| 1. |
- Ankerst, J., et al.
(författare)
-
Cross-reacting Tumor-associated Antigen(s) of Adenovirus Type 9-induced Fibroadenomas and a Chemically Induced Mammary Carcinoma in Rats
- 1974
-
Ingår i: Cancer Research. - 0008-5472. ; 34:8, s. 1794-1800
-
Tidskriftsartikel (refereegranskat)abstract
- Cross-reactivities among tumor-associated antigens of rat mammary fibroadenomas and among these fribroadenomas and a rat mammary carcinoma were investigated by in vitro techniques. Lymphocytes from five female W/Fu rats bearing mammary fibroadenomas were found to share a common reactivity against fibroadenoma target cells, as demonstrated by lymphocyte cytotoxicity tests on iododeoxyuridine-l25I-labeled target cells and by microcytotoxicity tests. These lymphocytes were also cytotoxic to target cells derived from a rat mammary carcinoma induced by 3,2'-dimethyl-4-aminobiphenyl. Inversely, lymphocytes from a female W/Fu rat bearing this 3,2'-dimethyl-4-aminobiphenyl-induced mammary carcinoma were cytotoxic to the carcinoma and the fibroadenoma target cells. Neither the immune lymphocytes from fibroadenoma-bearing rats nor those from the rats with the mammary carcinoma were cytotoxic to polyoma virus-induced sarcoma cells or to normal rat breast cells. Neither immune lymphocytes from rats with polyoma tumors nor those bearing chemically induced colon carcinomas demonstrated cellular immunity against either mammary fibroadenoma or mammary carcinoma target cells. Sera from each of the fibroadenoma-bearing rats inhibited the cytotoxic effect of lymphocytes from rats bearing fibroadenoma or carcinoma against both mammary fibroadenoma and carcinoma target cells. Sera from the rat with the 3,2'-dimethyl-4-aminobiphenyl-induced mammary carcinoma inhibited the activity of its own lymphocytes on either fibroadenoma or carcinoma target cells. They also blocked the cytotoxicity of fibroadenoma-immune lymphocytes to fibroadenoma or to carcinoma target cells. The blocking sera of mammary fibroadenomatous and carcinomatous rats did not inhibit the cytotoxic effect of lymphocytes from polyoma sarcoma-bearing rats against polyoma tumor cells. Additionally, sera from rats with either polyoma virus-induced tumors or colon carcinomas, which blocked in their respective systems, did not inhibit the in vitro activity of mammary fibroadenoma or carcinomaimmune lymphocytes on mammary fibroadenoma or cacinoma target cells. These results indicate a common tumor-associated antigenicity among the mammary fibroadenomas and a shared (tissue type-specific?) antigen between the mammary fibroadenomas and the chemically induced mammary carcinoma.
|
|
| 2. |
|
|
| 3. |
- Ankerst, Jaro
(författare)
-
Demonstration And Identification Of Cytotoxic Antibodies And Antibodies Blocking The Cell-Mediated Antitumor Immunity Against Adenovirus Type 12 Induced Tumors
- 1971
-
Ingår i: Cancer Research. - 0008-5472. ; 31:7, s. 997-1003
-
Tidskriftsartikel (refereegranskat)abstract
- Hyperimmune mouse antisera against syngeneic adenovirus type 12 induced tumors and their 7 S and 19 S fractions of immunoglobulins obtained after combined diethylaminoethyl cellulose and Sephadex G-200 separation were tested against a rat adenovirus type 12 induced tumor by 51 Cr release technique. The same sera and their fractions were investigated with the colony inhibition technique for ability to abrogate the inhibitory effect of mouse lymph node cells specifically immunized against syngeneic adenovirus type 12 induced tumors on rat adenovirus 12 target tumor cells. It was found that (a) hyperimmune antisera from mice which had received many immunization doses were cytotoxic to rat adenovirus 12 induced tumor cells at 37° in the presence of complement; (b) the same hyperimmune antisera abrogated specifically the inhibitory effect of specifically immune mouse lymph node cells on rat adenovirus 12 tumor cells; (c) the cytotoxic activity of the hyperimmune antisera at 37° in the presence of complement was found in 19 S fractions of γ-globulins; and (d) the serum factors causing abrogation of immune lymph node cells in vitro were found in 7 S fractions of immunoglobulins.
|
|
| 4. |
- 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.
|
|
| 5. |
- 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.
|
|
| 6. |
- 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.
|
|
| 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.
|
|
