Second malignant clone underlying a Burkitt-tumor exacerbation.
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Biomedical subjects
Publications and source records attributed to G Klein.
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Some murine sarcoma virus (MSV)-transformed mouse 3T3 cells contain the MSV genome in the absence of infectious helper murine leukemia virus (MuLV) and MSV production. These cells, designated S+L- (sarcoma positive, leukemia negative), were analyzed for the presence of a possible MSV-determined membrane antigen by the mixed hemadsorption test and in vitro lymphocyte cytotoxicity assay. Two different serological approaches were used: (a) isoantibody-free sera were obtained by immunizing with MSV of syngeneic origin or by allowing primary, autologous MSV sarcomas to regress, or (b) alloantisera obtained by immunizing C57BL mice with S+L- cells were absorbed with the corresponding nontransformed 3T3 cells until all activity against 3T3 had been removed. While MuLV-superinfected S+L- cells and a culture line of an MSV sarcoma known to produce both MSV and MLV were highly reactive, normal 3T3 and S+L- cells were negative. Similarly, lymph node cells from MSV immune mice or rats did not kill S+L- cells, although they were cytotoxic against target cells known to carry MuLV-associated antigens. Thus, the present study gives no positive evidence for the existence of any MSV-induced new surface antigen in the transformed target cell, known to carry the viral genome.
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The Ehrlich ascites tumor, which has been subjected to prolonged selection for growth in allogeneic hosts, possesses powerful mechanisms for the suppression of antigens normally found on the cell surface. It has previously been shown (1, 2) that when cells in which surface antigens are fully expressed are fused with Ehrlich cells, the suppressive mechanisms of the latter continue to operate and the new surface antigens introduced into the hybrid cell by the other partner are also suppressed. In the present paper we describe the properties of hybrids in which one parent cell was the TA3 ascites carcinoma. There are two sublines of this carcinoma which originally arose as a spontaneous mammary carcinoma in a strain A mouse. The TA3/St line has a high concentration of H-2(a) antigens and shows a strain-specific transplantation behavior; the TA3/Ha subline has a drastically reduced antigen concentration and readily transgresses histoincompatibility barriers. The immunoresistant TA3/Ha subline arose spontaneously without having been subjected to any known immunological selection pressure. Hybridization of TA3/Ha cells with normal diploid ACA fibroblasts reestablished full expression of H-2(a) antigens in nine independently derived hybrid clones. Full reestablishment of both D- and K-end components of the H-2(a) complex could be demonstrated. In some hybrid clones the concentration of H-2(a) antigens was found to be comparable to that seen in (A x ACA)F(1) fibroblasts, whereas in others a higher concentration was observed, even exceeding, in some cases, the levels found in the TA3/St line. The H-2(f) complex, contributed by the ACA parent cell, was fully expressed in eight of the nine hybrid clones studied. Antigen suppression thus behaves as a recessive character in the TA3/Ha hybrids, whereas in the Ehrlich hybrids antigen suppression is dominant.
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1. The larger rRNA molecules of different species of amphibia do not all have the same mobility on polyacrylamide gels, and the difference appears to be one between the Anuran and Urodele amphibia. 2. Alteration of conditions of electrophoresis so as to distinguish between differences of conformation and molecular weight does not affect the results. 3. The mobility on gel electrophoresis of the rRNA precursor in two species of amphibia is similar, although the intermediate processing products differ. 4. It is suggested that the mobility differences observed represent differences of molecular weight, and are an example of the variability of the products of transcription and processing of rRNA genes in two amphibian genera.
Herpesviruses have been implicated in oncogenesis. They have been found to be etiologic agents in certain chicken, primate, and frog neoplasms. There is suggestive evidence that herpesviruses may contribute to the genesis of certain human lymphomas.
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