First-line combination chemotherapy with mitoxantrone and cyclophosphamide in advanced breast cancer

Periti, P; Cuna, G.Robustelli Delia; Pannuti, F; Mazzei, Teresita; Preti, P.; Martoni, Andrea; Mini, Enrico

doi:10.1007/bf00174165

Cited by 7 publications

(1 citation statement)

References 9 publications

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“…15 (54) 3 (23) ...2 (24) 6 (33) 2 (15) Disappointing response rates have been found in teatment of colorectal carcinoma, renal cell carcinoma, melanoma, sarcomas, small-cell lung cancer, gastric, testicular, cervix, and ovarian cancer. 1.47-54 Negative results may have occurred in these studies because the patients were heavily pretreated.…”

Section: Lymphomasmentioning

confidence: 99%

Mitoxantrone

Poirier¹

1986

Drug Intelligence & Clinical Pharmacy

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Mitoxantrone is an anthraquinone antineoplastic agent with structural similarities to doxorubicin. It has a mechanism of action similar to the anthracyclines. Its primary elimination route is hepatic metabolism (only seven percent renal excretion) and it has a terminal half-life of -40 hours. Mitoxantrone has significant activity in the treatment of metastatic breast cancer, acute leukemias, and non-Hodgkin's lymphoma. Some activity is reported in head and neck cancer, Hodgkin's, myeloma, bladder cancer, prostate cancer, non-smallcell lung cancer, and liver cancer. There is a suggestion of incomplete cross-resistance between mitoxantrone and the anthracyclines in certain neoplasms. Some activity is reported with mitoxantrone in patients refractory to the anthracyclines in breast cancer, acute leukemias, and non-Hodgkin's lymphomas. The usual doses used in solid tumors and in lymphomas are mitoxantrone 12-14 mg/m' iv q3-4wk and in leukemias is mitoxantrone 12 mg/m'/d x 5 d iv for initial induction. Drug Inte/l Clin Pharm 1986;20:97-105.

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Section: Lymphomasmentioning

confidence: 99%

Mitoxantrone

Poirier¹

1986

Drug Intelligence & Clinical Pharmacy

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Candidate Agents for Papillary Thyroid Cancer Identified by Gene Expression Analysis

Zhu

2013

Pathol. Oncol. Res.

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A better understanding of the molecular mechanisms involved in papillary thyroid cancer (PTC) is needed to manage these patients effectively. Our objectives were to expand our understanding of this disease, and to identify biologically active small molecules capable to reverse PTC. We downloaded gene expression data of PTC from Gene Expression Omnibus database and employed computational bioinformatics analysis to compare gene expression patterns with normal tissues. Small molecules that induced inverse gene changes to the PTC were identified. A total of 2,154 differentially expressed genes (DEGs) with a false discovery rate of 0.01 were identified. These 2,154 DEGs were significantly enriched in 17 pathways, including pathways associated with signal transduction, tumorigenesis and lipid or amino acid metabolism. In addition, we identified large amount of small molecules that capable to reverse PTC. We found a group of small molecules that can provide new ideas for the therapeutic studies in PTC. These drugs are clearly a direction that warrants additional consideration.

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