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E Klein

Publications and source records attributed to E Klein.

At least 613 records · Page 34Linked to original sources
PubMed1973

Immunoglobulin and glucose-6-phosphate dehydrogenase as markers of cellular origin in Burkitt lymphoma.

Two independent marker systems, G-6-PD isoenzymes and cell membrane-associated IgM, were used to trace the cellular origin of Burkitt lymphoma. Application of the G-6-PD system is dependent upon the fact that, in accordance with inactivity of one X chromosome in each somatic cell, females heterozygous for the usual B gene (Gd(B)) at the X-linked G-6-PD locus and the variant allele Gd(A) (or Gd(A-)) have two types of cells. Gd(B) is active in one cell population, which consequently produces B type enzyme; in the other population Gd(A) is active, producing the variant A enzyme. Therefore, tumors with a clonal origin in a Gd(B)/Gd(A) heterozygote should exhibit only one enzyme type (B or A) whereas those with multicellular origin may show both A and B enzymes. Utilization of the immunoglobulin system is based upon the supposition that in lymphoid neoplasms with clonal origin either all or none of the tumor cells should have surface-associated IgM and kappa-reactivities. 33 of 34 relatively homogeneous (with respect to content of neoplastic cells) individual Burkitt tumors from 19 G-6-PD heterozygotes had single enzyme phenotypes. Similarly, of 95 tumors tested, 92 consisted essentially of IgM(+) or (-) cells. Two neoplasms could not be definitely classified and one tumor had two cell populations. These data suggest a clonal origin for most Burkitt tumors, but the one neoplasm with a double G-6-PD phenotype (A/B) and the one tumor that had two populations of cells with respect to surface IgM, could have originated from multiple cells. G-6-PD was determined in each of two tumors from seven heterozygotes and in all cases both tumors had the same single enzyme phenotype. Surface-associated IgM was tested in four tumors from one patient, three from another, and in two neoplasms from 11 patients. With one exception, all tumors from the same patient were concordant with respect to IgM. These findings suggest that the entire disease has a clonal origin, i.e., it emerges at one focus and then spreads to other parts of the body. Cells from 36 recurrent neoplasms were typed for G-6-PD (in heterozygotes) and/or IgM. In one previously reported patient, initial and recurrent tumors were discordant for G-6-PD. Two other patients had IgM phenotypes in recurrences that were discordant with those found in their initial tumors. Phenotypes from three of nine relapses which occurred after 5 mo were discordant for G-6-PD or IgM but no discordance was detected among 27 earlier recurrences. Thus, some "late" recurrences may be due to emergence of "new" maligant cell lines whereas most early relapses are due to reemergence of the original malignant clones. The probable unicellular origin of Burkitt lymphoma and the findings in tumor recurrences are discussed in terms of the disease's putative viral etiology.

Animals↗
PubMed1973

The lymphocyte response to primary Moloney sarcoma virus tumors in BALB-c mice. Definition of the active subpopulations at different times after infection.

Adult BALB/c mice were injected with Moloney sarcoma virus (MSV) after which the animals' lymphocytes were examined for activity against Moloney leukemia virus (MLV) antigen-bearing target cells at 5-day intervals for 30 days. Lymphocytes from these animals and appropriately matched controls were fractionated into B cell-deficient (primarily T cells) and T cell-deficient (primarily B cells) subpopulations. Macrophages were removed using iron powder and magnetism. The unfractionated lymphocytes, T cells, and non-T cells were then tested in microcytotoxicity tests. Antigen-specific activity was found in the unfractionated lymphocytes from animals that had not yet developed palpable tumors and from regressor animals. The T cells were active just before tumor development and just after regression; however, by day 30 after virus infection (8-10 days after regression) the T cell subpopulation was much less active. The non-T cell subpopulation was also active before tumor development and soon after regression. However, this activity continued to rise after regression and was highest at 30 days. At day 15 (peak tumor size) neither subpopulation was active. The activity was demonstrated to be specific for the MLV-determined cell surface antigen by testing on control target cells that were MLV antigen negative and by comparison of the inhibitory effects with lymphocytes immune to a nonpertinent antigen as well as normal lymphocytes. The non-T cells were tested for activity before and after removal of macrophages with iron powder and magnetism. Such cells were significantly more active after removal of the macrophages. These data demonstrate specific T cell and non-T cell activity in microcytotoxicity tests with a tumor-specific system and strongly suggest that the non-T cell activity described herein is a B cell function.

Animals↗
PubMed1973

The influence of the partner cell on the production of L virus and the expression of viral surface antigen in hybrid cells.

The C-type particles produced by the A9 and A9HT sublines of mouse L cells were shown to infect C3H (N type), but not C57BL (B type), mouse embryo fibroblasts. Infection was indicated by distinct single giant cell formation in the XC monolayer used to overlay the mouse embryo fibroblasts. On the basis of these results it was concluded that the L cell virus is N tropic. A9 and A9HT cells were fused to various mouse cells derived from tumors and normal tissues. The ability to produce the Moloney-type surface antigen and to release infectious virus was introduced by the A9 component into the hybrid cell. Virus production, measured by antigen induction on JLS-V9 cells, was suppressed in those hybrids in which the partner cell had a genotype determining low infectibility with that particular virus (B-type cell). It thus appears that the major genetic locus affecting resistance to infection with leukemia viruses, the Fv-1 locus, regulates infectious virus production in somatic cell hybrids also. The same genetic locus did not seem to govern the expression of all virus-related functions, for the virus-determined membrane antigen was demonstrated in many of the N x B-type hybrids in which production of infectious virus was suppressed.

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