Factors contributing to production of virus-free tumors in turkeys by Rous sarcoma virus

Virus-neutralizing factors in tumor extracts and sera, age of the tumor, and the infecting dose of virus are important factors contributing to the infective titer of tumor tissue. Tumors produced with small amounts of virus may contain no demonstrable infective virus, and detectable inhibitory factors may or may not be present in tumor extracts or sera.     

Mediation of wound-related Rous sarcoma virus tumorigenesis by TGF-beta

In Rous sarcoma virus (RSV)-infected chickens, wounding leads to tumor formation with nearly 100% frequency in tissues that would otherwise remain tumor-free. Identifying molecular mediators of this phenomenon should yield important clues to the mechanisms involved in RSV tumorigenesis. Immunohistochemical staining showed that TGF-beta is present locally shortly after wounding, but not unwounded controls. In addition, subcutaneous administration of recombinant transforming growth factor-beta 1 (TGF-beta 1) could substitute completely for wounding in tumor induction. A treatment protocol of four doses of 800 nanograms of TGF-beta resulted in v-src-expressing tumors with 100% frequency; four doses of only 10 nanograms still led to tumor formation in 80% of the animals. This effect was specific, as other growth factors with suggested roles in wound healing did not elicit the same response. Epidermal growth factor (EGF) or TGF-alpha had no effect, and platelet-derived growth factor (PDGF) or insulin-like growth factor-1 (IGF-1) yielded only occasional tumors after longer latency. TGF-beta release during the wound-healing response may thus be a critical event that creates a conducive environment for RSV tumorigenesis and may act as a cofactor for transformation in this system.     

Rous sarcoma virus nucleotide sequences in cellular DNA: measurement by RNA-DNA hybridization

Kinetic analysis of the hybridization of 71S RNA from Prague strain of Rous sarcoma virus with an excess of DNA from virus induced sarcomas indicated the presence of the majority of the viral genome sequences in cellular DNA with a very low average frequency per cell. About one-third of the viral sequences were at least partially complementary to DNA sequences with a higher average frequency on the order of 50 to 100 per cell. Normal chick embryo DNA was distinctly different, but contained sequences at least partially homologous to some fraction of the viral RNA.     

Tumors induced in primates by chicken sarcoma virus

A suspension of a variant of Rous sarcoma was injected into four adult and eight newborn rhesus monkeys. Seven newborns developed tumors, three of which were diagnosed as fibrosarcomas, in 2 to 6 weeks; none of the adults have tumors after 11 weeks. Virus was demonstrated in two of the tumors by injecting a tumor-suspension preparation into the chick wing-web where tumors subsequently appeared. To the best of our knowledge this is the first time that sarcomas have developed in primates after a virus has been injected.     

DNA of Rous sarcoma virus: its nature and significance

Purified preparations of Rous sarcoma virus (an avian tumor virus with an RNA genome) contain small amounts of double-stranded DNA. This DNA cannot be hybridized to viral RNA, but will reanneal completely with the DNA of avian cells. Extensive substitution of bromodeoxyuridine for thymidine in "viral" DNA does not photosensitize the biological activity of the virus. These observations indicate that the DNA associated with Rous sarcoma virus is derived from the DNA of the avian host cell, and is probably devoid of any function in the life cycle of the virus.     

Transformation of chick embryo neuroretinal cells by Rous sarcoma virus in vitro: induction of cell proliferation

Neuroretinal cells from 7-day-old chick embryos are transformed and induced to proliferate after infection with Rous sarcoma virus in vitro. Susceptibility of neuroretinal cells to the virus is also dependent on the stage of development since infection of cells from 10-day-old embryos is uneffective.     

Low malignancy of Rous sarcoma cells as evidenced by poor transplantability in turkeys

Homologous and isologous transfers of Rous sarcoma cells in turkeys indicate that growth of the implanted cells contributes little, if at all, to the formation of these neoplasms. Infection of normal host cells by virus appears to be, at least in this species, the major factor in the induction and progressive growth of Rous sarcomas.     

Differential reactivity of human serums with early antigens induced by Epstein-Barr virus

Inoculation of 64-10 or Raji cultures with Epstein-Barr virus derived from the HRI-K clone of the P3J Burkitt's lymphoma line caused abortive infections in most of the lymphoblastoid cells with synthesis of "early antigens" but few, if any, capsids. Antibodies to early antigens were detected by indirect immunofluorescence in serums of many patients with infectious mononucleosis, Burkitt's lymphoma, or nasopharyngeal carcinoma. These antibodies were rarely present in other serums even though some of them showed high titers of antibodies to Epstein-Barr virus when assayed on EB3 Burkitt tumor cells; they also prevented synthesis of early antigens, provided the serums were mixed with the virus prior to inoculation. Antibodies to early antigens possibly reflect current or recent disease processes that are associated with the virus.     

Leukemia, lymphoma, and osteosarcoma induced in the Syrian golden hamster by simian virus 40

Leukemia, lymphoma, and osteogenic and anaplastic sarcomas develop in Syrian golden hamsters inoculated intravenously at 3 weeks of age with simian virus 40, which is a popova virus. Previously, only RNA and herpes DNA viruses have been recognized as capable of inducing leukemia and lymphoma in mammals. The significance of these findings is emphasized in relation to the nature of viral agents that may be involved in analogous diseases of man.     

Neoplastic transformation of hamster astrocytes in vitro by simian virus 40 and polyoma virus

Astrocytes in cultures of brain cells from fetal or newborn hamsters undergo neoplastic transformation after infection with simian virus 40 or polyoma virus. Subcutaneous or intracerebral inoculation of the transformed brain cells into newborn or adult hamsters produces progressively enlarging astrocytomas at the sites of injection. Astrocytomas produced by polyomatransformed cell lines are histologically better differentiated, but grow more rapidly and metastasize more frequently, than astrocytomas produced by cell lines transformed by simian virus 40. These observations make available in vitro models of virus-induced oncogenesis in astrocytes and provide simple techniques for obtaining astrocytoma cell lines suitable for screening studies of chemical agents effective against astrocytomas.     

Neoplastic transformation in vitro of hamster lens epithelium by simian virus 40

Hamster lens epithelium infected with simian virus 40 underwent transformation in vitro and produced tumors when injected into homologous hosts. Undisturbed lens epithelium in man and experimental animals has not been observed to undergo neoplastic change. The virus-induced tumors contained undifferentiated cells that were either polygonal or spindle-shaped. Their origin from lens epithelium seems certain since it is possible to isolate this unique structure free of connective tissue and blood vessels.     

淀粉酶高产菌株的诱变选育

以浙江建德筛选得到的芽孢杆菌为出发菌种,对其进行紫外诱变,硫酸二乙酯及两者交替诱变,采用碘淀粉显色法进行初筛,即在淀粉培养基平板上挑取H/C(透明圈直径与菌圈直径的比值)较大的菌株,对这些菌株进行摇瓶复筛,测定发酵液淀粉酶酶活性,获得遗传稳定的菌株B2一株,其酶活性为2.01 U/mL,比原有菌株提高1.31倍.     

Congenital malformations induced by mescaline, lysergic acid diethylamide, and bromolysergic acid in the hamster

Malformations of the brain, spinal cord, liver, and other viscera; body edema; and localized hemorrhages were found in fetal hamsters from mothers injected subcutaneously with a single dose of mescaline, lysergic acid diethylamide, or 2-bromo-D lysergic acid diethylamide on the 8th day of pregnancy. In addition, all three drugs produced an increase in the percentages of small fetuses per litter, of resorptions, and of fetal mortality.     

Absence of polymerase protein in virions of alpha-type rous sarcoma virus

Noninfectious particles of a mutant of Rous sarcoma virus failed to exhibit DNA polymerase activity even with the use of the most sensitive synthetic template-primer complexes. A neutralization blocking test against antibody to DNA polymerase revealed that these mutants did not contain protein immunologically related to the DNA polymerase.