Chromosomal translocations activating myc sequences and transduction of v-abl are critical events in the rapid induction of plasmacytomas by Pristane and Abelson virus

Plasmacytomas with short latent periods can be induced in BALB/c mice by a single intraperitoneal (i.p.) injection of 0.5 ml pristane followed 20-40 d later by an injection of Abelson virus. The karyotypes of 18 such tumors were determined; 10 of these had rcpt 12;15, 5 had rcpt 6;15 and 3 had no translocations, but two of these have been shown to have interstitial deletions of chromosome 15. The specific breakpoints were the same as described in pristane-induced plasmacytomas, i.e., at 15D2/3, 6C2, and 12F2. Near diploid karyotypes and trisomy of chromosome 11 were frequently seen. All of the Abelson-plus-pristane-induced plasmacytomas (ABPC) were studied as transplanted tumors, contained integrated v-abl sequences, and actively transcribed v-abl mRNA. All but one of these tumors contained abundant myc RNA transcripts. The shortness of the latent periods of the ABPC suggests that the rcpt 12;15 and rcpt 6;15 occur soon after pristane administration and are present at the time Abelson virus is introduced. In this form of plasmacytomagenesis, activated v-abl genes appear to bypass other genetic changes that require a much longer period of time in pristane plasmacytomagenesis. Nonetheless, the consistent finding of chromosome-15 alterations and abundant myc expression in these plasmacytomas emphasize the apparent need for multiple events even in the genesis of some tumors induced by rapid transforming viruses

Etudes histologiques et histochimiques de surrénales de Cobayes traités par des extraits ascaridiens

Dans le présent travail les auteurs se sont proposé d’étudier les modifications histopathologiques et histophysiopathologiques des glandes surrénales, après l’action d’extrait ascaridien dans des conditions expérimentales.L’action non spécifique de la substance administrée se manifeste par une hyperplasie corticale, par une activité augmentée de la phosphatase acide et surtout de la succinodeshydrogénase, ce qui pourrait être en rapport avec les nécessités énergétiques augmentées de la glande dans la production des corticostéroïdes. Les signes inflammatoires, les infarctus anémiques des régions de la zone réticulaire, associés à une accumulation excessive de glycogène dans cette zone de nécrobiose, reflètent l’action toxique directe de l’extrait ascaridien