The taxanes: an update

Crown, John; O’Leary, Michael P.

doi:10.1016/s0140-6736(00)02074-2

Cited by 330 publications

(196 citation statements)

References 21 publications

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“…Microtubule-damaging agents (MDA), 1 including microtubule-stabilizing agents such as taxol and epothilone B and -destabilizing agents such as vinblastine and vincristine, are effective chemotherapeutic drugs against a variety of cancers (1)(2)(3). These drugs prevent cell cycle progression beyond the G 2 /M phase and subsequently kill cancer cells by activating apoptotic signaling pathway (4 -6).…”

mentioning

confidence: 99%

Regulation of Bax Activation and Apoptotic Response to Microtubule-damaging Agents by p53 Transcription-dependent and -independent Pathways

Yamaguchi

Chen

Bhalla

et al. 2004

Journal of Biological Chemistry

120

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Microtubule-damaging agents (MDA) are potent antineoplastic drugs that are widely used in clinical treatment for a variety of cancers. However, the precise mechanisms underlying MDA-induced cell death are largely unknown. Here, we report that both p53 and Bax are central participants in the MDA-mediated cell death machinery in HCT116 human colon cancer cells. MDA, including epothilone B analogue (BMS-247550) and vinblastine, induced apoptosis of Bax-positive HCT116 cells in a p53-dependent manner; p53 was required for MDAinduced Bax conformational change. In response to MDA treatment, the BH3-only proapoptotic protein PUMA was up-regulated in p53-positive but not in p53 knockout HCT116 cells. Moreover, PUMA knockout HCT116 cells were resistant to MDA-induced Bax conformational change and apoptosis. In addition, introducing p53 plasmid DNA into p53-deficient HCT116 cells restored PUMA expression and apoptotic response to MDA treatment. However, ectopic expression of the p53 point mutation L22Q/W23S, but not the proline-rich domain deletion mutants 83-393 and ⌬ProAE, could also sensitize p53 knockout HCT116 cells to MDA-induced Bax activation and apoptosis, although all mutants failed to restore PUMA expression. Together, these findings suggest that p53 acts upstream of Bax to promote MDA-mediated cell death in a proline-rich domain-dependent manner through both transcription-dependent (by up-regulating PUMA expression) and -independent mechanisms in human colon cancer HCT116 cells.

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mentioning

confidence: 99%

Regulation of Bax Activation and Apoptotic Response to Microtubule-damaging Agents by p53 Transcription-dependent and -independent Pathways

Yamaguchi

Chen

Bhalla

et al. 2004

Journal of Biological Chemistry

120

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“…Activation of PXR by paclitaxel has been suggested to account for the autoinduction of drug metabolism. Consistent with this notion, docetaxel shows better pharmacokinetic properties than paclitaxel [61,62].…”

Section: Othersmentioning

confidence: 86%

Pregnane X receptor and natural products: beyond drug–drug interactions

Staudinger

Ding

Lichti

2006

Expert Opinion on Drug Metabolism & Toxicology

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The pregnane X receptor (PXR, NR1I2) is a member of the nuclear receptor superfamily that is activated by a myriad of compounds and natural products in clinical use. Activation of PXR represents the basis for several clinically important drug-drug interactions. Although PXR activation has undesirable effects in patients on combination therapy, it also mediates the hepatoprotective effects exhibited by some herbal remedies. This review focuses on PXR activation by natural products and the potential therapeutic opportunities presented. In particular, the biological effects of St. John's Wort, gugulipid, kava kava, Coleus forskolii, Hypoxis, Sutherlandia, qing hao, wu wei zi, gan cao and other natural products are discussed. The impact of these natural products on drug metabolism and hepatoprotection is highlighted in the context of activation and antagonism of PXR.

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“…During the study period, treatment of metastatic breast carcinoma shifted toward agents such as the taxanes and vinorelbine, replacing less expensive agents like doxorubicin, cyclophosphamide, and methotrexate. 17,18 Much of this change likely resulted from increasing use of the newer drugs in adjuvant programs. 19 In colorectal carcinoma, irinotecan ($2080 per claim in our study) was approved for second-line therapy in 1996, 20 after firstline therapy with fluorouracil ($22 per claim in 1998) and leucovorin ($315 per claim).…”

Section: Commentmentioning

confidence: 99%

Outpatient cancer drug costs

Halbert

Zaher

Wade

et al. 2002

Cancer

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BACKGROUNDTo the authors' knowledge, no analysis has examined the specific components of drug spending for overall cancer care. The authors' objective was to quantify and characterize trends in outpatient drug expenditures for cancer patients.METHODSThe authors retrospectively analyzed pharmacy and outpatient professional claims data from commercial and Medicare health maintenance organization enrollees with a solid tumor diagnosis in 1995 and 1998. Charges were subdivided by type of drug (antineoplastic drugs, chemotherapy adjuncts, supportive drugs, and drugs unrelated to cancer treatment).RESULTSIn 1995, 14,663 cancer patients received outpatient drug treatment and 13,829 patients in 1998. Total charges increased from $17.9 million (mean charge of $1218 per patient) to $27.9 million (mean charge of $2003 per patient), an average annual increase of 16%. Antineoplastic therapy constituted the largest component of cancer‐related drug costs (67%) and represented 76% of the increase from 1995 to 1998. Most charges were incurred in the professional setting for agents administered by injection. The primary explanation for the increases appeared to be a shift in treatment patterns toward newer, more expensive antineoplastic agents. Supportive therapy represented 17% of the increase in cancer drug costs, followed by chemotherapy adjuncts (7%). Charges for drugs unrelated to cancer therapy increased by 21% per year.CONCLUSIONSAntineoplastic therapy administered in an office or clinic was the single most important cost driver, with newer more expensive agents replacing older, less expensive drugs. Attempts to understand and control outpatient drug cost increases for cancer patients should focus primarily on antineoplastic therapy, especially the appropriate substitution of newer agents for older, less expensive alternatives. Some nonchemotherapy cancer drugs may offer an opportunity to improve quality of life with a relatively small effect on overall cancer drug costs. Cancer 2002;94:1142–50. © 2002 American Cancer Society.DOI 10.1002/cncr.10347

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The taxanes: an update

Cited by 330 publications

References 21 publications

Regulation of Bax Activation and Apoptotic Response to Microtubule-damaging Agents by p53 Transcription-dependent and -independent Pathways

Regulation of Bax Activation and Apoptotic Response to Microtubule-damaging Agents by p53 Transcription-dependent and -independent Pathways

Pregnane X receptor and natural products: beyond drug–drug interactions

Outpatient cancer drug costs

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