Biweekly vinorelbine and tegafur/uracil in patients with metastatic breast cancer previously treated with anthracyclines and taxanes: GEICAM 2000–02 phase II study

Antón, Antonio; Barnadas, Agustí; Florián, Jesús; Ribelles, Nuria; Lomas, M.; Lao, Juan; González-Quintas, A.; Margelı́, Mireia; Paules, A. B.; Gayo, Javier; Ramos, Manuel

doi:10.1007/s12094-011-0654-5

Cited by 3 publications

(3 citation statements)

References 24 publications

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“…Conventional tubulin/microtubule inhibitor chemotherapeutics include colchicine (Levy, Spino, & Read, 1991), the vinca alkaloids (Antón et al, 2011; Dorsey et al, 2010; Honig et al, 2005; Hudis et al, 2004; Wong et al, 2010), taxanes (e.g. paclitaxel) (Chan, Miles, & Pivot, 2010; Dorsey et al, 2010; Rak Tkaczuk, 2011), podophyllotoxins (e.g.…”

Section: Introductionmentioning

confidence: 99%

“…The taxane class of anti-tubulin chemotherapeutics (e.g. paclitaxel, docetaxael) suffers from very similar disadvantages including acquired/intrinsic resistance (Antón et al, 2011; Dorsey et al, 2010; Dumontet, 1999; Kars et al, 2011) secondary to multidrug resistance protein (e.g. P-glycoprotein) over-expression (Harrison & Swanton, 2008; Overmoyer, 2008; Shen et al, 2011), hypersensitivity reactions (Feldweg, Lee, Matulonis, & Castells, 2005; Karacan, Eyüboglu, Akçay, & Ozyilkan, 2004; Lee, Gianos & Klaustermeyer, 2009; Rizzo, Spaggiari et al, 2010), hematopoietic toxicity (dose limiting feature) (Escuin et al, 2011; Manzoni, 2010; Pullarkat et al, 2009), and cumulative neurotoxicity (Cavaletti et al, 2000; Hershman et al, 2011; Windebank, 1999) that can all lead to termination of treatment protocols (Tang, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Influence of Alternative Tubulin Inhibitors on the Potency of Epirubicin-Immunochemotherapeutic Synthesized with an Ultra Violet Light-Activated Intermediate

Coyne¹,

Jones²,

Bear³

2012

CCO

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-10 M and 10 -6 M was determined by measuring the vitality/proliferation of chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3 cell type). Cytotoxic anti-neoplastic potency of benzimidazoles (albendazole, flubendazole, membendazole) and griseofulvin were assessed between 0-to-2 g/ml and 0-to-100 g/ml respectively while mebendazole and griseofulvin were analyzed at fixed concentrations of 0.35 g/ml and 35 g/ml respectively in dual combination with gradient concentrations of epirubicin-(C 3 -amide)-[anti-HER2/neu] and epirubicin-(C 3 -amide)-SS-[anti-HER2/neu].Cytotoxic anti-neoplastic potency for epirubicin-(C 3 -amide)-[anti-HER2/neu] and epirubicin-(C 3 -amide)-SS-[anti-HER2/neu] against chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3) was nearly identical at epirubicin-equivalent concentrations of 10 -10 M and 10 -6 M. The benzimadazoles also possessed cytotoxic anti-neoplastic activity with flubendazole and albendazole being the most and least potent respectively. Similarly, griseofulvin had cytotoxic anti-neoplastic activity and was more potent than methylselenocysteine. Both mebendazole and griseofulvin when applied in dual combination with either epirubicin-(C 3 -amide)-[anti-HER2/neu] or epirubicin-(C 3 -amide)-SS-[anti-HER2/neu] produced enhanced levels of cytotoxic anti-neoplatic potency.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of Alternative Tubulin Inhibitors on the Potency of Epirubicin-Immunochemotherapeutic Synthesized with an Ultra Violet Light-Activated Intermediate

Coyne¹,

Jones²,

Bear³

2012

CCO

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“…The taxane class of anti-tubulin chemotherapeutics (e.g. paclitaxel, docetaxael) suffers from very similar disadvantages that includes acquired and intrinsic tumor resistance [ 120 , 123 , 140 , 141 ] secondary to the over-expression of multidrug resistance proteins (e.g. P-glycoprotein) [ 110 , 144 , 145 ], hypersensitivity reactions [ 146 - 149 ], hematopoietic toxicity (dose limiting feature) [ 150 - 152 ], and cumulative neurotoxicity [ 133 , 134 , 153 ] which can all curtail administration of treatment protocols [ 154 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-Neoplastic Cytotoxicity of Gemcitabine-(C4-amide)-[anti-HER2/neu] in Combination with Griseofulvin against Chemotherapeutic-Resistant Mammary Adenocarcinoma (SKBr-3)

2013

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Introduction Gemcitabine is a pyrimidine nucleoside analog that becomes triphosphorylated and in this form it competitively inhibits cytidine incorporation into DNA strands. Diphosphorylated gemcitabine irreversibly inhibits ribonucleotide reductase thereby preventing deoxyribonucleotide synthesis. Functioning as a potent chemotherapeutic, gemcitabine decreases neoplastic cell proliferation and induces apoptosis which accounts for its effectiveness in the clinical treatment of several leukemia and carcinoma cell types. A brief plasma half-life due to rapid deamination, chemotherapeuticresistance and sequelae restricts gemcitabine utility in clinical oncology. Selective “targeted” gemcitabine delivery represents a molecular strategy for prolonging its plasma half-life and minimizing innocent tissue/organ exposure. Methods A previously described organic chemistry scheme was applied to synthesize a UV-photoactivated gemcitabine intermediate for production of gemcitabine-(C4-amide)-[anti-HER2/neu]. Immunodetection analysis (Western-blot) was applied to detect the presence of any degradative fragmentation or polymerization. Detection of retained binding-avidity for gemcitabine-(C4-amide)-[anti-HER2/neu] was determined by cell-ELISA using populations of chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3) that highly over-express the HER2/neu trophic membrane receptor. Anti-neoplastic cytotoxicity of gemcitabine-(C4-amide)-[anti-HER2/neu] and the tubulin/microtubule inhibitor, griseofulvin was established against chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3). Related investigations evaluated the potential for gemcitabine-(C4-amide)-[anti-HER2/neu] in dual combination with griseofulvin to evoke increased levels of anti-neoplastic cytotoxicity compared to gemcitabine-(C4-amide)-[anti-HER2/neu]. Results Covalent gemcitabine-(C4-amide)-[anti-HER2/neu] immunochemotherapeutic and griseofulvin exerted anti-neoplastic cytotoxicity against chemotherapeutic-resistant mammary adenocarcinoma (SKBr-3). Covalent gemcitabine-(C4-amide)-[anti-HER2/neu] immunochemotherapeutic or gemcitabine in dual combination with griseofulvin created increased levels of anti-neoplastic cytotoxicity that were greater than was attainable with gemcitabine-(C4-amide)-[anti-HER2/neu] or gemcitabine alone. Conclusion Gemcitabine-(C4-amide)-[anti-HER2/neu] in dual combination with griseofulvin can produce enhanced levels of anti-neoplastic cytotoxicity and potentially provide a basis for treatment regimens with a wider margin-of-safety. Such benefits would be possible through the collective properties of; [i] selective “targeted” gemcitabine delivery; [ii] relatively lower toxicity of griseofulvin compared to many if not most conventional chemotherapeutics; [iii] reduced total dosage requirements faciliated by additive or synergistic anti-cancer properties; and [iv] differences in sequelae for gemcitabine-(C4-amide)-[anti-HER2/neu] compared to griseofulvin functioning as a tubulin/microtubule inhibitor.

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Towards personalized medicine of colorectal cancer

Aziz

Yousef

Saleh

et al. 2017

Critical Reviews in Oncology/Hematology

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Biweekly vinorelbine and tegafur/uracil in patients with metastatic breast cancer previously treated with anthracyclines and taxanes: GEICAM 2000–02 phase II study

Abstract: The combination of biweekly vinorelbine and UFT in patients with metastatic breast cancer pretreated with anthracyclines and taxanes is a well tolerated and effective regimen. AEMPS Trial Registration No.: 00-0534.

Cited by 3 publications

References 24 publications

Influence of Alternative Tubulin Inhibitors on the Potency of Epirubicin-Immunochemotherapeutic Synthesized with an Ultra Violet Light-Activated Intermediate

Influence of Alternative Tubulin Inhibitors on the Potency of Epirubicin-Immunochemotherapeutic Synthesized with an Ultra Violet Light-Activated Intermediate

Anti-Neoplastic Cytotoxicity of Gemcitabine-(C4-amide)-[anti-HER2/neu] in Combination with Griseofulvin against Chemotherapeutic-Resistant Mammary Adenocarcinoma (SKBr-3)

Towards personalized medicine of colorectal cancer

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