Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The genetics of late appearing MSV tumors showing a progressive growth pattern in AKR mice was investigated. The late MSV tumor response in F1 hybrids depended on the genetic background of the non-AKR parent. Within the 4-month observation period following virus injection, (CBA X AKR) F1, (DBA/2 X AKR)F1, and (NIH X AKR)F1 developed progressing MSV tumors, which exhibited latency and growth behavior comparable to that seen in AKR mice, (BALB X AKR)F1, (B6 X AKR)F1, and (B10br x akr)f1 mice did not show any late MSV tumors. In contrast to early regressing M-MSV tumors, whose development is independent of Fv-1 genotype, late MSV tumor progression is largely a function of this gene, since all late tumors which appeared in (B10BR x AKR) x AKR were observed in Fv-1n homozygous mice, H-2k halotype is a further factor in the occurrence of late MSV tumors, at least in (B6 x AKR) x AKR mice. In crosses of AKR with Fv-1 compatible mice, tumor appearance was strongly associated with inheritance of AKR-Mulv, and MSV recovered from late tumors of first back-cross animals appeared to be a new pseudotype with the endogenous AKR-MuLV. It is suggested that the host genetic control in both early and late MSV tumors is exerted mainly on the helper component of the leukemia-sarcoma complex.
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PMID:Genetics of murine sarcoma virus (MSV)--induced tumors in AKR mice: Evidence that late progressing and early regressing tumors are controlled by different gents. 6 12

A 22-year-old man with a synovial cell sarcoma attained an excellent response to therapy with adriamycin (NSC-123127) and dimethyltriazeno imidazole carboxamide (NSC-45388). Therapy was discontinued at a cumulative dose of adriamycin of 600 mg/m2. Relapse occurred 13 1/2 months later, and therapy with adriamycin was restarted. Because of tumor progression, therapy was discontinued after a cumulative dose of adriamycin of 120 mg/m2. Ten weeks later, severe congestive heart failure developed which ultimately caused the patient's death. Exacerbations of the heart failure were temporally related to the administration of the antitumor antibiotics actinomycin-D (NSC-3053) and mithramycin (NSC-24559). Electron microscopic examination of the heart revealed changes characteristic of adriamycin cardiomyopathy. Thus, even after a long hiatus, it may not be safe to exceed the recommended maximum cumulative dose level of adriamycin. The pathogenic mechanisms involved in the development of adriamycin cardiomyopathy are reviewed, and the possible synergistic effect of other antitumor antibiotics is discussed.
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PMID:Cardiomyopathy after widely separated courses of adriamycin exacerbated by actinomycin-D and mithramycin. 17 14

Sublethally irradiated BALB/c mice innoculated with Moloney sarcoma virus (MSVm) develop progressively growing tumors and die within 30 days of virus innoculation. These animals can be protected from tumor progression (and death) by innoculation of small numbers of MSV-immune T lymphocytes from MSV-M innoculated (but unirradiated) animals. T lymphocytes in these donor animals have been shown to express immunity to a variety of viral and virally-induced antigens. We have investigated whether immunity to any one of these antigens was critically important in leading to protection of the irradiated animals by sensitizing normal T lymphocytes in vitro to different viral antigens and examining the ability of these sensitized cells to protect the irradiated recipients. Data is presented to show that cells sensitized in vitro to MSV-transformed fibroblasts, and to purified antigens with group specificity, but not to viral envelope antigens, or whole virus, are capable of protecting the irradiated MS innoculated animals.
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PMID:Cell-mediated immunity to Moloney sarcoma virus in mice. II. Analysis of antigenic specificities involved in T lymphocyte-mediated in vivo rejection of murine sarcoma virus-induced tumors. 108 21

The temporal development of antibodies to Moloney sarcoma virus (MSV)-induced antigens in relation to tumor progression was followed with the membrane immunofluorescence (MF) and antibody-dependent normal lymphocyte cytotoxicity (ADNLC) assays. Antibody was detected at 14 days following virus infection by MF. In mice that developed primary tumors which regressed, MF titers developed to high levels following a period between 2 and 4 weeks post-innoculation during which the titers remained at low and constant levels. The increase in MF titers corresponded closely on a temporal basis to the initiation of the regression process. In contrast, antibody remained at low levels in those mice that developed progressively growing tumors. ADNLC was detected in the sera of regressor mice approximately 6 weeks post-inoculation but was not detectable at any of the time interavals in sera from mice with progressively growing tumors. Attempts to enhance the cytotoxic activity of normal spleen cells directly with immune serum were unsuccessful. The synergistic effect of serum on the cytotoxic activity of immune lymphocytes was less pronounced than with normal lymphocytes in this system. Temporal studies indicated that there was an inverse relationship between the development of cellular immunity and the capablility of these cells to be activated in the ADNLC assay.
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PMID:Antibody production and interaction with lymphoid cells in relation to tumor immunity in the Moloney sarcoma virus system. 109 Jun 75

The efficacy of combined high-dose etoposide with standard dose cisplatin was evaluated in patients who had refractory lung cancer after standard chemotherapy. Each patient was given etoposide at 500 mg/m2/day on day 1 to 3 continuously (total dose 1,500 mg/m2) and cisplatin at 80 mg/m2 on day 1. Fifteen patients (7 adenocarcinoma, 5 small cell lung cancer, 2 squamous cell lung cancer and 1 sarcoma, which latter was difficult to distinguish from giant cell carcinoma) were entered in this study. The overall response was 41.7% (5 of 12); five partial response, 6 no change, and 1 progressive disease. Three treatment-related deaths were observed; one resulted from sepsis and two from respiratory failure because of tumor progression. All of the patients developed severe myelosuppression; the mean nadir white blood cell count was 400, and the mean nadir platelet count was 24,000 in 28 evaluable courses. The range of maximum concentration of etoposide determined by HPLC was from 17.4 to 39.1 micrograms/ml. These results suggest that high-dose etoposide combined with a standard dose of cisplatin is effective against refractory lung cancer.
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PMID:[Pilot phase II trial of high-dose etoposide combined with cisplatin in the treatment of refractory lung cancer]. 131 97

Interrelationships between neoplastic progression and the expression of intermediate filaments were examined in primary cultures, immortal lines, and Kirsten murine sarcoma virus (KiMSV) transformed lines of rat ovarian surface epithelial (ROSE) cells. Immunofluorescence microscopy revealed abundant keratin filaments in all cells of primary cultures. In immortal, nontumorigenic lines, keratin filaments were detected in fewer cells, in smaller numbers, and in microscopically altered forms. The percentage of keratin-positive cells ranged from 4 to 54%. Its expression was inversely proportional to cell density. Keratin expression was similar in the two immortal lines, although one had retained a monolayered epithelial growth pattern resembling primary cultures, while in the other the growth pattern of the cells was more atypical. The two KiMSV-transformed lines were previously shown to produce tumors in vivo that resemble human ovarian endometrioid stromal sarcomas. In spite of this histologic appearance, the proportion of keratin-positive cells in these cells was increased over the immortal lines. Keratin expression was unrelated to cell density, and keratin in most virally transformed cells was limited to few, fine filaments. In thymidine-labelled immortal and virus-transformed cultures stained for keratin, no correlation was found between keratin expression and proliferative activity. The keratin profiles of primary and immortal cultures were identical on Western blots, with subtypes ranging from 52 to 66 kDa. The two virally transformed lines lacked some of the subtypes. Vimentin networks were faint or absent in primary cultures. In the immortal and the virus-transformed lines, neoplastic progression was associated with increasing vimentin expression but with no changes in filament morphology and distribution. The results show that the abnormalities in intermediate filament expression that accompany immortalization do not preclude the retention of a normal epithelial morphology and growth pattern in this cell type. Furthermore, the number of intermediate filaments and their intracellular distribution appear to be altered at an earlier stage in neoplastic progression than those mechanisms that select for specific keratin subtypes, or those that respond to regulation by cell density. Finally, the presence of keratin in the KiMSV-transformed lines examined in this study supports the hypothesis that human ovarian stromal sarcomas can arise in the OSE.
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PMID:Intermediate filaments in rat ovarian surface epithelial cells: changes with neoplastic progression in culture. 137 15

We have investigated the in vivo role of 2 different adhesion molecules, LFA-1 and LECAM-1, in the immune reaction to Moloney-murine-sarcoma-virus(M-MSV)-induced tumors, which undergo a peculiar spontaneous regression due to generation of a strong virus-specific cytotoxic-T-lymphocyte(CTL) response. Repeated administration of anti-LFA-1 monoclonal antibody (FD441.8 MAb), i.p. or at the site of virus inoculation, enhanced tumor growth and delayed regression, while i.p. administration of anti-LECAM-1 MEL-14 MAb gave rise to tumors that grew progressively and caused host death. Evaluation of the immunological response in MAb-treated mice showed reduced generation of virus-specific CTL precursors (p) in the spleen of animals given FD441.8 MAb i.p.; CTLp frequency in locally treated mice overlapped with that of control mice injected with virus only. FD441.8 MAb treatment did not interfere with CTL homing in the tumor, since the frequency of M-MSV-specific CTLps in sarcomas was similar in treated and control mice. Cytofluorimetric analysis indicated that the majority of tumor-infiltrating lymphocytes (TIL) from MAb-treated mice were covered by anti-LFA-1 MAb, and lacked cytotoxic activity when assayed against target cells bearing relevant tumor antigens. Instead, in mice injected i.p. with MEL-14 MAb, a very low frequency of CTLps was detected in lymph nodes draining the tumor area, and within the tumor. Our results indicate that enhanced tumor growth, depending on the MAb used, is the resultant of an inhibitory effect on different T-lymphocyte functions. Tumor progression in anti-LFA-1 MAb-injected mice is explained mostly by blockage of CTL lytic activity at the tumor site; in mice receiving i.p. MEL-14 MAb treatment, by the failure of naive T lymphocytes to enter peripheral lymph nodes and subsequently by the lack of generation of tumor-specific CTLs.
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PMID:Role of adhesion molecules in the immune reaction to M-MSV-induced tumors. 138 41

In searching an animal model to study metastasis formation we used cultured cells of experimental rhabdomyosarcomas and their inoculation tumors in adult nude mice. Supplementing earlier observations (Katenkamp et al. 1987) we found that long-term cultured sarcoma cells induce tumors in adult nude mice which do not metastasize spontaneously but produce lung metastases after repeated incomplete tumor removal. Possible factors and mechanisms responsible for metastasis emergence are discussed. The metastasis model introduced may be apt to study cellular changes at cytogenetic and molecular biological level that occur during tumor progression and metastatic dissemination.
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PMID:Metastasis induction by incomplete tumor resection. A new metastasis model using inoculation sarcomas in adult nude mice after long-term cultivation of sarcoma cells. 139 12

Soft tissue sarcomas (STS) represent a heterogenous group of malignant tumors arising in mesenchymal tissue and in the autonomal and peripheral nervous systems. Only 1% of all malignancies in adults are STS. Most of them are localized at the extremities, but they also occur in the abdomen and the thorax as well as at the abdominal and chest wall. They are usually surrounded by a pseudocapsule which contains tumor cells and they can exhibit a discontinuous growth pattern. Macroscopically undetectable branches might grow along given anatomical structures. Thus the whole sarcoma-related anatomic compartment should be judged as tumor-contaminated. The high rate of local failure is often caused by insufficiently extended primary resections. Lymph node metastases are rare. The main prognostic factors are histological grading, tumor size and surgical radicality. Diagnosis of STS is often made at a rather late state of tumor progression often too late for curative therapy. Early histological diagnosis is thus of great importance. The operation aims at the removal of the whole tumor bearing anatomic compartment. Even wide excisions of the sarcoma surrounded by 3 cm of tumor free tissue will lead to at least 60% local recurrencies. Excisions along the pseudocapsule (enucleation) will most likely leave parts of the tumor behind. Insufficient surgical radicality cannot be compensated for by adjuvant therapies. The resection should be carried out without compromises.
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PMID:[Soft tissue sarcoma in adulthood]. 141 47

During the 5-year period between 1988 and 1989, five patients with primary sarcomas of the liver underwent surgery. Since the patients presented in an early stage of the tumor, all the sarcomas were resectable, in three cases with wide margins (R-0 resection). Five histological types were detected: malignant hemangiopericytoma, malignant fibrous histiocytoma, hemangiosarcoma, rhabdomyosarcoma, and embryonal sarcoma. Two patients with high-grade sarcomas received adjuvant chemotherapy. The follow-up was favorable in three patients with R-0 resections (two had adjuvant chemotherapy). They were still alive, with no evidence of disease 30, 46, and 63 months after the diagnosis. The two other patients had to be reoperated on for local recurrences. Both died of their tumor disease, 30 and 35 months after the initial diagnosis. Extensive chemotherapy in one of these cases failed to arrest tumor progression. Hence, liver resection with wide margins is a very important measure in such cases.
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PMID:Primary sarcoma of the liver in the adult. Report of five surgically treated patients. 142 75


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