Showing papers on "Tumor progression published in 1974"

Carcinoembryonic antigen: clinical correlation with chemotherapy for metastatic gastrointestinal cancer.

Abstract: Serial carcinoembryonic antigen (CEA) titers were measured in 38 patients receiving chemotherapy for metastatic carcinoma of the colon, pancreas, and stomach. CEA levels were initially elevated (over 2.5 ng/ml) in 26 patients (12/20 colonic, 8/10 pancreatic, 6/8 gastric). Seventeen patients had rising serial CEA values during therapy; 13 had evidence of tumor progression, 3 had stable disease, and 1 had no measurable disease. Nineteen patients had stable CEA levels which were either persistently elevated (11 patients) or normal (8 patients). Ten of 11 patients with elevated CEA levels developed tumor progression. In 8 patients with consistently normal CEA levels, 6 (colon) had no evidence of progressive tumor, and 2 (1 pancreatic and 1 gastric) eventually died of metastatic disease. CEA levels decreased in 2 patients with colon carcinoma during remission from chemotherapy. A rising CEA titer often presages clinical deterioration, although elevated CEA levels may remain stable despite progressive disease. Persistently normal CEA, however, is a favorable prognostic sign. The limited effectiveness of chemotherapy for gastrointestinal cancer in this series precludes any definitive conclusion regarding the effect of chemother-apeutically induced tumor regression on CEA levels, although there is suggestive evidence that CEA correlates with remission.

Proposed Mechanisms by Which Autochthonous Neoplasms Escape Immune Rejection

Abstract: The available evidence suggests that both human and animal cancers are generally recognized by their hosts to be antigenic. Both antibody- and cell-mediated immune reactions have been reported to occur in response to tumor cells in cancer-bearing animals. One of the major unanswered questions in cancer immunology is why these immune responses do not lead to the successful destruction of the tumor. For this presentation we have collected data in the autochthonous SV40 hamster sarcoma model system that suggest that cell-mediated and humoral responses against SV40 tumor surface antigens appear early after infection of neonatal animals with this oncogenic virus. Cell-mediated immunity measured in vitro in the microcytotoxicity assay against SV40 tumor target cells was demonstrable throughout several months prior to tumor appearance and thereafter until the death of the animals. Antibody, cytostatic to the growth of SV40 tumor cells when measured in vitro and in vivo , appeared early after the initial transformed cells were present but could never be detected during the several weeks prior to the visible appearance of s.c. autochthonous tumors. Lymphocytes from animals bearing SV40 sarcomas, although cytotoxic in vitro , were generally incapable of conferring protection against SV40 tumor challenge to normal syngeneic recipients, suggesting some additional functional impairment of antitumor cytotoxicity in vivo . The data collectively suggest that, early after the appearance of SV40 neoplasms, antibody inhibitory to the growth of tumor cells appears but is not cytotoxic. This antibody functions by restricting the initial growth of the tumor cells and perhaps serves to diminish tumor cell antigenicity (afferent and efferent inhibition). Cell-mediated immunity appears somewhat later but is obviously ineffective in destroying the tumor focus, as it grows slowly over many months and eventually metastasizes. Inhibititor, presumably circulating antigen released from the enlarging tumor mass, binds to circulating lymphocytes and inhibits their cytotoxicity against the spreading tumor. Thus the growth of the SV40-transformed cells, comprising the initial tumor focus, to a lethal, spreading cancer is permitted to occur because of a series of blocking and inhibitory events involving antibody initially, possibly antigen and antibody intermediately, and primarily antigen in the later stages of tumor progression.

Autonomous Derivatives of Estrogen-induced Renal Carcinomas and Spontaneous Renal Tumors in the Syrian Hamster

Abstract: A summary is given of the characteristics of autonomous or semiautonomous hormone-responsive or conditional renal tumor transplants available in a tumor bank. Also data from about 4000 Syrian hamsters used in many experiments from 1947 to 1974 are included. Transplanted tumors are referred to as autonomous whenever they grow progressively in intact hosts of either sex. Histologically the primary tumor its metastases its early and later serial transplants and metastases from them are essentially similar with some variations. Spontaneous tumors are undifferentiated and show many mitotic figures some of which are abnormal. Of induced tumors 30 primary estrogen-induced renal tumors have been transplanted into estrogen-treated hosts. Only a few have been continued long enough to have acquired autonomy. With the exception of the estrogen-induced kidney carcinomas induced kidney tumors or spontaneous ones are rare in hamsters. In some manner all of the autonomous lines are responsive to some steroidal hormones. Autonomy checks consisting of the transplantation of small random samples from hormone-dependent tumors into untreated hosts are not as significant as sometimes thought. After a variable number of serial passages in estrogen-treated hosts the estrogen-induced renal carcinoma contains areas of autonomous cells as well as areas of hormone-dependent ones. Chance plays a role in which areas may be selected for in vivo or in vitro transplants. The existence of specific protein receptors in estrogen target tissues of various animals is now established. The kidney in the Syrian hamster may be added to this list. Hormonal influences may be of secondary significance in neoplasia and although they are of clinical inportance in tumor progression they may not be primarily involved in tumor induction. The common origin of target tissues is undoubtedly involved in the tumorigenic properties of sex hormones. In hamsters carcinomas that are potentially hormone responsive demonstrate a different enzyme profile from those that are potentially independent. These observations suggest that isoenzyme differences may exist in human tumors and provide a reason for the clinical use of estrogen-dependent human tumors. 20 reproductions of the histology of these tumors are presented.

In Vitro Demonstration of Complement-Dependent Cytotoxic Antibodies to Moloney Sarcoma Cells

Abstract: An in vitro microcytotoxicity assay was used to demonstrate complement-dependent cytotoxic antibodies to Moloney sarcoma virus-induced cells throughout the stages of tumor progression and regression in BALB/c mice. Complement-dependent cytotoxic antibodies were present in the sera of mice whose tumors were in the late stages of tumor growth, and most consistently in the sera of mice whose tumors had completely regressed (regressors). Regressor sera were strongly cytotoxic for at least 125 days after the onset of tumor regression. Preliminary evidence indicates that the complement-dependent cytotoxic antibody in regressor sera is a 7S immunoglobulin.