Italian Society of Hematology, Italian Society of Experimental Hematology, and Italian Group for Bone Marrow Transplantation Guidelines for the Management of Indolent, Nonfollicular B-Cell Lymphoma (Marginal Zone, Lymphoplasmacytic, and Small Lymphocytic Lymphoma)

2015 ◽  
Vol 15 (2) ◽  
pp. 75-85 ◽  
Author(s):  
Corrado Tarella ◽  
Luca Arcaini ◽  
Luca Baldini ◽  
Giovanni Barosi ◽  
Atto Billio ◽  
...  
2002 ◽  
Vol 76 (6) ◽  
pp. 2857-2870 ◽  
Author(s):  
Katja C. Erlach ◽  
Jürgen Podlech ◽  
Aysel Rojan ◽  
Matthias J. Reddehase

ABSTRACT Tumor relapse and cytomegalovirus (CMV) infection are major concerns in the therapy of hematopoietic malignancies by bone marrow transplantation (BMT). Little attention so far has been given to a possible pathogenetic interplay between CMV and lymphomas. CMV inhibits stem cell engraftment and hematopoietic reconstitution. Thus, by causing maintenance of bone marrow aplasia and immunodeficiency, CMV could promote tumor relapse. Alternatively, CMV could aid tumor remission. One might think of cytopathogenic infection of tumor cells, induction of apoptosis or inhibitory cytokines, interference with tumor cell extravasation or tumor vascularization, or bystander stimulation of an antitumoral immune response. To approach these questions, the established model of experimental BMT and murine CMV infection was extended by the introduction of liver-infiltrating, highly tumorigenic variant clone E12E of BALB/c-derived B-cell lymphoma A20. We document a remarkable retardation of lymphoma progression. First-guess explanations were ruled out: (i) lymphoma cells were not infected; (ii) lymphoma cells located next to infected hepatocytes did not express executioner caspase 3 but were viable and proliferated; (iii) an inhibitory effect of virus on the formation of tumor nodules in the liver became apparent by day 7 after BMT, long before the reconstitution of immune cells; and (iv) recombinant tumor necrosis factor alpha (TNF-α) did not substitute for virus; accordingly anti-TNF-α did not prevent the inhibition. Notably, while the antitumoral effect required replicative virus, prevention of cytopathogenic infection of the liver by antiviral CD8 T cells did not abolish lymphoma control. These findings are paradigmatic for a novel virus-associated antitumoral mechanism distinct from oncolysis.


Blood ◽  
1990 ◽  
Vol 76 (11) ◽  
pp. 2411-2417
Author(s):  
LW Kwak ◽  
MJ Campbell ◽  
AD Zelenetz ◽  
R Levy

Recurrence of the underlying malignancy remains a major cause of treatment failure after autologous bone marrow transplantation (BMT) for patients with lymphoma. In this regard, we have developed an immunotherapeutic approach designed to induce resistance against residual tumor cells persisting after BMT. Previous studies in the model system of 38C13, a lethal B-cell lymphoma of C3H origin, have shown that active immunization with purified tumor-derived surface immunoglobulin (Id), as a tumor-associated antigen, produces resistance to tumor growth. Id immunization of lethally irradiated mice at 3 or 5 weeks after reconstitution with syngeneic bone marrow resulted in significantly prolonged survival after tumor challenge compared with nonspecifically immunized controls. Low levels of idiotype-specific antibody were also demonstrated in the sera of specifically immunized mice at this early time, when other functional studies in the literature of immunocompetence after syngeneic reconstitution might have predicted incomplete recovery. Immunization of mice before lethal irradiation and syngeneic marrow reconstitution also induced significant resistance to tumor challenge, suggesting the persistence of established host antitumor immunity through total body irradiation. These studies demonstrate the feasibility of id immunization in conjunction with bone marrow transplantation.


Blood ◽  
1990 ◽  
Vol 76 (11) ◽  
pp. 2411-2417 ◽  
Author(s):  
LW Kwak ◽  
MJ Campbell ◽  
AD Zelenetz ◽  
R Levy

Abstract Recurrence of the underlying malignancy remains a major cause of treatment failure after autologous bone marrow transplantation (BMT) for patients with lymphoma. In this regard, we have developed an immunotherapeutic approach designed to induce resistance against residual tumor cells persisting after BMT. Previous studies in the model system of 38C13, a lethal B-cell lymphoma of C3H origin, have shown that active immunization with purified tumor-derived surface immunoglobulin (Id), as a tumor-associated antigen, produces resistance to tumor growth. Id immunization of lethally irradiated mice at 3 or 5 weeks after reconstitution with syngeneic bone marrow resulted in significantly prolonged survival after tumor challenge compared with nonspecifically immunized controls. Low levels of idiotype-specific antibody were also demonstrated in the sera of specifically immunized mice at this early time, when other functional studies in the literature of immunocompetence after syngeneic reconstitution might have predicted incomplete recovery. Immunization of mice before lethal irradiation and syngeneic marrow reconstitution also induced significant resistance to tumor challenge, suggesting the persistence of established host antitumor immunity through total body irradiation. These studies demonstrate the feasibility of id immunization in conjunction with bone marrow transplantation.


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