Immunological Deficiency Disorders Associated with Chronic Lymphocytic Leukemia and Multiple Myeloma*

Cone, Lawrence A.; Uhr, Jonathan W.

doi:10.1172/jci105098

Cited by 194 publications

(46 citation statements)

References 31 publications

(29 reference statements)

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“…Diseases with increased numbers of lymphocytes in the circulation which are part of the neoplastic process, as in CLL and some FLL, have reduced lymphocyte transformation when stimulated with PHA. Antibody formation and the concentration of normal immunoglobulins are equally deficient in MM and CLL (Fahey et al, 1963;Cone and Uhr, 1964), but in our studies lymphocyte transformation was abnormal only in CLL. Conversely, cell-mediated (delayed) hypersensitivity, which is normal early in the evolution of CLL (Bernadou et al, 1971) and in MM (Cone and Uhr, 1964;Aisenberg, 1968), does not correlate well with our lymphocyte transformation findings.…”

Section: Discussioncontrasting

confidence: 64%

“…Antibody formation and the concentration of normal immunoglobulins are equally deficient in MM and CLL (Fahey et al, 1963;Cone and Uhr, 1964), but in our studies lymphocyte transformation was abnormal only in CLL. Conversely, cell-mediated (delayed) hypersensitivity, which is normal early in the evolution of CLL (Bernadou et al, 1971) and in MM (Cone and Uhr, 1964;Aisenberg, 1968), does not correlate well with our lymphocyte transformation findings. A lack of correlation between delayed hypersensitivity and lymphocyte transformation with PHA in CLL was also demonstrated by Bernadou et al (1971).…”

Section: Discussioncontrasting

confidence: 64%

“…These neoplastic proliferations of one or more of the cellular components of the immunological system have been shown to have several features in common, namely: (1) the proliferation of cells concerned in immunological responses; (2) immunodeficiences due to defective synthesis of antibodies, defective cellmediated (delayed) hypersensitivity or both (Miller, 1962;Good et al, 1962;Fahey et al, 1963;Cone and Uhr, 1964;Aisenberg, 1968); (3) the production of monoclonal immunoglobulins (" M " components) which is a feature of myelomatosis and Waldenstrom's macroglobulinaemia as well as of many cases of chronic lymphocytic leukaemia (CLL) and well differentiated (diffuse or follicular) lymphocytic lymphoma (Haller, 1966;Krauss and Sokal, 1966) and of cases of mixed lymphoid and plasma cell proliferation (Saunders et al, 1969); and (4) the well-recognized existence of cases with features intermediate between two or more of the diseases in the group (Vtander and Johnson, 1960;Weinreich and Krey, 1968;Zlotnick and Robinson, 1970;Galton et al, 1968;Forte et al, 1970;Jaeger and Lapp, 1970;Naidu and Rosner, 1971). An abnormal lymphocyte population, non-responsive or slowly responsive to mitogens, has been demonstrated in chronic lymphocytic leukaemia (CLL) (Quaglino and Cowling, 1964;Oppenheim et at., 1965;Thomson et al, 1966;Schrek, 1967;Lawler et al, 1968;Rubin et al, 1969).…”

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confidence: 99%

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Lymphocyte Transformation in Immunoproliferative Disorders

Catovsky¹,

Holt²,

Galton³

1972

Br J Cancer

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Summary.-Lymphocyte transformation with phytohaemagglutinin (PHA) was studied in 30 patients with immunoproliferative disorders (lymphoproliferative and plasma cell disorders).Lymphocyte transformation at 3 days was reduced in the lymphoproliferative disorders (chronic lymphocytic leukaemia (CLL), well-differentiated (lymphocytic) follicular lymphoma (FLL) and Waldenstrom's macroglobulinaemia (WM)), and normal in the plasma cell disorders (myelomatosis, primary systemic amyloidosis, a-chain disease and benign monoclonal gammopathy) and in idiopathic cold haemagglutinin disease. A case of plasma-cell leukaemia with increased numbers of abnormal cells in the circulation also showed reduced transformation. It is suggested that the presence in the circulation of abnormal lymphocytes (or plasma cells) accounts for the results in CLL and FLL, WM and plasma-cell leukaemia. In WM a correlation was found between the activity of the disease (expressed by the levels of IgM paraprotein) and the degree of blast transformation.The long-term (28 days) in vitro survival of lymphocytes using subconcentrations of PHA was also studied in 7 patients. The cell populations (PHA-non-responsive) of CLL and FLL, but not of WM, had a good in vitro survival, resembling in this respect the normal PHA-responsive population of lymphocytes, but they remained PHA-non-responsive after 4 weeks' culture. It is speculated that in CLL the long survival in vitro of the PHA-non-responsive (leukaemic) population corresponds to their long life-span in vivo.

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Section: Discussioncontrasting

confidence: 64%

Section: Discussioncontrasting

confidence: 64%

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confidence: 99%

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Lymphocyte Transformation in Immunoproliferative Disorders

Catovsky¹,

Holt²,

Galton³

1972

Br J Cancer

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“…MULTIPLE mnyeloma, both in man (Fahey et al, 1963;Cone and Uhr, 1964;Dammaco and Clausen, 1966) and the mouse (Smith et al, 1960;Fahey and Humphrey, 1962;Hirano et al, 1968;Zolla et al, 1974) often produces a marked humoral immunodepression. Associated with this depressed antibody response is the tendency of patients with myeloma to fall victim to infectious diseases (Fahey et al, 1963;Zinneman and Wall, 1964;Scharff and Uhr, 1965;Meyers et al, 1972).…”

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confidence: 99%

Lymphocyte Defect in Plasmacytoma-bearing Mice

Brus¹,

Brent²,

Hollander³

1978

Br J Cancer

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Multiple myeloma is often associated with humoral immunodepression in both man and mouse. When mice bearing the humorally immunodepressive plasmacytomas TEPC-183 and SPQC-11 were injected with SRBC, the rise of serum haemolysins was significantly less than that of non-tumour-bearing mice. Mice with the plasmacytomas MPC-11 and MOPC-315 have an antibody response similar to normal mice when injected with SRBC. Following immunization, normal mice and those bearing MPC-11 showed a 2- to 3-fold increase in total spleen lymphocytes. Mice bearing TEPC-183 or SPQC-11, the plasmacytomas causing an impaired antibody response, has significant increase in spleen lymphocytes under the same conditions. Mice bearing MOPC-315 had a very high initial count of spleen lymphocytes, which did not further increase upon immune stimulation. Incubation of lymphocytes from plasmacytoma-bearing mice with PHA did not produce an increase in TdR incorporation and in some cases even caused a decrease in TdR incorporation. Lymphocytes from mice bearing TEPC-183, SPQC-11, and MOPC-315 incorporated less TdR in response to LPS than did normal mice. On the other hand, mice bearing MPC-11 incorporated about as much TdR as did normal mice following LPS stimulation. Thus, the defect in the ability to respond to LPS in vitro correlated with the lack of an increase of spleen lymphocytes in mice bearing these tumours following antigenic stimulation in vivo . No immunodepressive properties of serum from mice with plasmacytoma could be detected.

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“…These are RNA viruses, whose oncogenic potential is realized in the central lymphoid organs. The abnormal lymphocytes, like those in human lymphomas, show a loss of their usual reactivity [7][8][9], and the diseased animals (or human subjects) express a corresponding diminution ofimmunologic responsiveness [10][11][12][13][14][15]. It now appears that the NZB mouse and related strains are hosts for a similar virus and develop lymphomas [16][17][18][19].…”

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confidence: 99%

Title Page / Index / Introduction

Progress in Allergy Vol. 12

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Immunological Deficiency Disorders Associated with Chronic Lymphocytic Leukemia and Multiple Myeloma*

Cited by 194 publications

References 31 publications

Lymphocyte Transformation in Immunoproliferative Disorders

Lymphocyte Transformation in Immunoproliferative Disorders

Lymphocyte Defect in Plasmacytoma-bearing Mice

Title Page / Index / Introduction

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