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Biomedical subjects

L Gross

Publications and source records attributed to L Gross.

At least 55 records · Page 3Linked to original sources

C-type virus particles in spontaneous and virus-induced leukemia and malignant lymphomas in mice and rats.

The presence and numbers of C-type virus particles in an animal model consisting of mice and rats with either spontaneous or virus-induced leukemia and lymphomas were studied, in order to determine the relation of the appearance of virus particles to viral etiology of such neoplasms. The numbers and distribution of C-type virus particles in organs from 13 mice with spontaneous leukemia and lymphomas were compared with the presence of virus particles in organs of 13 mice with leukemia and lymphomas induced by passage A (Gross) virus inoculation. C-type virus particles were present in organs of all mice with either spontaneous leukemia or leukemia and lymphomas induced by virus inoculation. However, the number of particles observed was significantly higher in those mice in which leukemia was induced by virus inoculation. Virus particles were also observed, but in substantially smaller numbers, in organs of 13 of 25 untreated, healthy mice of the nonleukemic C3H(f) inbred line. In contrast to mice, C-type, or any other virus particles, were not found in organs of 10 Sprague-Dawley, Long-Evans or Sprague-Dawley X Long-Evans F1 hybrid rats with spontaneous leukemia. However, C-type virus particles were consistently present in organs of 11 Sprague-Dawley rats with leukemia induced by rat-adapted passage A (Gross) mouse leukemia inoculation. The virus particles appeared in the organs of the inoculated rats 5 days after i.p., and 11 days after s.c. inoculation. Virus particles were not found in organs of 10 healthy untreated Sprague-Dawley rats. The implications of these observations are discussed.

Animals↗

[Regional transfemoral intra-arterial chemotherapy using selective catheter placement. Method and clinical results].

In a retrospective study on 108 arterial transfemoral perfusion treatments with cytostatic drugs, the authors describe the procedure and the response of patients shown by tumor markers, computed tomography, histologic findings, and subjective assessment by the patients. Then follows a critical discussion of the complication rate of a therapy which has proved since 1980 to be a valuable and effective treatment method. The objective remission rate was 67%, and a subjective response was observed in 75% of all cases. Compared to systemic chemotherapy, the tolerance was clearly better. Only in one case we found an arterial embolism which was treated by conservative measures. Intraarterial perfusion of cytostatic drugs is within the scope of palliative measures a very effective and, above all, relatively non-stressful treatment with regard to quality of life and survival time. This interventional therapy method should be offered by the radiologist to the clinical oncologist.

Adult↗

[Clinical aspects and pathology of primary tubal cancer].

Primary carcinoma of the fallopian tube is the least common of the malignant tumors of the female genital tract. Ten cases of primary fallopian tube carcinoma treated at the Women's Department of the University Hospital Mannheim between 1965 and 1983 are described. Four patients survived five years, of whom three had a stage I tumor. The most important factor affecting survival appeared to be the extent of the tumor at the time of diagnosis.

Adenocarcinoma, Papillary↗

Reduction in the incidence of radiation-induced tumors in rats after restriction of food intake.

In our inbred colony of Sprague-Dawley rats, fractionated total-body x-ray irradiation (150 rads five times at weekly intervals; 1 rad = 0.01 gray) increased the incidence of tumors from 22% to 93% in females and from 5% to 59% in males [Gross, L. & Dreyfuss, Y. (1979) Proc. Natl. Acad. Sci. USA 76, 5910-5913]. In experiments reported here, we investigated the influence of reduced food intake on the incidence of radiation-induced tumors in Sprague-Dawley rats. All rats in both groups received fractionated total-body x-ray irradiation similar to that specified above. Among the irradiated rats on full (ad lib) diet (five to six pellets of Purina Rodent Lab Chow per day, each) were 14 females and 9 males, and all (100%) developed tumors (or leukemia) at an average age of 13.7 months in females and 13.4 months in males. Among the litter mates on restricted diet (two pellets of Purina Rodent Lab Chow per day, each), only 9 out of 29 females (31%) developed tumors at an average age of 18.2 months and 1 out of 15 males (6.7%) developed a tumor at 9 months of age. In the full diet group, the majority of tumors developing in females were benign. Among the 9 irradiated males, 1 developed leukemia and the remaining 8 developed tumors; 7 of them were examined, 6 were found malignant, and 1 was benign. In the restricted diet group, of the 9 tumors that developed in females, 4 were malignant and 5 were benign. The tumor that developed in 1 male was a sarcoma.

Aging↗

In vitro gamma irradiation of leukemic cells in mice, rats, and guinea pigs.

In vitro gamma irradiation of virus-induced (Gross) mouse leukemia cells at doses of 350-1600 rads (1 rad = 0.01 gray) had no effect on their ability to induce leukemia, usually within 2 weeks, after transplantation into syngeneic mice. However, when cells irradiated at doses of 2000-20,000 rads were transplanted, they induced leukemia after a latency period exceeding 2.5 months, similar to the results observed in mice inoculated with filtered mouse leukemia extracts. Similar results were also obtained after irradiation of leukemic cells derived from rats in which leukemia had been induced by rat-adapted mouse leukemia virus. Apparently, gamma irradiation at a dose of, or exceeding, 2000 rads, inhibits the ability of mouse and rat leukemic cells to induce leukemia after transplantation into syngeneic hosts; however, it does not inactivate the virus carried by such cells nor prevent it from inducing leukemia. [In previous experiments, doses of more than 4,500,000 rads were needed to inactivate the passage A (Gross) leukemia virus carried in either mouse or rat leukemic cells.] In vitro gamma irradiation of L2C guinea pig leukemic cells at doses of 750-2500 rads had no apparent effect on their ability to induce leukemia after transplantation effect on their ability to induce leukemia after transplantation into strain 2 guinea pigs. However, irradiation at doses of 3250-20,000 rads inactivated their ability to do so. The morphology of mouse, rat, and guinea pig leukemic cells and the virus particles present in such cells was not affected by irradiation at doses of 20,000 rads.

Animals↗

Spontaneous tumors in Sprague-Dawley and Long-Evans rats and in their F1 hybrids: carcinogenic effect of total-body x-irradiation.

Rats frequently develop various tumors, many of them malignant; the majority of tumors in the females develop in the mammary glands. In primary spontaneous tumors and lymphomas virus particles cannot be found on electron microscopic examination; transmission of the tumors by filtered extracts has not been successful. In our colonies of Sprague-Dawley rats the incidence of tumors was 22% in females and 5% in males; in Long-Evans rats the incidence of tumors and 28% in females and 10% in males. In (Sprague-Dawley x Long-Evans) F1 hybrids the incidence of tumors was 67% in females and 32% in males, about twice as high as in the parental strains. Fractionated total-body x-irradiation (150 rads five times at weekly intervals) (1 rad = 0.01 gray) increased the incidence of tumors in Sprague-Dawley rats from 22% to 93% in females and from 5% to 59% in males. In Long-Evans rats, irradiation increased the incidence of tumors from 28% to 63% in females and from 10% to 42% in males. The incidence of malignant tumors was almost twice as high in irradiated Sprague-Dawley and Long-Evans rats as compared with nonirradiated animals of the same strains. Partial shielding during irradiation had no significant effect on the incidence or on the forms of tumors developing in the irradiated animals. In striking contrast to results of experiments carried out on mice, the incidence of leukemia and lymphomas was not increased in the irradiated rats, as compared with control animals.

Animals↗

Attempt to immunize guinea pigs against L2C leukemia with leukemia cells inactivated by gamma irradiation.

In previous studies, intradermal inoculation of small doses of L2C leukemic cell suspensions into strain 2 guinea pigs induced immunity against challenging reinoculation with leukemic cells; however, 50% of the guinea pigs developed leukemia in the course of immunization. We have now attempted to induce immunity by inoculation of L2C leukemic cells inactivated by in vitro gamma irradiation ranging from 750 to 8000 rads (1 rad = 0.01 gray). In preliminary experiments, irradiation with 750 to 2750 rads had no significant effect on leukemogenic potency of leukemic cells; however, doses exceeding 3000 rads inactivated the leukemogenic potency of L2C cells. Eighty-nine guinea pigs that survived intradermal, subcutaneous, or intraperitoneal inoculations with irradiated (1000-8000 rads) L2C cells were subsequently challenged by reinoculation with nonirradiated leukemic cells, and 83 of them (93%) developed leukemia. L2C leukemic cells contain spherical particles, about 103 nm in diameter; it is reasonable to assume that these particles represent the causative virus responsible for the development of L2C leukemia. Inactivation of leukemogenic potency of L2C leukemic cells by gamma irradiation in vitro does not necessarily imply that the virus particles consistently present in these cells were also inactivated. In previous experiments carried out on mouse leukemia, doses exceeding 1,000,000 rads were needed in order to inactivate the mouse leukemia virus in vitro.

Animals↗

Relative loss of oncogenic potency of mouse leukemia virus (Gross) after prolonged propagation in tissue culture.

Since the initial development of the "passage A" mouse leukemia virus in 1957, this virus has been propagated in our laboratory by serial passage in newborn C3H(f) mice. At the present time, 10(-2)-10(-3) dilutions in physiological saline solution of this mouse-passaged virus induce lymphatic leukemia in practically all inoculated mice after a latency of 3-5 months. On the other hand, when the same virus was propagated on NIH 3T3 mouse embryo cells in tissue culture for more than 10 years, its leukemogenic potency became considerably reduced. Recent bioassay experiments carried out in our laboratory demonstrated that after such prolonged propagation in tissue culture this virus now induced leukemia in less than 15% of the inoculated suckling C3H(f) mice; only undiluted or 10% dilutions of the tissue culture fluid (very occasionally 10(-2) or 10(-3) dilutions) induced leukemia after a prolonged latency varying from 5.5 to 18 months. The passaged and the tissue-culture-grown virus strains are identical immunologically and indistinguishable in their morphology when examined by electron microscopy. The tissue-culture-grown virus, attenuated in its leukemogenic potency, does not, however, confer immunity against a challenge with the mouse-passaged virus.

AKR murine leukemia virus↗