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

Between May 1980 and September 1983, 30 progestin-refractory patients with metastatic endometrial carcinoma were assigned at random to treatment groups receiving either cisplatin (CDDP) 60 mg/m2 every 3 weeks or a combination of cyclophosphamide, doxorubicin, and cisplatin every 4 weeks in doses of 400, 40, and 40 mg/m2, respectively. Those who failed cisplatin were then offered cyclophosphamide 500 mg/m2 plus doxorubicin 40 mg/m2 every 3 weeks. Reduced doses were utilized in both of the combination regimens for patients who had received extensive pelvic radiation. Of the 14 patients initially receiving cisplatin alone, 3 experienced objective tumor regression. One of these three and one other who failed primary cisplatin therapy later responded favorably to cyclophosphamide plus doxorubicin as secondary treatment. Among the 16 patients who took all three drugs simultaneously (CAP) 5 experienced objective partial tumor regression. Survival experience for these relatively late-stage patients has been uniformly poor, with only 7 and 12% surviving at 2 years after beginning CDDP and CAP, respectively. Thus, while cisplatin is clearly an active agent against endometrial carcinoma, its therapeutic index as a single drug or in combination (CAP) is not adequate to preclude new-agent Phase II studies early in patients with advanced disease.
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PMID:Randomized phase II studies of cisplatin and a combination of cyclophosphamide-doxorubicin-cisplatin (CAP) in patients with progestin-refractory advanced endometrial carcinoma. 365 66

The mouse mammary tumor and its associated virus, mouse mammary tumor virus, were chosen to test the possibility of using plasma levels of a Mr 52,000 viral glycoprotein (gp52) as a means for monitoring changes in tumor status during surgical adjuvant cyclophosphamide:doxorubicin (Adriamycin):5-fluorouracil treatment. Analysis of tumor recurrence and plasma gp52 concentrations during the postoperative period demonstrated that both parameters were significantly decreased in the group receiving cyclophosphamide:doxorubicin:5-fluorouracil treatment. This observation suggests that plasma gp52 levels may be a useful alternative measure of therapeutic effect during surgical adjuvant treatment. A retrospective analysis of gp52 plasma levels and tumor status of individuals during treatment has revealed the following associations. (a) An early sharp postsurgical elevation in plasma gp52 level was associated with subsequent death of treated animals. (b) Maintenance of postsurgical gp52 levels at a low level (less than or equal to 4.2 ng/ml) during and after treatment was characteristic of all tumor-free survivors. (c) A gradual rise in plasma gp52 level accompanied CAF-delayed tumor recurrence. gp52 levels increased in all treated animals 2 wk prior to detectable tumor regrowths, resulting in a statistically significant increase in mean gp52 level (2.2 to 5.4 ng/ml). However, the magnitude of this increase was small for the majority of animals with tumor regrowths, and greater, more definitive elevations in plasma gp52 levels were only detected at the time of frank tumor recurrence. In addition, comparisons of early mean gp52 levels (8 to 10 days after surgery) for controls and for animals receiving various forms of alternative treatment have indicated that differences in gp52 levels reflect subsequent differences in recurrence rates. The present data, obtained during surgical adjuvant treatment of BALB/c X DBA/8 F1 mice and viewed in a retrospective fashion, demonstrate that plasma gp52 concentrations reflected therapeutic effects.
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PMID:Plasma levels of a viral protein during adjuvant treatment: reflection of murine mammary tumor status and therapeutic effect. 375 89

The histogenesis of Ewing sarcoma, the second most frequent bone tumor in humans, remains controversial. Four Ewing cell lines were analyzed by immunological methods. A panel of antibodies directed to T, B, and myelomonocytic markers gave negative results. Surface antigens recognized on Ewing cells were found to be related to the neuroectoderm lineage. Ganglioside GD2, a marker of neuroectodermal tissues and tumors, was present on all lines. These were also stained by the mouse monoclonal antibody HNK-1, which detects a carbohydrate epitope present on several glycoconjugates of the nervous system, including two glycoproteins, the myelin-associated glycoprotein and the neural cell-adhesion molecule (N-CAM), and an acidic glycolipid of the peripheral nervous system. The P61 monoclonal antibody, which reacts with a peptide moiety of N-CAM, and a rabbit antiserum, raised to purified mouse N-CAM and not recognizing the HNK-1-defined epitope, were also reactive. By contrast, all antibodies specific for hematopoietic cell surface antigens were totally negative. Besides these antigenic features, Ewing sarcoma cells are characterized by a specific t(11;22)(q24;q12) translocation also observed in neuroepithelioma, a neuroectodermal tumor, suggesting a possible evolutionary related origin. The recent finding that the human N-CAM gene is located at the vicinity of the breakpoint on chromosome 11 indicates that it might be involved in genetic rearrangements occurring in this region.
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PMID:Phenotypic characterization of Ewing sarcoma cell lines with monoclonal antibodies. 376 36

Plasma concentrations of gp52, a Mr 52,000 glycoprotein of the mouse mammary tumor virus, have been measured during cyclophosphamide, doxorubicin (adriamycin) and 5-fluorouracil (CAF) treatment of mammary tumor-bearing CD8F1 mice. The value of plasma concentrations of gp52 as an indicator of CAF-mediated changes in tumor status was supported by each of the following findings: (a) CAF treatment did not interfere with the detection of elevated viral antigen levels in the plasma of tumor-bearing mice; (b) at 9-11 days after initiation of treatment, a significantly lower mean gp52 level, observed in the group of CAF-treated mice, provided definitive evidence of therapeutic effect; and (c) serial determinations of plasma gp52 levels in individual mice before, during, and after treatment provided a relative measure of therapeutic effect for each individual that was a reflection of corresponding changes in tumor size. Changes in viral antigen levels (i.e., decrease or increase) reflected inhibited tumor growth, as well as tumor regression. These findings demonstrate that plasma concentrations of gp52 can be utilized to provide an alternative measure of therapeutic effect in CAF-treated mice bearing significant tumor loads.
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PMID:Therapeutic effect reflected by plasma levels of a viral protein during combination chemotherapeutic treatment of mammary tumor-bearing mice. 384 Apr 11

Between December 1979, and October 1981, the Eastern Cooperative Oncology Group (ECOG) compared four cisplatin-containing regimens in the treatment of patients with metastatic non-small-cell bronchogenic carcinoma (NSCBC). CBP (cyclophosphamide, bleomycin, and cisplatin) and AFP (doxorubicin, 5-fluorouracil, and cisplatin) had shown activity in generation II of this study (EST 2575). These were compared to MVP (mitomycin C, vinblastine, and cisplatin) and CAP (cyclophosphamide, doxorubicin, and cisplatin) which were reported efficacious in single institution studies. A total of 479 previously untreated patients with metastatic NSCBC (ECOG performance status 0, 1, or 2) were entered, and of these, 432 (90%) were evaluable. Although MVP resulted in a higher response rate (5 complete responses [CRs], 22 partial responses [PRs], 26% overall) than CBP (4 CRs, 18 PRs, 20% overall), AFP (0 CRs, 18 PRs, 17% overall), or CAP (1 CR, 23 PRs, 23% overall), the difference was not significant. Survival by treatment did not differ significantly. There were 45 life-threatening and six lethal complications of therapy. Although each of the above regimens offers a modest chance of inducing greater than 50% tumor shrinkage (17% to 26%, 21% overall) the effect that these responses have an overall median survival (21.6 to 23.7 weeks, 22.9 weeks overall) is unclear.
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PMID:Chemotherapy for metastatic non-small-cell bronchogenic carcinoma: EST 2575, generation V--a randomized comparison of four cisplatin-containing regimens. 388 Aug 10

Between February 1980 and August 1982, the Cancer and Leukemia Group B (CALGB) performed a randomized study aimed to compare chemotherapy with CAF (Cyclophosphamide, Adriamycin, 5-Fluorouracil) versus the same chemotherapeutic regimen plus tamoxifen (T-CAF) in stage IV breast cancer patients. Patients were stratified on the basis of menopausal status, estrogen receptors (ER) status, dominant site of metastasis and prior adjuvant treatment. Overall 474 patients were entered into the study of whom 433 were assessable for response. 314 patients were postmenopausal, 85 premenopausal and 34 patients were unknown as far menopausal status was concerned. No difference was evident among postmenopausal patients in overall response rate and duration of responses between T-CAF and CAF (52% vs 50% respectively). Similarly no difference was shown among premenopausal patients, response rates being 63% with T-CAF and 60% with CAF. Lack of benefit from adding T to chemotherapy was seen also according to the different strata, including patients with ER positive tumors. The failure for this combination to be synergistic might reflect an effect of T on tumor kinetics interfering with the activity of chemotherapy.
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PMID:Chemotherapy with cyclophosphamide, adriamycin, and 5-fluorouracil compared to chemotherapy plus hormonal therapy with tamoxifen in the treatment of advanced breast cancer: an interim analysis. 391 18

Experimental chemotherapies for 15 human cancers xenografted into nude mice were performed using 14 anticancer agents including 6 drugs in clinical use. Treatment with each single agent was performed for every cancer line using the maximum tolerated dose through continuous daily (antimetabolites) or intermittent (cytocidal agents) schedules. Effectiveness of each drug was evaluated by inhibition rate (IR) calculated from mean tumor weights of both treated and untreated groups. Response to a treatment was judged as effective when the IR was higher than 58%. Response rate of each drug was as follows; MMC was 67%, UFT 67%, CPA 47%, FT-207 40%, ACNU 33%, ADR 27%, SOAz 87%, 5'-DFUR 80%, MXT 20%, Leakadine 17%, M-83 17%, CAM 0% and GANU 0%. Generally, the experimental results for each drug on the xenografts was in good accordance with the known clinical effect of each drug on the same type of cancer. On the other hand, individual cancer xenografts showed considerable differences in chemosensitivity. Some tumors were sensitive to a majority of the drugs, whereas some were resistant to many of them. Each cancer line seemed to retain individuality in its spectrum of chemosensitivity irrespective of whether it originated from the same organ or whether it was of similar histologic type. This fact suggests the necessity of selecting drugs effective to the individual tumor when considering a patients chemotherapy regime.
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PMID:[Chemosensitivity of human gastrointestinal and breast cancer xenografts in nude mice]. 397 May 56

Authors report on their experiences concerning in vitro clonogenic assay performed according to Hamburger and Salmon on solid tumor tissue samples (13 cases) and ascites cells (5 cases) obtained from 16 ovarian cancer patient. Out of the 13 solid tumors they got single cell suspension with sufficient number of cells in each case. Colony formation was observed in 10 out of 18 specimens. Dose-response curves were determined after incubation of cells with different concentrations of the following drugs: cis-platin, adriamycin and melphalan. Patients were treated with the CAP combination chemotherapy. The correlation between clinical responses and in vitro sensitivity was evaluated retrospectively. The analysis of the in vitro-in vivo correlation showed that in case of in vitro resistance against two components of the CAP combination the tumor progressed during CAP treatment. In case of in vitro resistance against one component except cis-platin CAP therapy could cause even complete response. By in vitro cis-platin resistance the maximum response with CAP treatment was partial remission.
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PMID:[Pretherapeutic chemosensitivity testing of ovarian cancer and possibilities for its clinical use]. 406 Sep 13

The studies presented herein were designed to directly evaluate the effects of a transient GVH reaction on T lymphocyte functions. To this end, we have shown that generation of carrier-specific helper cell function can be significantly influenced by the allogeneic effect. Thus, carrier-primed helper cells derived from CAF(1) donor mice were generally much more active in specifically cooperating with syngeneic 2,4-dinitrophenyl (DNP)-primed B cells in adoptive recipients when parental A strain lymphocytes had been administered at some time during the priming regimen. This was true when allogeneic cells were administered concomitantly with the initial priming dose of carrier protein as well as when the GVH was induced in animals that had been exposed to antigen several days previously. This indicates that the allogeneic enhancing effects can be manifested on either primed or unprimed T cell populations. The ultimate effect of the GVH reaction on the development of helper T cell activity was found to be related to the number of allogeneic cells employed and the duration of the resultant GVH reaction in the carrier-primed host animal. Hence, allogeneic stimulation of slightly greater magnitude and/or longer duration resulted in marked suppression rather than enhancement of helper cell function in such donor mice. These findings may have general relevance to problems in autoimmune diseases and tumor immunity.
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PMID:The allogeneic effect in inbred mice. IV. Regulatory influences of graft-vs.-host reactions on host T lymphocyte functions. 412 47

A graft-vs.-host reaction (GVHR) was induced in young male CAF(I) and CB6F(1) mice by the administration of BALB/cJ spleen cells. A proportion of such mice subsequently developed lymphoreticular rumors. Cell-free extracts (CFEs) prepared from the reticular tissues of CAF(1) mice killed at intervals after the induction of the GVHR were tested for their capacity to produce the same tumors in a litter of syngeneic mice inoculated at birth. 12 of 29 (41.4%) such extracts were positive, causing lymphoreticular tumors in one or more littermate recipients. The positive CFEs came from donors killed at all stages of the GVHR, from tumor-bearing mice as well as from non-tumor-bearing mice. However, whereas less than 30% of CFEs from mice killed within 12 mo of GVHR induction were oncogenic, the incidence of oncogenic extracts from mice killed 12-15 mo after GVHR induction rose to 75%. None of the CFEs prepared from nine normal uninjected male CAF(1) mice killed between the ages of 8 and 18 mo transmitted tumors to recipients. CFEs prepared from CAF(1) mice with the GVHR were tested for infectious murine leukemia virus (MuLV) using the XC assay and also for complement-fixing (CF) group-specific MuLV antigen. Substantial titers of B-tropic MuLV and CF antigen were detected in at least half the extracts from mice killed 11-14 mo after GVHR induction. During the first few months of GVHR induction, MuLV titers were low and CF antigen was absent. Neither infectious MuLV nor CF antigen were detected in CFEs prepared from normal control mice. Serially passed CFEs originating from a CB6F(1) GVHR-induced RCN caused similar tumors in successive generations of syngeneic recipient mice. These lymphoreticular tumors were shown to contain infectious MuLV, CF MuLV antigen, and C-type particles. These data together provide evidence that MuLV is activated during the GVHR and that it is responsible for the eventual development of lymphoreticular tumors.
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PMID:Tumor induction by immunologically activated murine leukemia virus. 414 84


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