Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A group of 32 patients with disseminated breast cancer were submitted to polychemotherapy following Cooper's protocol. Vincristine, cyclophosphamide, 5-fluorouracil, and prednisone were administered. The fifth drug used by Cooper, methotrexate, was not included in the therapy program because of difficulties in obtaining it. Both the objective and subjective results were similar to those of other authors using similar drug associations, while toxicity was moderate. Although this treatment is effective to some degree, the authors feel that further research should be carried out on more potent drugs, or in different combinations, in order to get a more definite chemotherapeutic effect in patients with breast cancer.
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PMID:[Association of VCR-5FU-CYCLO-PDN in the treatment of disseminated carcinoma of the breast (author's transl)]. 48 Oct 10

Three patients with breast cancer with poor prognosis were treated with high-dose chemotherapy (HD-CT) and peripheral blood stem cell transplantation (PBSCT) as adjuvant treatment. After radical mastectomy, the consolidation chemotherapy with Adriamycin 50 mg/m2, Cyclophosphamide 1,000 mg/m2, Vincristine 1.0 mg/m2 and Methotrexate 200 mg/m2 with Leucovorin rescue was started. Recombinant human granulocyte colony stimulating factor (rhG-CSF) was also added for early recovery from myelosuppression. This combination chemotherapy was given every 3 weeks for 3 courses, and after the 2nd and 3rd courses, peripheral blood stem cells (PBSC) were collected and cryopreserved. HD-CT with Cyclophosphamide 2,000 mg/m2/day, Thio-TEPA 200 mg/m2/day, and Etoposide 300 mg/m2/day, were administered for 3 consecutive days, and after 48 hours of last doses, frozen-thawed PBSC (6.4-8.9 x 10(4)/kg of CFU-GM) were administered. rhG-CSF was also added. HD-CT and PBSCT were well tolerated, recovery from myelosuppression of the HD-CT was very quick and no serious side effects were observed.
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PMID:[High-dose adjuvant chemotherapy with peripheral blood stem cell transplantation for breast cancer with poor prognosis--a pilot study]. 138 71

Of 47 consecutive patients with advanced breast cancer, we randomly assigned 24 to receive Arm A; ACF alone (Adriamycin, Cyclophosphamide, Ftorafur) and 23 to receive Arm B; 2 cycles of ACF alternating one cycle of MVMF (Mitomycin C, Vincristine, Methotrexate, Ftorafur--a combination of drugs not cross-resistant with ACF). The response rate was 66% in Arm A and 52% in Arm B. The median duration of response was significantly longer in Arm B (11 months in Arm A, 28.8 months in Arm B) due to prolongation of duration to administer adriamycin in Arm B. But the median survival time was 30.7 months in Arm A and 24.5 months in Arm B, and significantly longer in Arm A until 10 months. These results were due to the difference in response rate during induction therapy (58% in Arm A, 26% in Arm B) reflected in the dose intensity of Adriamycin (13 mg/m2/w in Arm A, 6.7 mg/m2/w in Arm B) and the higher CR rate in Arm A, because CR cases had a significantly longer survival than PR and NC cases in both arms. We suppose that achieving CR by an intensive regimen containing adriamycin and adopting a non-cross-resistant regimen can help prolong survival in advanced breast cancer.
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PMID:[A randomized trial comparing ACF (adriamycin, cyclophosphamide, ftorafur) and ACF/MVMF (mitomycin C, vincristine, methotrexate, ftorafur)--a non-cross-resistant alternating chemotherapy of recurrent and advanced breast cancer]. 249 47

The sensitivity of cancer cells to anti-cancer agents (ACA) was assessed in 110 cases of breast cancer (87 primary cases and 23 recurrent cases). The cancer cells were cultured with ACAs: Mitomycin C (MMC), Adriamycin (ADR), 5-Fluorouracil (5-FU), Cytosine Arabinoside (Ara-C), Carboquone (CQ), Nimustine Hydrochloride (ACNU), Cis-platinum Diammine Dichloride (CPDD) or Vincristine (VCR) for 3 days and their sensitivity was estimated by the inhibition rate (I.R.) of DNA synthesis (3H-thymidine uptake) of cancer cells. The DNA synthesis was higher in recurrent cases than in primary cases. The primary cases showed high sensitivity to ADR or CQ, and the recurrent cases showed high sensitivity to ADR. Histologically, papillotubular or medullary tubular carcinoma showed high sensitivity to CQ, and scirrhous carcinoma showed high sensitivity to ADR, CQ or 5-FU. The sensitivities of medullary tubular or scirrhous carcinoma to ADR, 5-FU and CQ in patients with stage III and IV were lower than those in patients with stages I and II. No difference of ACA sensitivity was observed between estrogen receptor (+) and (-) cases. All recurrent cases were treated with 5-FU or its derivatives. The 50% survival period in the 5-FU high sensitivity (I.R. greater than 80%) group was 7.0 months and that of the low sensitivity (I.R. less than 80%) group 3.0 months, respectively.
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PMID:[An in vitro sensitivity assay for anti-cancer agents by measuring the inhibition rate of DNA synthesis (3H-thymidine uptake of cancer cells). II. Clinical study of 110 cases of breast cancer]. 301 95

We have examined the effects of a 24-h exposure to clinically achievable concentrations of adriamycin, melphalan, 5-fluorouracil, and vincristine on the estrogen binding capacity of MCF-7 human breast cancer cells using a whole cell binding assay. Adriamycin (0.018 to 1.8 microM), melphalan (0.1 to 5 microM), 5-fluorouracil (0.077 to 15.4 microM), and vincristine (0.01 to 1 nM) reduce the estrogen binding capacity in a dose dependent manner. The rate of protein synthesis is reduced following exposure to 5-fluorouracil but not following exposure to adriamycin, melphalan, or vincristine. The rate of cell proliferation, influx of the ligand, and the Kd of remaining estrogen receptor are unaltered following drug exposure. These drugs may, therefore, be inducing a nonspecific reduction in the rate of receptor recycling and/or synthesis. Vincristine (1 nM) abolished estrogen receptor expression but following removal of the drug receptor levels did not reach that expressed in untreated cells for at least 48 h. Prior exposure to vincristine (1 nM) reduced the antiproliferative effects of tamoxifen (2 microM) toward MCF-7 cells.
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PMID:Effect of cytotoxic drugs on estrogen receptor expression and response to tamoxifen in MCF-7 cells. 377 32

Two hundred and twenty-three patients with disseminated breast cancer entered in a randomized trial: Group I: 130 patients were given a monthly 5 day- course of a cytotoxic chemotherapy protocol including Adriamycine, Vincristine, Cyclophosphamide, 5 Fluoro-uracile (A.V.L.F.); Group II: 93 patients were given alternatively the same program and a non cross resistant program including: VM 26, Mitomycine C, Methotrexate (V.M.M.). The patients of these groups were randomized into three subgroups: Subgroup O: chemotherapy alone; Subgroup N: chemotherapy + Tamoxifen (20 mg/m2/day); Subgroup NN: chemotherapy + Tamoxifen + Norethisterone (40 mg/m2/day). Objective response rates to cytotoxic chemotherapy were respectively of 65 per cent and 68 per cent in groups I and II of chemotherapy. Further more mean-duration of response and survival were not different. Objective response rates were comparable in the three subgroups of chemo-hormonotherapy. However, the survival was significantly better in the subgroup N (with Tamoxifen) when compared with the subgroup O (without hormonotherapy), and marginally better (p = 0,09) when compared with the NN subgroup (with Tamoxifen + Norethisterone).
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PMID:[Metastatic breast cancer: controlled trial of chemotherapy with and without hormones]. 639 20

Eighteen patients with advanced refractory breast carcinoma were treated with vincristine (VCR), 0.5 mg I.V. bolus followed by continuous I.V. infusions of 0.25 mg/m2/day for 5 days every 3 weeks. The daily dose of VCR was infused in 1000 ml D5W to which was added hydrocortisone 50 mg and heparin 3000 U. Patients received from one to six courses (mean 2.3 courses). No objective responses were observed. Stable disease was noted in five patients who had skeletal metastases only. Disease progression occurred in the remaining 13 patients, 10 of whom had received prior VCR by bolus injection. The principal toxicity consisted of constipation without ileus and hyporeflexia-paresthesias. Vincristine, administered by continuous I.V. infusion according to this dose and schedule does not appear to be effective in the treatment of patients with advanced refractory breast cancer.
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PMID:Vincristine by continuous infusion in refractory breast cancer: a phase II study. 661 19

Vincristine (VCR) and etoposide (VP-16) have been shown to be synergistic in a murine model, and this combination was studied in a phase II trial. Eligibility required measurable disease, a performance status of 0-2, a life expectancy of > or = 2 months, an interval of at least 3 weeks since the receipt of previous radiation therapy or chemotherapy and recovery from related toxicity, no prior treatment with VCR or VP-16, and no more than two prior chemotherapy regimens (only one for treatment of metastatic disease). Treatment consisted of 0.5 mg i.v. (bolus) VCR followed by 200 mg/m2 VP-16 given over 2 h. Both drugs were given daily for 3 consecutive days every 3 weeks (total dose: VCR, 1.5 mg; VP-16, 600 mg/m2). A total of 18 patients with metastatic breast cancer were accured; 14 had adjuvant chemotherapy and 8 had chemotherapy for advanced disease. As judged by International Union Against Cancer (UICC) criteria, one complete response (CR) and three partial responses (PR) were obtained, for a CR + PR rate of 22% (95% confidence interval, 6%-48%). All responders had soft-tissue involvement only. Six patients had stable disease and 8 showed progression. The median time to treatment failure was 3.5 months, and the median survival from study entry was 8.3 months. The major toxicity was myelosuppression, with 9 patients (50%) experiencing a total WBC of < 1,000/mm3. Grade 2-3 neurologic toxicity was noted in 6 patients (33%) and grade 3 nausea and vomiting was noted in 5 (28%). The combination of VCR and VP-16 is active in advanced breast cancer but is not convincingly superior to either of these agents used alone.
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PMID:Vincristine with high-dose etoposide in advanced breast cancer: a phase II trial of the Piedmont Oncology Association. 798 95

2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite which disrupts microtubule function, has been shown to inhibit proliferating cells in vitro and suppress certain murine tumors in vivo. In vitro screening has determined that breast cancer cell lines are most sensitive to inhibition by 2-ME. Additionally, 2-ME has been shown to inhibit angiogenesis in vitro. We tested whether 2-ME suppresses cytokine-induced angiogenesis in vivo and inhibits growth of a human breast carcinoma in severe combined immunodeficient mice. A model of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF)-induced corneal neovascularization in C57BL/6 mice was used to evaluate the antiangiogenic effects of 2-ME and other microtubule inhibitors such as Taxol, vincristine, and colchicine. 2-ME (150 mg/kg p.o., n = 20) inhibited bFGF and VEGF-induced neovascularization by 39% and 54%, respectively. Taxol (6 mg/kg i.p., n = 17) inhibited bFGF and VEGF-induced neovascularization by 45% and 37%, respectively. Vincristine (0.2 mg/kg i.p., n = 8) and colchicine (0.25 mg/kg i.p., n = 8) had no effect. Treatment with 2-ME (75 mg/kg p.o., n = 9) for 1 month suppressed the growth of a human breast carcinoma in mice by 60% without toxicity. Recognition of the antiangiogenic and antitumor properties of 2-ME and Taxol may be crucial in planning clinical applications to angiogenesis-dependent diseases.
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PMID:Inhibition of angiogenesis and breast cancer in mice by the microtubule inhibitors 2-methoxyestradiol and taxol. 898 45

We designed three new four-drug cisplatin-containing combinations and evaluated their activity in a randomized phase II study including patients with locally advanced (stage III) and locally recurrent breast carcinoma. All combinations included methotrexate (M) on day 1 and cisplatin (P) on day 2 (MVAC-like combinations) and differed from one another by the addition of Epirubicin (Epi), Vincristine (V), Etoposide (E), Mitomycin (Mi). Based on the administered agents, they were named MPEMi, MPEpiE, MPEpiV. The combinations were randomly assigned to 101 patients, 57 with locally advanced and 44 with locally recurrent breast carcinoma. Response was evaluated after 4 cycles. The complete response (CR) rates were 7% and 43% and the CR plus partial response (PR) rates were 84% and 89% in locally advanced and in locally recurrent disease, respectively. In locally advanced disease, a pathologic CR (pCR) was assessed in seven of 57 patients (12%). There were no significant differences among the three combinations. The toxicities were at times severe, but generally tolerable, as demonstrated by the high cumulative doses of the drugs received by the patients. In conclusion, these three innovative chemotherapy regimens induced high CR plus PR rates in the neoadjuvant treatment of stage III and of locally recurrent breast carcinoma, and a high rate of pCR in stage III disease. These regimens warrant testing in phase III trials.
Breast Cancer Res Treat 1999 Jul
PMID:Three new active cisplatin-containing combinations in the neoadjuvant treatment of locally advanced and locally recurrent breast carcinoma: a randomized phase II trial. 1057 5


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