A total of 289,868 locus tests, based on 28 different protein phenotypes and using one-dimensional electrophoresis to detect variant proteins, has yielded one probable mutation in the offspring of "proximally exposed" parents, who received an estimated average gonadal exposure of 31 to 39 rem in the atomic bombings of Hiroshima and Nagak. There were no mutations in 208,196 locus tests involving children of "distally exposed" parents, who had essentially no radiation exposure. Studies of the genetic effects of atomic bombs have been in progress in Hiroshima and Nagasaki since 1946 (1-5). The first generation of studies was essentially morphological in nature. More recently, profiting from technological developments, studies have been undertaken at the cytogenetic (6, 7) and biochemical (8) levels. We present here a progress report on the results of the biochemical approach at approximately the midpoint of the study. No statistically significant difference between the children of exposed and control parents can be demonstrated at this time (nor was it expected at this juncture in the study). In addition to the timeliness of a progress report, however, the present publication is dictated by three other considerations. (i) The current intense interest in the genetic effects of low-level ionizing radiation has prompted a complete re-evaluation of 30 years of genetic studies on the effects of the atomic bombs; the present data can be integrated into that treatment. (fi) The control aspects of the data of this study can be combined with similar data from other studies to yield a direct estimate of the rate at which spontaneous mutation results in electrophoretic variants of proteins; this should be useful in planning the feasibility and magnitude of any other genetic studies of this type. (Wi) A wealth of data on biochemical variants in Japanese has accumulated during the past 7 years; this description should clear the way for the presentation of this information.
The MHC class II I‐A(s) positive B cell lymphomas reticulum cell sarcoma (RCS) that arise in > 90% of SJL mice by the age of 12 months have superantigen‐like stimulating properties. In the present study, therefore, RCS cell lines were examined for abnormal expression of endogenous mouse mammary tumor virus (MMTV) proviruses. Extraordinarily high expression of a 1.8 kb mRNA hybridizing with the long terminal repeat (LTR) of MMTV was found in both primary lymphomas and in vitro RCS lines, but not in an SJL B cell lymphoma, NJ101, that does not stimulate syngeneic T cells, or in LPS activated SJL B cells. A cDNA was cloned from cRCS‐2 and sequenced. A 31mer oligonucleotide probe, prepared based on the unique C‐terminal sequence of this RCS‐Mtv LTR, detected the 1.8 kb mRNA in all RCS lymphomas, while a similar probe for the C‐terminal sequence of Mtv‐8 LTR hybridized with the larger mRNA present in normal B cells and in NJ101. Preincubation with 19mer antisense S‐oligonucleotides, prepared based on the sequences of the first two potential translation initiation sites common to both Mtv‐8 and the RCS‐Mtv LTR, significantly reduced the ability of RCS cells to stimulate syngeneic T cells. Moreover, transfection of NJ101 cells with the cloned RCS‐MMTV cDNA conferred V beta 16 T cell stimulating properties on to these cells. It is concluded that expression of the product of this MMTV‐LTR mRNA provides RCS with the strong T cell stimulating properties that it needs for its growth. These results thus identify a novel oncogenic property of MMTV‐LTR.
Determination of the LC50 may be useful in predicting the efficacy of GC treatment in SLE patients, and may be of use in considering other treatment options. CD8 and Bcl-2 double-positive lymphocytes that are insensitive to the apoptotic effect of GCs may play a role in the resistance to these agents in SLE patients.
Genetic variation has been studied in plasma samples from 107 Amerindian children and their parents, and 110 Japanese children and their parents by means of two-dimensional polyacrylamide gel electrophoresis. Twenty-three polypeptides were scored; the identity of nine of these is at present still unknown. Genetic variation was encountered in 11 of these polypeptides. We have previously reported that the index of heterozygosity was 6.2 +/- 0.7% for 20 "randomly selected", silver stained polypeptides scored for genetic variation in Caucasoids (Rosenblum et al. 1983b). For technical reasons only 11 of these 20 polypeptides could be routinely scored in preparations from the Amerindian samples. For these 11 polypeptides, the indices of heterozygosity in the three populations were: Amerindians, 4.5 +/- 0.6%; Japanese, 5.7 +/- 0.7%; Caucasoids, 8.0 +/- 1.1%. Even with these relatively small numbers some striking ethnic differences as regards individual polypeptides are apparent.
Altered genomic methylcytosine content has been described for a number of tumor types, including neuroblastoma. However, it remains to be determined for different tumor types whether specific loci or chromosomal regions are affected by a methylation change or whether the change is random. We have implemented a computer‐based approach for the analysis of two‐dimensional separations of human genomic restriction fragments. Through the use of methylation‐sensitive restriction enzymes, methylation differences in genomic DNA between tumor and normal tissues can be detected. We report the cloning and sequencing of two fragments detectable in two‐dimensional separations of genomic DNA of neuroblastomas. These fragments were found to be a part of repetitive units that exhibited demethylation in neuroblastoma relative to other tumor types. Our finding of a distinct pattern of methylation of repetitive units in neuroblastoma suggests that altered methylation at certain loci may contribute to the biology of this tumor. Genes Chromosom Cancer 17:234–244 (1996). © 1996 Wiley‐Liss, Inc.
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