Concurrent Paclitaxel and Radiation in the Treatment of Locally Advanced Head and Neck Cancer

Sunwoo, John B.; Herscher, Laurie L.; Kroog, Glenn; Thomas, Giovana R.; Ondrey, Frank G.; Duffey, Dianne C.; Solomon, Beth; Boss, Carol; Albert, Paul S.; McCullugh, Linda; Rudy, Susan F.; Muir, Chris; Zhai, Suoping; Figg, William D.; Cook, John A.; Mitchell, James B.; Waes, Carter Van

doi:10.1200/jco.2001.19.3.800

Cited by 57 publications

(33 citation statements)

References 38 publications

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“…Complete tumor clearance was documented in 74% of the patients with an overall response rate of 71% and a 2 year survival of 32%. Sunwoo et al [25], administered Paclitaxel as a 120-hour continuous infusion every 3 weeks to 33 previously untreated patients with stage III or IV tumors. Sixteen patients received a Paclitaxel dose of 105 mg/m 2 , and 17 patients received 120 mg/m 2 .…”

Section: Discussionmentioning

confidence: 99%

Chemoradiation in Advanced Head and Neck Cancers: A Comparison of two Radiosensitizers, Paclitaxel and Cisplatin

Kanotra

Gupta

et al. 2011

Indian J Otolaryngol Head Neck Surg

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Section: Discussionmentioning

confidence: 99%

Chemoradiation in Advanced Head and Neck Cancers: A Comparison of two Radiosensitizers, Paclitaxel and Cisplatin

Kanotra

Gupta

et al. 2011

Indian J Otolaryngol Head Neck Surg

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“…In vivo, bortezomib inhibited growth of murine and human SCC in mice, which was associated with a marked decrease in vessel density. In addition, bortezomib inhibited expression of proinflammatory and proangiogenic factors GRO-1 and VEGF by SCC in the range at which bortezomib inhibits NF-κB [71].…”

Section: Nf-κb Regulated Proteomes and Transcriptomes As Biomarkers Amentioning

confidence: 93%

“…The inhibitory activity of bortezomib has been demonstrated against a spectrum of cancer cells in culture [57][58][59][60][61][62][63][64][65][66][67] and in animal models [50,[68][69][70] including suppression of NF-κB and other signal transcription pathways with induction of cell apoptosis and cell cycle arrest. The molecular and clinical effects of bortezomib and potential mechanisms of sensitivity and resistance have been most extensively studied in multiple myeloma (MM) and certain other hematopoietic malignancies [58,[60][61][62][63], and to a lesser extent in solid cancers [31,50,57,[64][65][66][67][68]70,71].…”

Section: Nf-κb Regulated Proteomes and Transcriptomes As Biomarkers Amentioning

confidence: 99%

“…We examined the effects of bortezomib on activation of NF-κB, cell survival, growth, and angiogenesis in murine and human SCC cell lines, as well as in tumor models in vivo [49,50,71]. Bortezomib inhibited activation of NF-κB DNA binding and functional reporter activity in the nanomolar concentration range.…”

Section: Nf-κb Regulated Proteomes and Transcriptomes As Biomarkers Amentioning

confidence: 99%

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Role of the NF-κB Transcriptome and Proteome as Biomarkers in Human Head and Neck Squamous Cell Carcinomas

2008

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NF-κB is a family of signal-activated transcription factors comprising hetero- or homodimers from five different subunits, NF-κB1, NF-κB2, RELA, cREL and RELB. NF-κBs are normally transiently activated in response to infection or injury, but in cancers are aberrantly activated, regulating a transcriptome of hundreds of genes and corresponding proteome that promote pathogenesis and therapeutic resistance. In head and neck squamous cell carcinomas, an important role of NF-κB in the regulation of the altered transcriptome and proteome has been established, providing a catalog of activating and target genes and proteins that may be useful as biomarkers of alterations in this pathway for this and other cancers. An emerging appreciation that NF-κB and other signal pathways form an altered regulatory network highlights the need to use biomarkers and combine targeted agents for personalized therapy of cancer.

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“…Paclitaxel (Taxol), a novel naturally occurring antineoplastic agent, has shown great promise in the treatment of a variety of tumor types including breast, head and neck, ovarian, and lung cancers (1)(2)(3). Although the exact mechanism of the cytotoxicity of paclitaxel against tumor cells is not entirely clear, previous studies demonstrated that paclitaxel is a unique antimicrotubule agent that acts by inhibiting microtubule depolymerization and thereby disrupting the normal dynamic reorganization of the microtubule network required for mitosis and cell proliferation (4,5).…”

Section: Introductionmentioning

confidence: 99%

Cell Cycle–Dependent Antagonistic Interactions between Paclitaxel and γ-Radiation in Combination Therapy

Sui

Dziadyk

Zhu

et al. 2004

Clinical Cancer Research

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Purpose: The promising clinical activity of paclitaxel, a naturally occurring antimicrotubule agent, has promoted considerable interest in combining this drug with radiation therapy, but it remains unclear whether such a combination would increase the therapeutic efficacy. This study is to assess the potential interactions between paclitaxel and ␥-radiation against human tumor cells in vitro.Experimental Design: Paclitaxel and ␥-radiation were administered in three different sequences designated as preradiated, co-radiated, and post-radiated to BCap37 (human breast cancer cell line) and KB (human epidermoid carcinoma cell line) cells. The cytotoxic interactions between and mutual influences of these two agents on their antitumor activities were analyzed by a series of assays including cytotoxic, morphological, and biochemical examinations.Results: The combination of paclitaxel and ␥-radiation did not produce a synergistic or additive effect. Instead, the overall in vitro cytotoxicity of these combinations was much lower than that of paclitaxel treatment alone. DNA fragmentation and flow cytometric assays showed that the addition of ␥-radiation interfered with paclitaxel-induced apoptosis. Further analyses indicated that the addition of ␥-radiation resulted in a transient or prolonged cell cycle arrest at G 2 phase, which likely prevented the cytotoxic effects of paclitaxel on both mitotic arrest and apoptosis. In addition, biochemical examinations revealed that ␥-radiation inhibited paclitaxel-induced IB␣ degradation and bcl-2 phosphorylation and increased the protein levels of cyclin B1 and inhibitory phosphorylation of p34 cdc2 . Conclusions: Our results suggest that ␥-radiation might specifically block the cell cycle at G 2 phase, which in turn prevents the cytotoxic effects of paclitaxel on both mitotic arrest and apoptosis. Therefore, it eventually results in a cell cycle-dependent antagonistic effect on the antitumor activity of paclitaxel. This finding may be relevant to the clinical application of combination therapy with paclitaxel and radiation.

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Concurrent Paclitaxel and Radiation in the Treatment of Locally Advanced Head and Neck Cancer

Abstract: Paclitaxel administered as a 120-hour continuous infusion in combination with radiotherapy is a feasible and promising treatment for patients with advanced HNSCC.

Cited by 57 publications

References 38 publications

Chemoradiation in Advanced Head and Neck Cancers: A Comparison of two Radiosensitizers, Paclitaxel and Cisplatin

Chemoradiation in Advanced Head and Neck Cancers: A Comparison of two Radiosensitizers, Paclitaxel and Cisplatin

Role of the NF-κB Transcriptome and Proteome as Biomarkers in Human Head and Neck Squamous Cell Carcinomas

Cell Cycle–Dependent Antagonistic Interactions between Paclitaxel and γ-Radiation in Combination Therapy

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