Leiomyosarcoma of the inferior vena cava. Ultrasonographic appearance.

Ultrasonographic features of six leiomyosarcomas of the inferior vena cava are described. In most cases, the presentation is typical enough to strongly suggest the histologic diagnosis. The tumor is usually greater than 10 cm long, hypoechoic, heterogeneous. Cystic components can be found. It is sharply demarcated from neighboring organs which are displaced. The mass is located at the very place of the inferior vena cava, the lumen of which is no longer seen. It is fusiform shaped, surprisingly sparing the aorta. Differential diagnosis along with other radiologic examinations, pathologic findings, and prognosis are discussed.

[Leiomyosarcomas of the inferior vena cava]. / Les léiomyosarcomes de la veine cave inférieure.

Leiomyosarcoma of the inferior vena cava in a rare tumor which is predominantly seen in women. The symptomatology is non specific and depends mostly of the segment of the vessel which is involved. Radiologic approach for correct preoperative diagnosis is based on ultrasonography, computed tomography and inferior vena cavography. The best treatment is en bloc resection of the mass associated with pre and post-operative chemotherapy. Although the tumor is slow-growing, the prognosis is poor and the average survival is less than two years, due to local recurrence and metastases.

Saccharomyces cerevisiae ARS on a plasmid from Staphylococcus aureus.

Staphylococcus aureus plasmid pC194 carries three sequences closely related to a consensus sequence defined previously by analysis of different genetic elements which replicate autonomously in yeast Saccharomyces cerevisiae. Two of these enable the plasmid to replicate in yeast, the third does not. A new consensus sequence A/T T T T A T R T T T, 1 bp shorter than the previous one, can be deduced from our results. Replacement of the T with G at the position 9 of the sequence abolishes its activity. The presence of the two active sequences on pC194 genome can be explained by the A + T-rich base composition of the plasmid.

Replication functions of pC194 are necessary for efficient plasmid transduction by M13 phage.

Escherichia coli plasmids pBR313 and pBR322 were transduced by phage M13 with low efficiency (10(-8) transductants/phage). Hybrid plasmids pHV12 or pHV33, composed of Staphylococcus aureus plasmid pC194 and pBR313 or pBR322, respectively, were transduced much more efficiently (10(-4) transductants/phage). Inactivation of either of the two zones necessary for pC194 replication, one coding for a protein, the other not, reduced the transforming efficiency of hybrids to the level of pBR322. Activity of the pC194 replication region was not necessary for the formation of chimeras between M13 and the transduced plasmid in the donor cells, but rather for the establishment of the plasmid in the recipient cells.

Insertional mutagenesis in Bacillus subtilis: mechanism and use in gene cloning.

The plasmid pHV32, which replicates in Escherichia coli but not in Bacillus subtilis, transformed B. subtilis-competent cells efficiently when linked in vitro to EcoRI B. subtilis DNA segments. The transformed clones carried pHV32 inserted in their chromosomes, and often displayed a mutant phenotype. One of the transformed clones carried pHV32 inserted close to the thyB gene. We cleaved the DNA extracted from this clone with BglII restriction endonuclease, for which no sites exist on pHV32, ligated the released segments and used them to transform E. coli selecting for pHV32-carried genetic markers. The transformants harbored a hybrid plasmid which carried the B. subtilis thyB gene. Circular molecules composed of pHV32 joined to B. subtilis DNA inserted into the chromosome by a Campbell-like recombination event. Linear molecules, in which pHV32 was flanked by two non-adjacent DNA segments, underwent a double cross-over recombination with the chromosome. In this case the chromosomal sequences between the non-adjacent segments were deleted, and replaced by pHV32 sequences.

Plasmids from Staphylococcus aureus replicate in yeast Saccharomyces cerevisiae.

It is known that some plasmids, such as RP4, can replicate in many Gram-negative bacteria. Certain small Staphylococcus aureus plasmids have an even broader host range, being able to replicate in not only phylogenetically distant Gram-positive bacteria such as Bacillus subtilis or Streptococcus pneumoniae, but also in the Gram-negative bacterium Escherichia coli. Here we have examined whether these plasmids can also replicate in a lower eukaryote, the yeast Saccharomyces cerevisiae. For this purpose we constructed hybrids between a S. aureus plasmid pC194 and an E. coli plasmid YIp5, which carries a ura-3 gene easy to select for in yeast but cannot replicate in this host. We found that the hybrids transformed yeast with high efficiency (as did hybrids between YIp5 and three other S. aureus plasmids); were maintained extrachromosomally in yeast; and were not modified during residence in yeast. We conclude from this evidence that S. aureus plasmids can replicate in yeast, which raises the questions of whether the replication signals used by prokaryotes and eukaryotes are similar, and how far up the phylogenetic tree the organisms still able to be hosts to S. aureus plasmids may be.

Replication of plasmids from Staphylococcus aureus in Escherichia coli.

Plasmid pBR322 derives from plasmid ColE1 and does not replicate in Escherichia coli strains lacking DNA polymerase I. Hybrids between pBR322 and a plasmid isolated from Staphylococcus aureus, pC194, replicate in such E. coli strains, provided that the pC194 replication region is intact. Inactivation of the pBR322 replication region does not interfere with the replication of hybrids in E. coli. Hybrids between pBR322 and two other plasmids from S. aureus, pT127 and pUB112, and replicate at the restrictive temperature in E. coli having thermosensitive DNA polymerase I. Similar hybrids involving pC221 and pHV400, plasmids from S. aureus and Bacillus subtilis, respectively, do not replicate under such conditions. These results show that some plasmids from a Gram-positive bacterium, S. aureus, can replicate in a Gram-negative one, E. coli.

Repair promoted by plasmid pKM101 is different from SOS repair.

In E. coli K12 bacteria carrying plasmid pKM101, prophage lambda was induced at UV doses higher than in plasmid-less parental bacteria. UV-induced reactivation per se was less effective. Bacteria with pKM101 showed no alteration in their division cycle. Plasmid pKM101 coded for a constitutive error-prone repair different from the inducible error-prone repair called SOS repair. Plasmid pKM101 protected E. coli bacteria from UV damage but slightly sensitized them to X-ray lesions. Protection against UV damage was effective in mutant bacteria deficient in DNA excision-repair provided that the recA, lexA and uvrE genes were functional. Survival of phages lambda and S13 after UV irradiation was enhanced in bacteria carrying plasmid pKM101; phage lambda mutagenesis was also increased. Plasmid pKM101 repaired potentially lethal DNA lesions, although wild-type DNA sequences may not necessarily be restored; hence the mutations observed are the traces of the original DNA lesions.

Increased UV-inducibility of SOS functions in a dam-3 mutant of Escherichia coli K12 uvrA.

The dam-3 mutation caused a 2--4 fold increase in the susceptibility of E. coli K-12 uvrA to UV induction of prophage lambda, induced reactivation and mutagenesis of lambda, and mutation to histidine prototrophy. The increased inducibility exceeded the level expected by UV and dam-3 acting additively and independently, and suggests that the effects of UV and dam-3 interact in some way to potentiate induction of SOS functions.

Induced reactivity of UV-damaged phage gamma in E. coli K12 host cells treated with aflatoxin B1 metabolites.

The metabolites of aflatoxin B1, the most potent hepatocarcinogen so far known, promote in E. coli K12 cells the reactivation of phage lambda damaged by ultraviolet (UV) radiation. This reactivation process is error prone; 25% of the phage DNA lesions are repaired, but mutagenesis, scored as clear plaque formation, is increased as much as 10-fold. Such reactivation of UV-damaged phage lambda, which occurs in wild-type and in uvrA but not in recA bacteria, is inducible: phage reactivation is obtained even after a long delay following treatment of the host by the short-lived metabolites. This induced reactivation of UV-damaged phage in hosts treated with metabolites of aflatoxin B1 is similar to direct of indirect UV reactivation. Metabolites of aflatoxin B1 produce induced phage reactivation as well as prophage lambda induction in lysogens and cell filamentation in non-lysogens. These cellular events are also triggered by DNA lesions caused by UV radiation and result from the induction of a metabolic pathway (SOS functions). We postulate that, in eucaryotes, carcinogens may induce cellular SOS functions similar to those in E. coli. Induction of such functions might be responsible for the transformation of mammalian cells.

Induction and mutagenesis of prophage lambda in Escherichia coli K12 by metabolites of aflatoxin B1.

Like most carcinogens, aflatoxin B1 must be activated by mammalian microsomal enzymes to give rise to coupounds active on bacteria. These compounds act as inducers of E. coli K12 (lambda) at a high efficiency, whereas unmodified aflatoxin B1 has no effect. Moreover, metabolites of aflatoxin B1 have a mutagenic action on phage lambda, as shown by the appearance of clear plaque mutants. We propose the hypothesis that the same derivative is responsible for carcinogenesis of liver cells by aflatoxin B1. Therefore, our system provides a simple way of measuring in vitro, in the same assay, the mutagenic and inducing activities of compounds to which the cells are permeable, thereby detecting potentially carcinogenic agents.