| 1. |
- Ankerst, Jaro, et al.
(författare)
-
Demonstration of two group‐specific TSTAs in adenovirus‐induced tumors
- 1970
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 6:1, s. 84-92
-
Tidskriftsartikel (refereegranskat)abstract
- Infection of mice and rats with any one of five tested human adenovirus types belonging to groups A and B (types 3, 7, 12, 18 and 31) induced an immunity to the TSTAs of type 12 tumors as detected by the colony inhibition (CI) test. No immunity was found against an adenovirus type 1 tumor. Two adenovirus types belonging to group C (types 1 and 5) were similarly tested and found to induce a clear‐cut immunity to the adenovirus type 1 tumor but not to tumors induced by adenovirus of groups A and B. The only tested virus type of group D (type 4) did not induce any clear‐cut immunity to either adenovirus 12 tumors or the adenovirus 1 tumor. Immunization of rats with rat adenovirus 12 tumor cells induced a cellular immunity to adenovirus 12 mouse tumor cells but not to a mouse polyoma tumor. Adenovirus 1 rat tumor cells induced no such immunity. Immunization of rats with syngenic adenovirus 12 tumor cells induced a cellular immunity to adenovirus 12 rat and mouse tumors and an adenovirus 7 hamster tumor, but not to an adenovirus 1 rat tumor or BHK‐C13 control hamster cells. The result of a tumor prevention experiment is consistent with the existence of a common TSTA induced by types 7 and 12 and a different TSTA induced by type 5 virus. It is concluded that the highly oncogenic group A and the weakly oncogenic group B adeno virus types all induce a common TSTA. Another TSTA is induced by the group C viruses, while no evidence has been obtained for the existence of any TSTA induced by a group D virus type.
|
|
| 2. |
- Ankerst, J., et al.
(författare)
-
Induction of mammary fibroadenomas in rats by adenovirus type 9
- 1974
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 13:3, s. 286-290
-
Tidskriftsartikel (refereegranskat)abstract
- After inoculation of adenovirus type 9 into newborn Wistar/Furth rats, seven out of seven females developed one or several mammary fibroadenomas within 14–25 weeks after virus inoculation. No tumours were observed in male rats inoculated with the same virus or in untreated controls. Neonatal inoculations of adenovirus type 5, produced on the same HeLa cells, gave negative results in both sexes. The results indicate that benign mammary tumours can be induced in rats by a virus and that mammary fibroadenomas are induced by adenovirus type 9, previously known to be capable of transforming cells in vitro but not of inducing tumours in vivo.
|
|
| 3. |
- Ankerst, Jaro, et al.
(författare)
-
Inhibitory effects of BCG on adenovirus tumorigenesis : Dependence on administration schedule
- 1972
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 10:2, s. 351-356
-
Tidskriftsartikel (refereegranskat)abstract
- The cumulative incidence of tumours was registered in CBA mice inoculated with adenovirus type 12 when newborn and treated with BCG in different ways during the latency period. A single subcutaneous dose of BCG at 3–4 weeks of age had a preventive effect, while no prevention could be recorded after a single BCG dose at 9 weeks of age or eight BCG injections at intervals of 1 week. Sera obtained during the latency period were tested for capacity to block lymph‐node cell‐mediated tumour immunity. Blocking activity was detectable in pooled serum of the mice which had been infected with BCG at 9 weeks of age, already at 10 weeks, i.e. 1 to 2 weeks before the appearance of palpable tumours. Blocking activity could not be demonstrated in a serum pool from control mice until 14 weeks after virus inoculation, at which time sera from mice inoculated with BCG at the age of 3 weeks were still negative. The results indicate that the effect of BCG upon tumour development is dependent upon the point of time of BCG treatment and further suggest that BCG treatment initiated at a stage when serum blocking activity is already present can further stimulate the production of blocking factors and tentatively promote tumour development.
|
|
| 4. |
- Fäldt, R., et al.
(författare)
-
Demonstration of antibody‐associated cellular cytotoxicity in patients with acute myelogenous leukemia before and after chemotherapy
- 1979
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 24:1, s. 17-26
-
Tidskriftsartikel (refereegranskat)abstract
- This study demonstrates that a cytotoxic serum reactivity not requiring the presence of complement appears in the sera of patients with acute myelogenous leukemia. The reaction is detected upon short‐term incubation of sera in vitro with autochthonous mononuclear white blood cells from peripheral venous blood of patients at the acute stage of the disease. This reactivity was demonstrated in 18/18 patients. Generally, the cytotoxicity was low in patients at the acute stage of the disease, but increased after chemotherapy and reached the highest level at the onset of clinical remission or just before. No cytotoxicity could be demonstrated against autochthonous remission white blood cells. The serum activity could be absorbed and eluted from protein A‐Sepharose CL‐4B and was recovered in the 7S‐fraction of the sera after gel filtration on Sephadex G‐200 and ion exchange chromatography. This indicates that the demonstrated cytotoxicity is due to immunoglobulins of IgG‐class. It is believed that Fc‐receptor‐bearing cells present in the target cell preparations function as effector cells. The reaction is designated antibody‐associated cellular cytotoxicity (AACC).
|
|
| 5. |
- Fäldt, R., et al.
(författare)
-
Tumor‐associated humoral cytotoxicity in patients with acute myelogenous leukemia before and after chemotherapy
- 1977
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 20:6, s. 824-833
-
Tidskriftsartikel (refereegranskat)abstract
- Sera of eight unselected adult patients with acute myelogenous leukemia obtained before and after chemotherapy were repeatedly tested for specific complement‐dependent cytotoxicity against autochthonous peripheral white blood cells from the acute leukemia stage and from the remission stage, respectively. Complement‐dependent cytotoxicity against white blood cells from the acute leukemia stage was demonstrated in all of the eight patients, while none of three patients' sera were reactive against white blood cells from the remission stage tested in parallel. The cytotoxicity was increased after chemotherapy, also in those patients in whom remission was not achieved.
|
|
| 6. |
- Steele, G., et al.
(författare)
-
Absorption of blocking activity from human tumor‐bearer sera by staphylococcus aureus, cowan I
- 1975
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 15:2, s. 180-189
-
Tidskriftsartikel (refereegranskat)abstract
- Staphylococcus aureus, strain Cowan I, contains a cell‐wall substance, protein A, which combines with the Fc part of IgG in most mammalian species. It can therefore be used as a solid‐phase immunoabsorbant for elimination of the reacting immunoglobulins. Since it has been shown that Cowan I could absorb out the blocking activity of sera from rats bearing isografts of polyoma‐virus‐induced sarcomas or chemically induced colon carcinomas, we investigated what effects Cowan I absorption of human tumor‐bearer sera might have. In all tumor‐bearer sera tested, from patients with melanomas or colon carcinomas, treatment with protein‐A‐containing staphylococci decreased the sera's ability to inhibit lymphocyte‐mediated cytotoxicity in vitro. Cowan‐I‐treated sera from healthy controls had no effect on lymphocyte cytotoxicity. Nor did Cowan‐I‐treated tumor‐bearer sera potentiate or „arm” normal lymphocytes against tumor target cells. There was no evidence of complement‐dependent cytotoxicity with added human complement in sera from melanoma and colon carcinoma bearing patients either before or after absorption with Staphylococcus aureus, Cowan I. The concentrations of IgA, IgG and IgM were determined in sera used for in vitro tests of blocking activity and complement‐dependent cytotoxicity before and after absorption. No reduction of IgA, reduction to undetectable levels of IgG and 20–30% reduction of IgM immunoglobulins as compared to unabsorbed sera were demonstrated.
|
|
| 7. |
- Steele, G., et al.
(författare)
-
Alteration of in vitro anti‐tumor activity of tumor‐bearer sera by absorption with Staphylococcus aureus, cowan I
- 1974
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 14:1, s. 83-92
-
Tidskriftsartikel (refereegranskat)abstract
- Staphylococcus aureus, strain Cowan I, has been shown to contain a cell‐wall substance, protein A, which combines with the Fc part of IgG in most mammalian species. Since the blocking activity of sera from tumor‐bearing individuals has previously been found to be associated with 7S immunoglobulins, it was investigated whether Cowan I could absorb out the blocking activity of sera from rats carrying either isografted polyoma virus induced sarcomas or chemically induced colon carcinomas. In all sera tested, treatment with protein A abrogated the sera's ability to inhibit lymphocyte‐mediated cytotoxicity in vitro. Absorption of sera with Staphylococcus aureus, strain Wood 46, not containing protein A, had no effect on the blocking activity. Admixtures of protein‐A‐treated blocking sera to untreated blocking sera from animals bearing the same tumor type, specifically abrogated the blocking activity, while admixture of Wood 46 absorbed sera, protein‐A‐treated normal sera, or protein‐A‐treated sera from animals bearing a different tumor type did not cause a similar abrogation. The blocking sera from tumor‐bearing rats were not cytotoxic to their specific tumor target cells in the presence of homologous complement. After protein A treatment, serum from rats bearing isografts of sarcomas induced by polyoma virus showed specific complement‐dependent cytotoxicity to polyoma tumor target cells. Serum from primary colon carcinoma bearing rats also had complement‐dependent cytotoxic effect on colon tumor target cells after protein A treatment. Sera used for in vitro tests of blocking activity and complement‐dependent cytotoxicity were analyzed for IgG concentration before and after absorption with S. aureus, Cowan I. A 20‐30% reduction of IgG class immunoglobulins as compared to unabsorbed or control (Wood 46) treated sera was demonstrated.
|
|
| 8. |
- Steele, G., et al.
(författare)
-
Immune responses of adenovirus type‐9 infected (tumor‐free) male rats against adenovirus type‐9 induced mammary fibroadenomas and A chemically induced mammary carcinoma
- 1974
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 14:3, s. 359-366
-
Tidskriftsartikel (refereegranskat)abstract
- Lymphocytes from five non‐tumor‐bearing male W/Fu rats infected with human adenovirus type‐9 as newborns or as adults share a common reactivity against rat mammary fibroadenoma target cells and rat mammary carcinoma target cells, as demonstrated by microcytotoxicity tests. Mammary fibroadenomas were induced by adenovirus type‐9 infection of newborn female W/Fu rats, littermates of three of the male lymphocyte donors. The mammary carcinoma target cells were derived from a single rat mammary carcinoma induced by 3,2′‐dimethyl‐4‐amino‐biphenyl (DMABP). Lymphocytes from the male adenovirus type‐9 infected rats were not cytotoxic to normal rat breast epithelial cells, nor to target cells explanted from a polyoma‐virus‐induced sarcoma. Sera from each of five mammary fibroadenoma‐bearing female rats inhibited the cytotoxic effect of lymphocytes from the adenovirus type‐9 infected males against both mammary fibroadenoma and carcinoma target cells. Sera from the female W/Fu rat bearing the DMABP induced mammary carcinoma also inhibited the male lymphocyte cytotoxicity against both fibroadenoma and carcinoma target cells. Serum from rats bearing a polyoma‐virus‐induced sarcoma, though actively blocking in its own system, had no effect on lymphocytes from the adenovirus type‐9 infected males. Anti‐viral antibody response was demonstrated 8 days following adenovirus type‐9 infection of adult males. No anti‐tumor humoral response was demonstrated in either newborn‐infected or adult adenovirus type‐9 infected W/Fu male rats. Sera were checked for cytotoxicity against fibroadenoma and mammary carcinoma target cells in the presence of active homologous complement. No complement‐dependent cytotoxicity was evident. Sera from infected males were admixed to known blocking sera from mammary fibroadenoma‐ and carcinoma‐bearing rats, with no significant abrogation of the blocking effect. These results indicate that, despite the lack of tumor development, infection of male W/Fu rats by adenovirus type‐9 has produced an antigen which is at least partially common to the antigen (s) shared by adenovirus type‐9 induced mammary fibroadenomas and a DMABP induced mammary carcinoma.
|
|
| 9. |
- Steele, G., et al.
(författare)
-
The effects of cyclophosphamide on in vitro correlates of tumor immunity
- 1974
-
Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 14:6, s. 743-752
-
Tidskriftsartikel (refereegranskat)abstract
- The effects of cyclophosphamide (CY) on tumor immunity against isografts of rat sarcomas induced by polyoma virus were studied using in vitro techniques. Groups of sarcoma‐bearing animals received CY (250 mg/kg intraperitoneally 11 days after isografting) CY (150 mg/kg IP 8 days after isografting), or IP injections of 0.9% NaCl. In control rats tumor growth was progressive. All CY‐treated animals showed transient tumor regression of at least 50% of their pretreatment tumor volume. Despite a drastic depression in numbers of blood leukocytes as well as lymph‐node cells following CY treatment, animals treated with 150 mg/kg CY were shown to have blood lymphocyte and lymph‐node cell cytotoxicity in vitro against plated sarcoma target cells comparable to untreated sarcoma‐bearing animals. Sera obtained from sarcoma‐bearing rats prior to CY treatment specifically blocked lymphocyte cytotoxicity against sarcoma target cells. After CY treatment serum blocking activity could not be demonstrated during the period of tumor regression, but reappeared in parallel with tumor regrowth. Antibodies cytotoxic to sarcoma target cells when homologous complement was added could not be demonstrated in sera obtained from animals before CY treatment, but were present after treatment during tumor remission. Following CY treatment, sera obtained from treated animals, when mixed with blocking sera from control animals, could counteract or unblock the blocking activity of tumor‐bearer sera. Unblocking capacity was present only in sera obtained during CY‐induced tumor remission. Serum IgG concentration was significantly and temporarily decreased after CY treatment.
|
|
