Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently we reported that the highly metastatic MSC-10 (mouse squamous carcinoma) is incapable of inducing transplantation immunity. Studies reported here were undertaken to determine whether or not the tumor is devoid of tumor-associated antigen. We found that sera from MSC-10 tumor-bearing mice contain soluble protein antigens which react with rabbit antisera made against the MSC-10 tumor, as demonstrated by immuno-diffusion. Such proteins were not detected in the sera of normal mice or mice bearing fibrosarcomas. A close temporal relationship was demonstrated between the appearance of circulating antigens and the occurrence of lung metastases. Protein components serologically indistinguishable from the circulating antigens were isolated from tumor cells. The molecular weight of these proteins is between 30,000 and 100,000 daltons. Studies with antisera to mouse leukemia virus showed that hte MSC-10 tumor antigens are not viral proteins. The lack of immunogenicity of this tumor for syngeneic hosts as well as its high metastatic activity may be due to the early appearance of soluble antigens in the circulation.
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PMID:Detection of circulating tumor antigens in mice carrying a highly metastatic pulmonary squamous--cell carcinoma. 7 59

Tests were made to determine whether cell surface tumor antigens of metastases differed from the tumor antigens of the cell population of the local tumor growth. C57BL/6 mouse spleen lymphocytes sensitized against monolayers of the local growth of the 3LL Lewis lung carcinoma (L-3LL) in the presence of syngeneic serum generated lymphocytes that were cytotoxic to L-3LL but significantly less cytotoxic to target cells derived from lung metastases (M-3LL). Lymphocytes sensitized against M-3LL were significantly more cytotoxic against M-3LL than against L-3LL cells. Anti-M-3LL cytotoxic lymphocytes but not anti-L-3LL, admixed with either L-3LL cells or M-3LL tumor cells, when injected into syngeneic recipients reduced lung metastasis significantly. Results indicated that cells with high metastatic capacity and distinct antigenic properties exist within the tumor cell population and that immunoselection might be involved in the production of lung metastases.
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PMID:Differences in cell surface antigens of tumor metastases and those of the local tumor. 8 91

Exposure of cells in tissue culture to bleomycin or Adriamycin during 43 degrees C hyperthermia increased cytotoxicity dramatically compared to exposure at 37 degrees C. This study was designed to test whether this interaction was useful in tumor-bearing animals. C3H mice bearing the KHT tumor were treated with bleomycin (7 or 15 mg/kg) or with Adriamycin (2.5 or 5 mg/kg) with or without local heating of the tumor to 43 degrees C for 30 minutes by 13.56 MHz radiofrequency fields. The effects were assessed by growth delay (mean tumor diameter doubling time) and cure rate. In separate experiments, BALB/c mice bearing EMT6 tumors were treated identically, but tumors were excised 2 hours after treatment and tumor cell survival was assayed by colony formation. Antitumor effects of systemic bleomycin were potentiated by local hyperthermia. The two modalities had to be administered close together in time to observe the potentiation, suggesting a true interaction. There was a "threshold" for bleomycin potentiation in vivo between 42 degrees C and 43 degrees C, just as observed in tissue culture experiments. The antitumor activity of Adriamycin was not potentiated in vivo in these tumor systems except in cell survival experiments at doses higher than those compatible with survival of the host. The toxicity of drug combined with heat was greater than that of either modality alone. Hyperthermia did not adversely affect the incidence or severity of spontaneous lung metastases from KHT tumors. In fact, groups treated with heat and bleomycin had less severe lung metastases than groups treated with bleomycin alone. We conclude that local heating of tumors may be a useful adjunct to systemic bleomycin therapy. In vivo potentiation of Adriamycin by heat, however, could not be demonstrated in these tumor systems.
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PMID:Effects of systemically administered bleomycin or adriamycin with local hyperthermia on primary tumor and lung metastases. 8 6

The existence of antigenic differences between cell populations in the local growth of the 3LL tumor (L-3LL) and its lung metastases (M-3LL) was studied. Normal C57BL/6 spleen cells sensitized in vitro for 5 days against L-3LL monolayers lysed preferentially L-3LL targets but not M-3LL tumor cell targets. Conversely, anti-M-366-sensitized lymphocytes killed M-3LL targets more efficiently than they killed L-3LL targets. Furthermore, spleen cells from mice bearing subcutaneous L-3LL tumors were significantly more cytotoxic to L-3LL targets than to M-3LL targets and vice versa. M-3LL cells were found also to be more resistant in vitro and in vivo to natural killer cells than were L-3LL tumor cells. M-3LL cells were more resistant than L-3LL cells to hybrid resistant mechanisms when they were inoculated into F1 (C3Heb x C57BL/6) or F1 (BALB/c x C57BL/6) mice. Anti-M-3LL lymphocytes generated both in vitro and in vivo, but not anti-L-3LL lymphocytes, admixed with L-3LL or M-3LL tumor cells and inoculated into footpads of syngeneic recipients suppressed the development of lung metastases. These results suggest that metastatic cells are indeed phenotypic variants of the local growing tumor cell populations. Presumably, these variants are selected for their capacity to home to and grow in the lungs, and for their resistance to specific immune effects initially evoked against the local tumor and to nonspecific natural killer cells. These data may prove to be of importance with respect to any rational approach to the problem of immunotherapy.
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PMID:Tumor-associated antigenic differences between the primary and the descendant metastatic tumor cell populations. 9 33

Inoculation of Moloney sarcoma virus into the marrow cavity of the tibia of newborn Wistar-Lewis rats resulted in the appearance of an initially localized osteosarcoma in 97.7% of these animals. At least 77.9% of the rats developed lung metastases and died, usually within 6 weeks of inoculation. The remaining 22.1% showed regression of disease after initial growth of the tumor. Tumor cells were maintained in tissue culture and used as target cells for a visual and isotopic (3H-thymidine or 125IUdR) microcytotoxicity assay. Cell-mediated immunity could be measured by these methods throughout the course of the illness in animals with progressive disease as well as in those whose tumors eventually regressed. The presence of serum factors capable of modifying the level of CMI was documented. This Moloney-sarcoma-virus-induced rat osteosarcoma and human osteosarcoma thus appear to have several basic pathologic and immunologic similarities. The model may be useful for studying the effects of a variety of treatment protocols upon the clinical course and immune response to osteosarcoma.
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PMID:A laboratory model for the study of the immunobiology of osteosarcoma. 17 15

Growth characteristics, metastatic spread, and survival times were evaluated in a transplantable Wistar/Furth rat Wilms' tumor model. Tumor suspensions of various tumor cell dosages were injected in an attempt to find the optimum level of tumor take. Lung metastases were frequent following tumor injection by all routes. However, tumor spread to the lungs was the least frequent following subcutaneous (SC) injection of the tumor. Survival time for the intramuscular (IM) group was statistically longer at all tumor dose levels. For the 1 X 10(5) tumor dosage, survival time ranged from a mean of 27 days for the intrarenal (IR) group to a mean 42 days for the IM group. For the 1 X 10(4) dosage, survival time ranged from a mean of 37 days for the intraperitoneal (IP) group to a mean of 51 days for the IM group. It is concluded that this animal tumor closely resembles the human Wilms' tumor, and that the point at which the transplanted tumor fails to be successfully transplanted is below the dosage level of 1 X 10(3) tumor cells.
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PMID:The growth characteristics of the metastatic Wistar/Furth Wilms' tumor model. 17 97

The growth properties of single-tumor-cell suspensions prepared by enzymatic digestion of solid tumors from Morris hepatomas 7777, 5123tc, and 3924a and the presence of tumor-specific transplantation antigen for tumor lines 7777 and 3924a were described. Two of the tumor cell lines (7777 and 3924a) showed consistent i.m. tumor growth following the inoculation of 1 x 10(5) tumor cells, and a similar dose of 5123tc tumor cells resulted in inconsistent tumor growth. Two of the tumor lines (5123tc and 7777) were associated with rapid appearance of lung metastases, whereas with line 3924a metastatic lung lesions rarely developed despite its rapid i.m. tumor growth rate. Tumor resistance to rechallenge with a threshold inoculum of tumor cells was present in approximately 15 to 50% of the animals following amputation of an existing tumor mass. Resistance to a challenge tumor cell inoculum could also be accomplished by immunization with irradiated tumor cells. Tumor-specific resistance was demonstrated to tumor line 3924a in that "immune" animals were able to resist a challenge with 3924a tumor cells but did not resist a challenge with tumor line 9098.
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PMID:Characterization of growth properties and demonstration of the tumor-specific transplantation antigens of Morris hepatomas. 17 9

The effects of long-term administration of nafenopin, a potent hypolipidemic drug with marked hepatomegalic and peroxisome-proliferative properties, were studied in wild-type (Csa strain) and acatalasemic (Csb strain) mice. Nafenopin was administered in the diet at a concentration of 0.1% during the first 12 months and then at 0.05% until the termination of the experiment at 20 months. By 56 weeks, 100% mortality occurred in both male and female wild-type mice, whereas the mortality rate in acatalasemic mice was approximately 50%. Between 18 and 20 months of the experiment, 9 of 9 male and 12 of 12 female acatalasemic mice that survived chronic nafenopin treatment developed hepatocellular carcinomas, some of which metastasized to the lungs. None of the 15 male and 15 female acatalasemic controls developed liver cancers. Numerous peroxisomes were seen in the lung metastases of these hepatocellular carcinomas on electron microscopic examination; in contrast the number of peroxisomes in primary liver tumor cells varied considerably. The hepatocarcinogenicity of nafenopin strongly suggests the need for long-term studies with other hypolipidemic drugs that cause hepatomegaly and peroxisome proliferation to clarify the role, if any, of peroxisome proliferation in liver carcinogenesis.
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PMID:Hepatocellular carcinomas in acatalasemic mice treated with nafenopin, a hypolipidemic peroxisome proliferator. 17 2

In this case report, the patient had been delivered by Caesarean section and weighed only 4 pounds at birth. The mother was O negative, the father A positive, and the infant A positive. Initial red cell count was 2.85 million/cu mm; white cell count, 19,200/cu mm; and hemoglobin 70% of normal. At 3 months of age hemoglobin was 10% of normal. Bone marrow examination revealed marked erythroid hyperplasia. A diagnosis of Blackfan-Diamond syndrome was made. He received blood transfusions every 2 or 3 weeks for the first 4 years of his life. During his lifetime he received 433 units of packed cells for the treatment of congenital hypoplastic anemia. Vitamin-B12, folic acid, and iron were given without benefit. At 8 years of age a spelectomy was done. 20 months after surgery he recovered from pneumonococcal meningitis without sequelae. Progressive signs of hemochromatosis developed and finally progressive signs of heart failure with edema. At 24 years of age severe epigastric pain developed. An open liver biopsy disclosed multiple liver nodules which proved to be hepatoma. Severe ascites followed the surgery. Pulmonary metastases of the liver tumor developed and heart failure. He died at age 25. This patient had received no androgen. He was consistently hepatitis antigen negative. He was prepubertal at the age of 25 and had almost no endogenous androgens. Alpha-fetoglobin was present. This test may be useful as a screening test for hepatoma.
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PMID:Hepatocellular carcinoma, transfusion-induced hemochromatosis and congenital hypoplastic anemia (Blackfan-Diamond syndrome). 18 Aug 2

From 1950 through 1975, 671 patients with malignant major salivary gland neoplasms were referred to M. D. Anderson Hospital and Tumor Institute. Thirty-six patients with advanced local or metastatic disease subsequently underwent 62 evaluable trials with a variety of chemotherapeutic agents, either alone or in combination. Six patients achieved a partial response, with a median duration of 3 months. Ten additional patients had stable disease for 2 or more months. Anthracyclines appeared to be the most effective agents in this study, with three partial responses of six evaluable trials. The longest partial response (10 months) occurred in a patient receiving combination chemotherapy plus BCG immunotherapy. Pulmonary metastases were most commonly responsive to chemotherapy. The median intervals from diagnosis to death or to last follow-up and from initiation of chemotherapy to death or to last follow-up were 30 months and 6 months, respectively. Further therapeutic trials are necessary before response rates to single chemotherapeutic agents or combinations can be accurately assessed. In view of the poor prognosis of patients with recurrent disease, postoperative adjuvant studies with chemoimmunotherapy in patients with a high risk of recurrence are planned.
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PMID:Chemotherapy of malignant major salivary gland neoplasms: a 25-year review of M. D. Anderson Hospital experience. 19 35


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