Growth inhibitory effects of paclitaxel on human epithelioid sarcoma in vitro

Reinecke, Petra; Knopf, Christiane; Schmitz, Michael; Schneider, Eva; Gabbert, Helmut E.; Gerharz, Claus Dieter

doi:10.1002/(sici)1097-0142(20000401)88:7<1614::aid-cncr16>3.0.co;2-x

Cited by 10 publications

(6 citation statements)

References 34 publications

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“…Using verapamil and cyclosporine A to reverse multidrug resistance, the authors showed increased sensitivity to doxorubicin and vincristine ( 83 ). For the GRU cell line, expression of P-glycoprotein and MRP could also be observed ( 84 ). However, one study identified an absence of expression of P-glycoprotein and MRP in the ES-OMC-MN and SFT-8606 cell lines ( 85 ).…”

Section: Tyrosine Kinase Inhibitorsmentioning

confidence: 99%

Epithelioid Sarcoma: Opportunities for Biology-Driven Targeted Therapy

et al. 2015

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Epithelioid sarcoma (ES) is a soft tissue sarcoma of children and young adults for which the preferred treatment for localized disease is wide surgical resection. Medical management is to a great extent undefined, and therefore for patients with regional and distal metastases, the development of targeted therapies is greatly desired. In this review, we will summarize clinically relevant biomarkers (e.g., SMARCB1, CA125, dysadherin, and others) with respect to targeted therapeutic opportunities. We will also examine the role of EGFR, mTOR, and polykinase inhibitors (e.g., sunitinib) in the management of local and disseminated disease. Toward building a consortium of pharmaceutical, academic, and non-profit collaborators, we will discuss the state of resources for investigating ES with respect to cell line resources, tissue banks, and registries so that a roadmap can be developed toward effective biology-driven therapies.

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Section: Tyrosine Kinase Inhibitorsmentioning

confidence: 99%

Epithelioid Sarcoma: Opportunities for Biology-Driven Targeted Therapy

et al. 2015

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“…Although the aggressiveness with which tumor may grow and spread varies from patient to patient, RCCs remain one of the most clinically drug-resistant human cancers, consistent with intrinsic and acquired MDR. The mechanisms of MDR have been investigated biochemically in RCCs and they include P-gp [64][65][66][67][68][69][70][71], glutathione metabolism [68], topoisomerase enzymes [69], and MRP [70]. MDR1 mRNA has been found in 80% of renal tumors that were not pretreated [64][65][66].…”

Section: Expression Of Drug Resistance Markers In Childhood Renal Tumorsmentioning

confidence: 99%

“…Calcium antagonists, tamoxifen and oligomycin have been individually effective chemotherapy adjuvants for overcoming the innate or acquired MDR in RCC in vitro [75]. Reinecke et al [70] studied the expression of P-gp and MRP in RCC cell lines of different histological types and correlated with taxol sensitivity. The expression of MRP was low in RCC cell lines and was not related to taxol sensitivity.…”

Section: Expression Of Drug Resistance Markers In Childhood Renal Tumorsmentioning

confidence: 99%

Drug Resistance in Renal Tumors of Childhood

Ramachandran

2007

CPB

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Renal cancers are as one of the most common drug resistant neoplasms affecting children and multidrug resistance (MDR) happened to be an important reason for the failure of chemotherapy in refractory cancers of childhood. MDR can be intrinsic or acquired, depending on the time of its occurrence, either at diagnosis or during chemotherapy. Renal cancers often have intrinsic form of MDR because of de novo expression of P-glycoprotein (P-gp) in renal cells. Molecular investigations on MDR during the past two decades have led to the isolation and characterization of genes coding for P-gp, multidrug resistance-associated protein (MRP), lung resistance-related protein (LRP), breast cancer resistance protein (BCRP/MXR), drug resistance-associated protein (DRP), and ATP-binding cassette protein (ABCP). Several molecular probes, primer pairs, and monoclonal antibodies have been developed over the years to quantify the regulation and expression of these drug resistance markers in tumor cells. Methodologies have also been standardized to estimate the gene amplification, mRNA and protein expression, and functionality of drug resistance proteins in clinical specimens from cancer patients. Because of the recent developments in microarray technology, DNA and protein arrays against drug resistant genes are available commercially now. This review includes techniques for detection and quantification of the expression and function of these drug resistance genes in childhood renal tumors. Since these markers have clinical significance, currently available technology warrants the application of these markers in clinical oncology. Moreover, the first, second and third generation drug resistance modifiers have been developed over the past several years for overcoming drug resistance problem in tumor cells. Unfortunately, these reversing agents are yet to be proved successful clinically. Since treatment protocols are usually adopted from adult tumor patients into childhood population, clinical trials with modifying agents are yet to be undertaken and/or concluded in pediatric renal cancer patients. More clinical studies may be required to analyze the genes involved in the MDR of childhood renal cancer patients and trials have to be undertaken to evaluate the efficacy of MDR modifying agents in them, at least in parallel with adult patients.

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“…The other ''C resonances for the E and Z isomers are overlapping. Comparison of the 'rC chemical shifts of the E and Z olefinic methines of dimethyl fumarate(6 133.5 ppm) and dimethyl maleate (6 129.9 ppm) to 63, enabled us to tentatively distinguish between the E and Z isomers of dimer 63 and conclude that the E:Zratio is approximately 2:1.…”

mentioning

confidence: 99%

“…'H l.[l4R: 67.74 (dd, "/ =7.2,1.2112,2H),7.68 (dd, J ='l.5,l.2lfz,2H), 7.42 (m, 6H), 4.20 (m, lH), 3.52 (dd, J = 9.0,2.L Hz, lH), 2.61 (dd, "/ = 16.2, 6. 6 (3RS'7R)-7-tert-Butyldiphenylsiloxy-3-hydroxy-2,8-dimethylnonan-5-one (96b), The aldol reaction of 95a (l 19 mg, 0.32 mmol) and isobutylaldehyde gave 96b (125 mg,86Vo yield), ds = 2.5:1. Spectral data reported for one diastereomer (separated by flash chromatography).…”

mentioning

confidence: 99%

Studies Towards the Synthesis of Peloruside A

Stocker¹

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<p>In the search for new treatments for cancer, advances in biology have provided targets for the destruction of cancer cells. One such structure the microtubule, a protein required for cell division, has been the target of many successful anticancer agents including the multi-million dollar earning Taxol [trademark] (paclitaxel) and the epothilones, currently in late-stage clinical trials. More recently it has been shown that peloruside A 1, a secondary metabolite isolated from the New Zealand marine sponge Mycale hentscheli, prevents cell division by stabilising microtubules, and thus offers promise as a novel anticancer agent. However, due to its limited natural abundance, significant quantities of peloruside A can only be obtained through chemical synthesis. A retrosynthetic analysis of peloruside A divided the molecule into four key fragments: a) the commercially available C-l to C-2 benzyloxy acetic acid fragment; b) the C-3 to C-7 fragment; c) the C-8 to C-11 fragment and d) the remaining C-12 to C-24 portion of the macrocycle and side chain. The C-3 to C-7 and C-8 to C-11 fragments combine to form a key intermediate pyranose ring. This thesis however, addresses the synthesis of two of these key fragments, namely the C-8 to C-11 and C-12 to C-24 fragments. An efficient synthesis of the C-8 to C-11 fragment of peloruside A, starting from commercially available pantolactone, has been developed. This synthesis proceeds in good overall yield, and has been successfully reproduced on the multigram scale. The significant portion of this thesis, however, is dedicated to the synthesis of the C-12 to C-24 fragment. After our initial strategy proved unviable, a short, facile method for the synthesis of the C-12 to C-24 fragment, involving the formation of a bis-silyl ether, was developed. The protocol for its desired coupling, via a boron_mediated, remote 1,5-anti-induction aldol reaction has also been established. These and subsequent studies provided valuable insight into the origin of 1,5-anti induction in boron-mediated aldol reactions.</p>

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Growth inhibitory effects of paclitaxel on human epithelioid sarcoma in vitro

Cited by 10 publications

References 34 publications

Epithelioid Sarcoma: Opportunities for Biology-Driven Targeted Therapy

Epithelioid Sarcoma: Opportunities for Biology-Driven Targeted Therapy

Drug Resistance in Renal Tumors of Childhood

Studies Towards the Synthesis of Peloruside A

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