Adenovirus Tumor Research Articles

In vitro transformation by the adenovirus-SV40 hybrid viruses. 3. Morphology of tumors induced with transformed cells.

Tumors induced with hamster kidney cells transformed by the adeno 2-, adeno 3-, adeno 7-, and adeno 12-SV40 hybrid viruses, and by adenovirus type 12, were examined histologically. The tumors induced with adeno 2-, adeno 3-, and adeno 7-SV40-transformed cells were similar to tumors induced with SV40-transformed hamster kidney cells but contained cells intermediate in morphology between SV40 and adenovirus tumor cells and occasionally contained nests of adenovirus-like cells. Cells transformed by the adeno 12-SV40 hybrid and by adenovirus type 12 gave rise to morphologically similar tumors. The results suggest that both viral genomes are operative in hybrid-transformed cells but that one genome is apparently responsible for the predominant morphology of the tumor. Evidence that the morphology of a single transformed target cell is determined by the transforming genome was discussed.

Antigenic Analysis of Tumors and Sera from Animals Inoculated with Para-Adenovirus Populations

Summary The oncogenicity for hamsters of a PARA-adenovirus 7 population carrying SV40 determinants was confirmed and the immunologic events studied. Tumors induced by PARA-adenovirus 7 were virus-free but synthesized SV40 tumor antigen. Almost all the animals bearing tumors induced by this virus produced antibodies against SV40 tumor antigen and 50 percent also produced antibodies against adenovirus tumor antigen. Transcapsidation of PARA from adenovirus type 7 to adenovirus type 2 conferred oncogenic properties to the previously nontumorigenic adenovirus 2. Again, the resulting tumors were virus-free. Cells established in culture from the tumors synthesized SV40 tumor antigen. In addition, most of the animals produced antibodies against both SV40 and adenovirus tumor antigens.

Effect of spleen and lymph node removal on adenovirus tumor growth.

REGIONAL lymph node removal has been an established procedure for the treatment of cancer. Recently this concept has been challenged because of the lymphocytes' important role in the hosts' immune response. Much of the stimulus for questioning lymph node excision has come from the expanding field of organ transplantation immunity. Homografts were shown to release antigens which drained to the regional lymph nodes at which site antibodies were formed. 1 Numerous experimental studies indicated that this cell-bound antibody was of prime importance in the rejection of the graft. 2 It was of interest, therefore, to investigate the regional lymph nodes' influence on tumor growth. Tumors were induced in newborn hamsters at the site of injection by adenovirus type 12 and later transplanted to adult hamsters where progressive growth occurred in the majority of the animals. 3 Infectious virus was not identified in these tumors, but a specific complement-fixing antigen was

Studies on induction of virus from adenovirus and SV40 hamster tumors 2. "Helper" viruses.

SummaryCell culture lines of virus-free hamster tumors which were initiated by ade-novirus 7 (Pinckney and Grider) or by adenovirus 18 and which synthesized “T” antigen were tested exhaustively for release of infectious adenovirus following addition of candidate “helper” viruses including SV40 respiratory syncytial virus and reovirus type 1. Attempts to detect adenovirus were by copropagation with susceptible indicator cells and by subculture of supernatant fluid or of disrupted cells in a sensitive assay cell system. In no case was infectious adenovirus recovered. The data permit speculation that the adenovirus genetic material retained in the tumor cells which was sufficient to code for “T” antigen might have been too highly integrated in the cell or might have been insufficient in amount to produce infectious virus. Alternatively, the “helper” viruses chosen might not have been appropriate to demonstrate the effect. Whatever the factors involved, it appeared quite clear that SV40, RS and reovirus 1 age...

Studies on induction of virus from adenovirus and SV40 hamster tumors 1. Chemical and physical agents.

SummaryCell culture lines of virus-free hamster tumors initiated by SV40 virus or by the Pinckney and Grider strains of adenovirus 7 were tested exhaustively by procedures which might be hoped to induce the virus or to increase its chance for detection. This included treatment with actinomycin D, mito-mycin C, puromycin, proflavine, hydrocorti-sone, ACTH, thyroxine, insulin, H2O2, increased O2, γ-radiation and copropagation with indicator cells. In no case was infectious virus recovered. Superinfection of SV40 hamster tumor with SV40 virus could not be established and hypothetical inapparent super-infection was not demonstrated following treatment with mitomycin C, proflavine or H2O2. No virus was detected in the cell cultures of any of 3 human tumors tested. The findings supported the concept that viral genetic materials in the animal tumors which are sufficient to code for “T” antigen may be insufficient to replicate the complete infectious virus.

The mechanism of viral carcinogenesis by DNA mammalian viruses: viral-specific RNA in polyribosomes of adenovirus tumor and transformed cells.

The mechanism of viral carcinogenesis by DNA mammalian viruses: viral-specific RNA in polyribosomes of adenovirus tumor and transformed cells.

Inhibition of Adenovirus Replication by l- -D-Arabinof uranosylcytosine.

The effect of 1-β-D-arabinofu-ranosylcytosine on replication of human adenovirus types 2, 7, and 12 in human embryonic kidney, KB, and HeLa cells was investigated. The results indicate that 10 μg/ml of ara-C inhibits replication of these adenoviruses in all 3 human cell types. Inhibition of synthesis of infectious virus ranged from 70 to greater than 99% when yields from infected cultures incubated in the presence of ara-C were compared to drug-free controls. Immunofluorescence studies of infected human embryonic kidney cells revealed that ara-C prevents synthesis of adenovirus viral antigens, but does not inhibit synthesis of adenovirus tumor antigens. However, appearance of the tumor antigen in the presence of ara-C was restricted to fleck- or fiber-like structures in contrast to the appearance of both flecks and globular masses in the absence of the drug.

Interaction of a simian papovavirus and adenoviruses. I. Induction of adenovirus tumor antigen during abortive infection of simian cells.

Feldman, Lawrence A. (Baylor University College of Medicine, Houston, Tex.), Janet S. Butel, and Fred Rapp. Interaction of a simian papovavirus and adenoviruses. I. Induction of adenovirus tumor antigen during abortive infection of simian cells. J. Bacteriol. 91:813-818. 1966.-Adenovirus types 2, 7, and 12 undergo an abortive growth cycle in green monkey kidney cells; they induce the formation of adenovirus tumor antigen, but synthesis of adeno capsid antigen and infectious adenovirus was observed only when cultures were concomitantly infected with a simian papovavirus (SV40). Several other viruses, including herpes simplex and measles which replicate in monkey cells, and rabbit papilloma and human wart papovaviruses which do not, failed to stimulate adenovirus replication in the monkey cells. Adenovirus tumor antigen was detected 8 to 10 hr postinfection by immunofluorescent techniques. The antigen induced by adenovirus types 2 and 7 appeared as intranuclear masses; adenovirus type 12 tumor antigen also appeared as cytoplasmic and nuclear flecks. Sera from hamsters bearing tumors induced by adenovirus type 12 cross-reacted with tumor antigens induced by types 2 and 7 but not with antigens induced by SV40.