Pulmonary Complications of Novel Antineoplastic Agents for Solid Tumors

Vahid, Bobbak; Marik, Paul E.

doi:10.1378/chest.07-0851

Cited by 223 publications

(171 citation statements)

References 108 publications

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“…Interstitial pneumonitis has been recognised as being associated with sustained treatment with rapamycin and other rapamycin derivatives (Pham et al, 2004;El-Maraghi et al, 2006). Pulmonary toxicity is a potential toxicity associated with the use of newer anti-neoplastic agents (Vahid and Marik, 2008). In this study, interstitial pneumonitis was of short duration and recovered under corticosteroid therapy.…”

Section: Discussionmentioning

confidence: 66%

Safety and pharmacokinetics of paclitaxel and the oral mTOR inhibitor everolimus in advanced solid tumours

et al. 2009

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Everolimus displays antiproliferative effects on cancer cells, yields antiangiogenic activity in established tumours, and shows synergistic activity with paclitaxel in preclinical models. This study assessed the safety and the pharmacokinetic interactions of everolimus and paclitaxel in patients with advanced malignancies. Everolimus was dose escalated from 15 to 30 mg and administered with paclitaxel 80 mg m À2 on days 1, 8, and 15 every 28 days. Safety was assessed weekly, and dose-limiting toxicity (DLT) was evaluated in cycle 1. A total of 16 patients (median age 54.5 years, range 33 -69) were entered; 11 had prior taxane therapy for breast (n ¼ 5), ovarian (n ¼ 3), and vaginal cancer (n ¼ 1) or angiosarcoma (n ¼ 2). Grade 3 neutropenia in six patients met the criteria for DLT in two patients receiving everolimus 30 mg weekly. Other drug-related grade 3 toxicities were leucopenia, anaemia, thrombocytopenia, stomatitis, asthenia, and increased liver enzymes. Tumour stabilisation reported in 11 patients exceeded 6 months in 2 patients with breast cancer. Everolimus showed an acceptable safety profile at the dose of 30 mg when combined with weekly paclitaxel 80 mg m À2 , warranting further clinical investigation.

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Section: Discussionmentioning

confidence: 66%

Safety and pharmacokinetics of paclitaxel and the oral mTOR inhibitor everolimus in advanced solid tumours

et al. 2009

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“…Nevertheless, most tumour types are only marginally sensitive to mTORC1 inhibitors either because of redundant signal transduction pathways, lack of functional apoptosis/autophagy, or expression of VEGF/VEGFR-independent angiogenesis. Furthermore, although acute toxicity of rapalogues is fairly acceptable, long-term exposure to several rapalogues is associated with interstitial pneumonitis (Vahid and Marik, 2008) that may require treatment discontinuation and jeopardise efficacy. It is thus important to consider other drugs blocking the mTOR signalling pathways by different mechanisms of action with distinct toxicity and overcoming current mechanisms of resistance to rapalogues.…”

Section: 'Non-rapalogues' Mtor Kinase Inhibitorsmentioning

confidence: 99%

mTORC1 inhibitors: is temsirolimus in renal cancer telling us how they really work?

et al. 2008

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The proof of principle that a drug targeting mTOR can improve survival has been obtained recently from a large randomised trial using temsirolimus as a first-line therapy in patients with advanced poor prognostic renal cell carcinoma. Consistent data have recently shown the important role of the PI3K/AKT/mTOR signalling pathway in the regulation of crucial metabolic and mitotic functions of cancer cells and endothelial cells allowing a better understanding of the role of mTOR in controlling cancer cell proliferation and survival as well as tumour angiogenesis. As a result, rapamycin derivatives (rapalogues) that block mTOR/Raptor complex 1 were shown to exert direct antiproliferative effects against endometrial cancers, in which cancer cells frequently lose PTEN function as well as mantle cell lymphomas, in which cancer cell proliferation appears to be driven primarily by cyclin D1 overexpression. The overall antitumour effects of rapalogues in renal cell carcinoma appear to be more complex with tumour growth inhibition resulting from direct G1/S cell cycle blockage and/or apoptotic effects in carcinoma cells along with the inhibition of downstream signalling of the HIF1a-induced VEGF/VEGFR autocrine loop in endothelial cells shutting down the maintenance of tumour angiogenesis. Despite extensive cognitive researches, it is difficult to appraise which of those mechanisms is predominant in patients. This review focuses on mechanisms of action of rapalogues focusing on antitumour effects in patients with renal cell carcinoma.

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“…The incidence of trastuzumab-induced pneumonitis has been reported in the literature as 0.4-0.6%. [19] Of our patients 97.5% including this restrictive patient had been given taxancontaining regimen although this regimen was not found efficient on PFTs in our study. Paclitaxel cause There are some limitations of this study.…”

Section: Discussionmentioning

confidence: 54%

Evaluation of Pulmonary Function After Radiotherapy Using Helical Tomotherapy for Breast Cancer Treatment: Prospective Study

Teke¹

2016

TJ Oncol

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Pulmonary Complications of Novel Antineoplastic Agents for Solid Tumors

Cited by 223 publications

References 108 publications

Safety and pharmacokinetics of paclitaxel and the oral mTOR inhibitor everolimus in advanced solid tumours

Safety and pharmacokinetics of paclitaxel and the oral mTOR inhibitor everolimus in advanced solid tumours

mTORC1 inhibitors: is temsirolimus in renal cancer telling us how they really work?

Evaluation of Pulmonary Function After Radiotherapy Using Helical Tomotherapy for Breast Cancer Treatment: Prospective Study

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