Friend leukemia

About: Friend leukemia is a research topic. Over the lifetime, 319 publications have been published within this topic receiving 7463 citations.

Differentiation of Friend Leukemia Cells Induced by β-, γ-, δ- and Aza-β-Mactam, and Thiaziadine Compounds

Abstract: β-, γ-, δ- and aza-β-lactam, and thiaziadine compounds induced the differentiation of Friend leukemia cells and hemoglobin was produced. Modification of the lactam rings of γ- and (δ-lactam compounds with aromatic side chains and bromine atoms enhanced their differentiation-inducing-activities to Friend leukemia cells. On the other hand, 4 thiaziadine compounds (AKT-1, AKT-2, AKT-3 and AKT-4), which commonly contain a -N(CH3)-N(CH3)-moiety, also promoted the differentiation of Friend leukemia cells. They had specific differentiation-inducing-abilities without toxic effects to Friend leukemia cells. 5-Aza-β-lactam compounds showed differentiation-inducing-activity toward all of three types of Friend leukemia cells, two of which were dimethylsulfoxide (DMSO)-sensitive and the other of which was DMSO-resistant. But we did not find any correlation between the differentiation-inducing-activity and the chemical group at the 1-imino position. The presence of an amino bond, which commonly exist in differentiation...

Origin of spleen colonies generated by Friend virus-infected cells in mice.

Abstract: “Tumor colonies” develop in the spleen of unirradiated C57BL/6 × DBA/2 F 1 (hereafter called BD2F 1 ) mice ( H-2 b /H-2 d ) 9 days after iv injection of spleen cells from N-tropic Friend virus-infected DBA/2 donors ( H-2 d /H-2 d ) To determine whether these spleen colonies resulted from donor or host cell proliferation, we compared the histocompatibility antigen markers of cell populations from dissected colonies and intercolonial areas Cytotoxic tests with mouse antisera specific for H-2D b and H-2D d antigens revealed the presence of both antigen specificities on cells from both sources, thus indicating that the majority of cells were of host BD2F 1 origin The presence of donor cells in spleen colonies could be detected, however, when the recipients were lethally irradiated (800 R) BD2F 1 mice, the colonies of which consisted exclusively of cells bearing H-2D d and not H-2D b (recipient) antigens Analogous results were obtained by cytotoxic analysis of spleen colonies in C57BL/6 × C3H/An F 1 mice injected with Friend virus-infected C3H/An spleen cells In addition, direct visualization of virus-induced antigens and H-2 antigens by immunofluorescent staining confirmed the cytotoxicity data Finally, the colony-forming efficiency of H-2 d cells was found to vary only slightly among unirradiated recipients of different H-2 haplotypes These findings indicate that spleen colony formation by Friend virus-infected leukemia cells was based on donor cell proliferation in irradiated hosts and on host cell proliferation in unirradiated hosts, for the strains used here The spleen colony assay for Friend leukemia cells in unirradiated hosts is therefore an assay for infectious centers where virus is apparently released from donor cells in quantities sufficient to infect Fv-1 -restrictive host cells and to initiate their proliferation

Suppression of in vitro antibody response by spleen cells of mice infected with Friend-associated lymphatic leukemia virus.

Abstract: The ability of spleen cells of mice infected with oncornaviruses to depress the in vitro antibody responsiveness of normal lymphoid cells was exploited in an attempt to clarify the role played by the lymphatic leukemia virus (LLV) component in the immunodepressive properties of the Friend leukemia complex. Spleen cells of mice infected with LLV or, for comparison, with the entire complex were added to cultures of sheep erythrocyte-primed uninfected spleen cells, and the antibody-forming cells produced by the latter, after antigen restimulation, were assayed. The addition within 2 days from culture initiation of low numbers of cells infected with either virus preparation suppressed all stages of the response affecting the production of both immunoglobulin M and immunoglobulin G antibody. The activity of infected cells resisted doses of ultraviolet radiation which inhibit cell multiplication but was abolished by disrupting the cells and was prevented by the presence of anti-LLV antibodies. The LLV-infected spleen cells responsible for suppression were not removed by treatments which selectively remove or kill macrophages and exhibited surface properties of B lymphocytes. These results were interpreted as indicating that the effect is due to virus (or viral products) released by B cells. The suppressing cells in the spleens of mice in the early days of Friend leukemia complex infection presented superimposable properties, supporting the concept that their activity is also due to the LLV they release in large quantities. However, in later stages of infection, the spleens of Friend leukemia complex-infected mice also contained non-B-suppressing cells possibly derived from the proliferation of nonlymphoid LLV-producing cells caused by the neoplastic process.