was similar in PLL and CLL. In conclusion, PLL can be distinguished from CLL by morphological and immunological features. The distinction is important clinically, because the survival of PLL is shorter than that of CLL.

Aged↗

Increase in T gamma lymphocytes in B-cell chronic lymphocytic leukaemia.

A significant increase in the proportion (mean 38% +/- 9.3 SD) and absolute number of T gamma (suppressor) lymphocytes was observed in 13 patients with chronic lymphocytic leukaemia (CLL) compared with 20 normal controls (mean 19% +/- 6.5). Conversely, the proportion of T mu (helper) lymphocytes was lower in CLL (mean 27% +/- 9.3) than in the controls (mean 40% +/- 4), although the absolute numbers were normal or increased. It is suggested that an imbalance of T-lymphocyte subsets controlling B-lymphocyte differentiation may be relevant in the pathogenesis of CLL or some of its associated features.

B-Lymphocytes↗

Mouse RBC rosettes in chronic lymphocytic leukaemia: different expression in blood and tissues.

Mouse RBC (M) rosettes were investigated on lymphocytes from peripheral blood (PB) and various tissues in twenty patients with chronic lymphocytic leukaemia and one with follicular lymphoma. In all cases studied, the percentage of M rosettes was significantly higher in PB (median 64%) than in bone marrow (median 15%) and lymph node (median 12%). These differences were statistically significant (P less than 0.01). The possibility that these differences were related to technical factors was ruled out by a number of control procedures. It is suggested that the different expression of M rosette formation reflects the property which determines whether a lymphocyte enters the peripheral blood or remains fixed in the tissues.

Animals↗

Inhibition of T-lymphocyte colony formation by inhibitors of mitochondrial protein synthesis.

A double layer technique which requires an underlayer of peripheral blood leucocytes, in addition to phytohaemmagglutinin (PHA) in the overlayer, to obtain good T-lymphocyte colony formation, was used to assess the effect of two inhibitors of mitochondrial protein synthesis, chloramphenicol and ethidium bromide. A significant inhibition of the colony growth of peripheral blood T lymphocytes was observed when either of the drugs was incorporated in the underlayer. The inhibitory effect was always smaller (c. 50%) when the drugs were added to the overlayer. These findings point to the existence of a T-lymphocyte colony stimulating factor(s), released mainly by the leucocyte-rich underlayer and essential for T-colony formation, the production of which is inhibited by these mitochonrial inhibitors.

Chloramphenicol↗

Evidence that T colony formation is a property of T mu (helper) lymphocytes.

The T-colony-forming capacity of different T lymphocyte subsets was studied in normal peripheral blood. Unfractionated lymphocytes (after 'Lymphoprep' separation) gave rise to a mean of 150 +/- 27 . 7 s.d. T colonies per 1 x 10(5) cells, while purified T lymphocytes by sheep RBC rosetting formed 110 +/- 32 . 2 colonies. Two subpopulations of T lymphocytes were further isolated according to the presence of Fc receptors for IgG (T gamma) or IgM (T mu) by ox RBC rosetting. T gamma cells were found to have a very low or absent T colony-forming capacity (23 +/- 26 . 2), while T mu cells produced normal colony numbers (106 +/- 28 . 4). Co-culture experiments showed that T gamma cells do not inhibit the T colony growth of normal T cells in our system. Our findings indicate that in human peripheral blood not all T lymphocytes are capable of forming T colonies and that this property is confined to the T mu (helper) lymphocyte subset.

Cell Separation↗

T-lymphocyte colonies in human cord blood.

The capacity of human cord blood (CB) lymphocytes to form T-colonies was studied with a double layer technique. The mean number of colonies in CB was 91 +/- 70.5 SD (X 10(5) cells), significantly lower than in adult blood, mean 182 +/- 58.0 (X 10(5). In 28 of the 50 CB samples tested the colony numbers were below the normal range for adult lymphocytes. There was no direct correlation between number of colonies and percentage of E-rosette-forming cells in CB. Some CB samples with a high proportion of E-rosettes formed few T-colonies, suggesting that not all E-rosette positive cells are capable of producing T-colonies. On the other hand, some CB samples with a low proportion of E-rosettes formed normal numbers of T-colonies. Purification of two populations of T-cell enriched and T-cell depleted lymphocytes confined the T-colony growth in CB, as in adult blood, to the former fraction, excluding that T-colonies could be obtained from E-rosette negative lymphocytes. This indicates that, from birth onwards, T-lymphocyte colonies originate from E-rosette positive cells. Whether the low growth observed in CB results from lack of maturation of T-lymphocytes or from the presence of specific subsets of T-lymphocytes is not clear at the present time.

Colony-Forming Units Assay↗

Immunoreactive calcitonin in leukaemia.

A radioimmunoassay was used to measure concentrations of immunoreactive human calcitonin (HCT) in plasma and leucocytes from patients with various leukaemic and myeloproliferative disorders. Plasma immunoreactive HCT concentrations were increased in 32 out of 33 patients with chronic granulocytic leukaemia (CGL) and in all eight patients with acute myeloid leukamia (AML) at presentation or in relapse. Out of 11 patients with other myeloproliferative disorders, eight had increased plasma immunoreactive HCT concentrations. Buffy-coat-cell extracts and culture media from peripheral leucocytes of patients with CGL also contained increased immunoreactive HCT concentrations. In contrast, plasma from patients with chronic lymphocytic leukaemia, acute lymphoblastic leukaemia, and AML in remission had low or undetectable immunoreactive HCT concentrations. Increased plasma and cellular concentrations of immunoreactive HCT may be a consequence of abnormal proliferation of myeloid cells and might prove to be valuable in predicting relapse in patients with myeloid leukaemias.

Calcitonin↗

Hairy-cell leukaemia with polyarteritis nodosa.

In four patients a systemic vasculitis similar to polyarteritis nodosa developed within 2 years of the onset of hairy-cell leukaemia. Arteriographic studies in two patients revealed microaneurysms, and biopsy specimens in three patients revealed a vasculitis affecting medium-sized vessels. Blood neutrophilia and neutrophilic vascular infiltrate were absent. One patient had circulating immune complexes. Two patients responded to corticosteroids alone, one required cyclophosphamide as well as steroids, and one improved without chemotherapy. The association of vasculitis with hairy-cell leukaemia may provide insight into the pathogenesis of arteritis.

Adult↗

Cryopreserved peripheral blood cells functioning as autografts in patients with chronic granulocytic leukaemia in transformation.

Six patients with chronic granulocytic leukaemia (CGL) in transformation were treated with cytotoxic drugs or cytotoxic drugs plus total body irradiation, followed by infusion of reconstituted autologous peripheral blood cells that had been collected from them at diagnosis and stored in liquid nitrogen for up to 58 months. In four cases the blood and bone-marrow appearances were rapidly restored to those of typical chronic-phase disease. In three of these patients transformation recurred at 74, 32, and 26 weeks respectively. One patient was still in second chronic phase at eight weeks. One of the patients who entered a second transformation was restored to a third chronic phase by further treatment with cytotoxic drugs and a second autograft. Cryopreserved autologous blood cells may thus restore some patients with CGL in transformation to chronic-phase disease and so may help to prolong life.

Adult↗

Alkaline phosphatase in human lymphocyte subpopulations.

The levels of membrane alkaline phosphatase have been measured on different lymphocyte fractions from human peripheral blood separated on bovine serum albumin discontinuous gradients. The peak in enzyme activity was observed in a non-T-, non-B-cell fraction, rich in "null" lymphocytes; the lowest values were found in the fraction with the highest proportion of T-cells.

Alkaline Phosphatase↗

Clinical staging and immunological findings in chronic lymphocytic leukemia.

Several immunological markers were tested in 52 untreated cases of chronic lymphocyte leukemia (CLL) to see whether their frequency differed according to the clinical stage in Rai's system. The leukemic cells in all cases had B-cell features as shown by monoclonal immunoglobulins on the cell surface (SmIg) and/or a high percentage of mouse RBC (M)-rosettes. Of the two B-cell markers, the M-rosette test was the more consistently positive. The frequency of these markers did not correlate with clinical staging. The percentage of T-lymphocytes, low in all cases, was found to correlate inversely with the lymphocyte counts, which were higher in advanced stages. The absolute number of T-lymphocytes was above normal in most cases, but did not relat to staging. At least one of the serum Ig, most commonly IgA, was decreased in 87% of cases. Low Ig were slightly less common in Stages 0-I than in advanced stages (II-IV). The above features were also examined in two groups of CLL patients: with stable (9) or progressive (16) disease. The only difference observed between the two groups was that surface IgM only was present in 1 of the 9 stable cases as compared to 9 of the 16 progressive ones. Our findings do not support the suggestions that surface IgM is a feature of a benign form of CLL or that the absolute number of T-lymphocytes correlates with prognosis.

Adult↗