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)

Chemotherapy of metastatic breast cancer induces temporary tumor responses, without any incidence on vital prognosis. New drugs are sometimes less toxic than previous but are not more efficient. Such findings are observed with other schedules of chemotherapy. It is necessary to adapt treatment to expected goal: optimal efficacy or minimal toxicity.
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PMID:[New agents in chemotherapy and new methods of their administration in the treatment of metastatic cancer of the breast]. 271 19

Thirty-six patients with metastatic breast cancer, 23 with documented progression of the disease after first-line chemotherapy (CAF or CMF) and 13 without prior chemotherapy, were treated with a simultaneous 120-h infusion of cisplatin (CDDP) and 5-fluorouracil (5-FU). Objective response was demonstrated in 19 patients (52.7%), stable disease in 7 patients (19.4%) and progression of the disease in 10 patients (27.7%). Similar response rate was observed according to tumor site (soft tissues, 50%; bone, 52%; lung, 63%; liver, 55%; and pleura and peritoneum, 42%) and previous treatment (previous chemotherapy, 48%; previously untreated, 61%). Median duration of response was 8 months. Toxicity was characterized by stomatitis and myelodepression and required dose adjustments in 30% of patients. CDDP and 5-FU infusion deserve further investigation because it appeared to have substantial activity in this preliminary study in metastatic breast cancer.
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PMID:120 hours simultaneous infusion of cisplatin and fluorouracil in metastatic breast cancer. 280 99

In an attempt to increase the clinical activity of 5-fluorouracil (5-FU) by blocking the thymidine salvage pathway, 15 patients with refractory metastatic breast cancer (MBC) were treated with oral dipyridamole (D): 75 mg p.o. q.i.d. and 5-FU: 400 mg/m2 i.v. by bolus for 5 consecutive days, every 28 days. All the patients were pretreated with 5-FU and an anthracycline-based regimen. Toxicity was minimal, with 8 patients experiencing a D-related moderate headache. Although no objective responses were seen, two patients with 5-FU refractory disease showed tumor shrinkage. A different D schedule and the addition of folinic acid (FA) to 5-FU might provide better results and deserves further evaluation.
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PMID:5-Fluorouracil and dipyridamole in metastatic breast cancer: a pilot study. 280 94

A mucin-like carcinoma-associated antigen (MCA) was recently identified on the surface of established breast cancer cell lines by several monoclonal antibodies. The antibody b-12 was used in a sandwich enzyme immunoassay to measure MCA concentrations in serum samples and other biological fluids. The upper limit for noncancerous women and men was 14 U/ml. MCA levels were independent of estrogen or prolaction secretion, 63% of patients with metastatic breast cancer had elevated serum concentrations of MCA. Elevated MCA levels were also associated with cervical, ovarian or endometrial cancer and carcinoma of the prostate. In metastatic breast cancer, MCA and CA 15.3 showed similar sensitivity. Carcinoembryonic antigen levels did not correlate with MCA. Serum concentrations of MCA increased during pregnancy and remained elevated in nursing mothers. Amniotic fluid was found to be rich in MCA. In contrast, CA 15.3 showed only small changes during pregnancy and was low in amniotic fluid. From binding tests with antibodies used in the MCA and CA 15.3 assays, we conclude that the monoclonal antibodies b-12 as well as 115-D8 and DF3 (CA 15.3 assay) recognize coexisting epitopes on mucin-like antigens, which belong to a polymorphic family of glycoproteins suitable for tumor monitoring. Differences in the behavior of MCA and CA 15.3 may emerge from the complexity and heterogeneity of these mucin-like antigens.
Tumour Biol 1989
PMID:MCA, a monoclonal-antibody-defined breast-tumor-associated antigen and its relation to CA 15.3. 281 32

In this study we report on some lines of ongoing research performed in our laboratory, in relation to the increased expression of FcR on tumor cells, as well as on cells present in the tumor-bearing host, and its possible role in tumor progression. In a previous study we have shown that a Polyoma virus (PyV)-induced anaplastic carcinoma (SEYF-a tumor) contained an FcR-expressing subpopulation of tumorigenic cells. We tested the effect of in vivo passaging of FcR-expressing and of non-FcR-expressing sub-populations of SEYF-a tumor cells on the expression of FcR, as revealed by the ability of these cells to bind the 2.4G2 monoclonal antibody, which is directed against mouse Fc gamma 2b/gamma 1R. It was found that upon in vivo passaging these two sub-populations became practically identical in their ability to bind anti-Fc gamma R antibody. On the other hand, in vitro passaging of FcR-expressing SEYF-a cells resulted in a gradual decrease in the expression of Fc gamma R. These results, indicating that the expression of Fc gamma R on tumor cells, per se, is dependent on a factor present in the in vivo environment were confirmed using 3T3 cells transformed in vitro by PyV (C) and forming tumors at first injection to mice (CTC). C cultures of various clones did not express Fc gamma R, while CTC cultures (cultures from tumors) became positive. We also detected an increase in the level of a soluble form of Fc gamma 2b/gamma 1R in the circulation of mice bearing PyV induced tumors. This increase paralleled the appearance of palpable tumors. A similar pattern of increase was observed in mice inoculated with the c-H-ras transformed tumorigenic clone 8/F/5, but not in mice inoculated with non-tumorigenic 3T3 cells. Data published by us show that metastatic breast cancer patients had significantly elevated Fc gamma R levels on their peripheral blood mononuclear cells (PBMC). Experiments presented here indicate a direct correlation between increased Fc gamma R levels on PBMC and tumor mass in colon, ovary and lung metastatic carcinoma patients. The possibility that malignantly transformed cells have the potential to cause proliferation of Fc gamma R expressing T cells was tested. It was found that extract derived from r-H-ras transformed 3T3 cells triggers the proliferation of a T cell hybridoma expressing Fc gamma R.
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PMID:Increased expression of Fc gamma receptor in cancer patients and tumor bearing mice. 285 35

Plasma fibronectin was determined by laser nephelometric immunoassay in two populations: healthy individuals and patients with metastatic or non-metastatic breast cancer. The results showed that the fibronectin concentration was higher in the patient group than in the healthy controls of similar age, with a significant difference (p less than 0.05). The patients who had metastatic breast cancer tended to show higher levels than those with no detectable metastasis, but such a difference was not statistically significant. Since fibronectin is sensitive to clinical events unrelated to the malignancy status, it does not seem suitable as a tumor marker.
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PMID:Level of plasma fibronectin in patients with breast cancer. 285 55

Medroxyprogesterone acetate (MPA) has been used in high doses as hormone treatment for metastatic breast cancer. We treated five intracranial meningiomas with MPA expecting that MPA would reduce the volume or decrease the growth rate. All five patients were postmenopausal women, aged 47 to 73 years. Before treatment, the growth rate of each tumour was assessed by two consecutive CT scans (CT 1 and CT 2). Tumours 1 to 4, histologically benign meningiomas, grew slowly as the tumour volumes were not found to increase in 21 to 45 months between CT 1 and CT 2. Tumour 5 was an anaplastic meningioma the rapid growth of which was evident in 8 weeks between CT 1 and CT 2. After CT 2, MPA was given 1,000 mg intramusculary once weekly for 17 to 29 weeks until CT 3 which showed the response. Tumours 1 to 4 had neither reduced in volume nor developed necroses, and tumour 5 continued its fast growth at the same rate as before.
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PMID:Hormone treatment of meningiomas: lack of response to medroxyprogesterone acetate (MPA). A pilot study of five cases. 293 93

Using ascitic fluid or pleural effusion obtained from 13 ovarian or metastatic breast cancer patients, we separated tumor cells from effusion-associated lymphocytes (EAL) with Percoll density centrifugation. Lymphocytes were incubated with recombinant interleukin 2 (IL-2) for 3-4 days and then assessed for tumoricidal activity in a 51chromium-release assay. The IL-2-activated EAL were found to lyse autologous fresh tumor cells, as well as allogeneic fresh tumor cells and FMEX tumor cells, a melanoma cell line which is resistant to natural killer cell activity but is sensitive to lysis by lymphokine-activated killer cells. There was little or no tumoricidal activity seen in freshly isolated EAL or in EAL which were cultured in medium without IL-2. Phenotypically, the IL-2-activated EAL were largely CD3-, although some cytolytic activity was found in CD3+ populations. Also, most activity was found in cells positive for CD2 (OKT11) and CD16 (Leu 11b), and negative for the monocyte marker Leu M3. These results indicate that the activated cell types found in EAL were predominantly natural killer/lymphokine-activated killer-like with a small contribution from T-cells. Finally, EAL were readily activated by IL-2 in medium containing autologous effusion fluid, indicating that in situ activation of tumoricidal activity by IL-2 can occur in the face of potentially inhibitory substances or cells that may exist in the effusions. Direct introduction of IL-2 may therefore be a potential therapeutic modality of effusion-forming cancers.
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PMID:Infiltration of interleukin-2-inducible killer cells in ascitic fluid and pleural effusions of advanced cancer patients. 297 57

Progestational agents, such as megestrol acetate and medroxyprogesterone acetate, are effective hormonal treatments for metastatic breast cancer in postmenopausal women. Clinical trials of these agents have demonstrated that 30% to 60% of patients will experience objective tumor response, depending on pretreatment prognostic variables. Although optimal doses and schedules have not been fully defined, current studies are investigating the therapeutic effectiveness of high-dose progestins. Toxicity of these drugs is mild and generally limited to weight gain related to their anabolic activity. Progestins are active second-line agents for metastatic breast cancer in postmenopausal women. In selected patients, they appear to be equivalent to tamoxifen as first-line therapy for metastatic disease. As more patients are exposed to prolonged adjuvant tamoxifen therapy, the role of progestins as first-line hormonal therapy at the time of relapse is likely to expand.
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PMID:Progestational agents in advanced breast cancer: an overview. 302 51

Cells from some, but not all, tumor biopsy samples form colonies when cultured in semi-solid media. The possibility that colony formation by progenitor cells in these tumors may reflect a more "aggressive" phenotype bearing clinical implications was examined in a series of 61 patients with primary breast cancer. Tumor cells from 32 samples formed colonies in vitro. There was no correlation between colony formation and any of the standard clinical parameters such as tumor size, nodal status, metastatic spread, or hormone receptor levels. Eighteen patients had inflammatory, locally advanced and/or detectable metastatic breast cancer at the time of surgery. Sixteen of these patients have progressed and 15 have died, with no relationship between colony formation and survival. For the 43 remaining patients, 23 had a tissue sample that gave rise to colonies in vitro; 14 of these have relapsed, with a median relapse-free survival (RFS) of 37.6 months, and eight have died with a median survival time of 46.8 months. This is compared with four relapses (median RFS not reached, P = .0043, Peto-Pike), and four deaths (median not reached, P = .1175) in the group without growth of the tumor specimen. These results indicate that colony formation is an independent prognostic parameter for breast cancer, which may be useful for selecting patients who would benefit from more intensive therapy.
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PMID:Colony formation in vitro as a prognostic indicator for primary breast cancer. 303 10


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