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  • American Association for Cancer Research (AACR)  (26)
  • 1
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 23 ( 2019-12-01), p. 5930-5943
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 23 ( 2019-12-01), p. 5930-5943
    Abstract: The genetic events occurring in recurrent nasopharyngeal carcinoma (rNPC) are poorly understood. Here, we performed whole-genome and whole-exome sequencing in 55 patients with rNPC and 44 primarily diagnosed NPC (pNPC), with 7 patients having paired rNPC and pNPC samples. Previously published pNPC exome data were integrated for analysis. rNPC and pNPC tissues had similar mutational burdens, however, the number of clonal mutations was increased in rNPC samples. TP53 and three NF-κB pathway components (TRAF3, CYLD, and NFKBIA) were significantly mutated in both pNPC and rNPC. Notably, mutations in TRAF3, CYLD, and NFKBIA were all clonal in rNPC, however, 55.6% to 57.9% of them were clonal in pNPC. In general, the number of clonal mutations in NF-κB pathway–associated genes was significantly higher in rNPC than in pNPC. The NF-κB mutational clonality was selected and/or enriched during NPC recurrence. The amount of NF-κB translocated to the nucleus in samples with clonal NF-κB mutants was significantly higher than that in samples with subclonal NF-κB mutants. Moreover, the nuclear abundance of NF-κB protein was significantly greater in pNPC samples with locoregional relapse than in those without relapse. Furthermore, high nuclear NF-κB levels were an independent negative prognostic marker for locoregional relapse-free survival in pNPC. Finally, inhibition of NF-κB enhanced both radiosensitivity and chemosensitivity in vitro and in vivo. In conclusion, NF-κB pathway activation by clonal mutations plays an important role in promoting the recurrence of NPC. Moreover, nuclear accumulation of NF-κB is a prominent biomarker for predicting locoregional relapse-free survival. Significance: This study uncovers genetic events that promote the progression and recurrence of nasopharyngeal carcinoma and has potential prognostic and therapeutic implications. See related commentary by Sehgal and Barbie, p. 5915
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 2
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 15, No. 5 ( 2016-05-01), p. 899-910
    Abstract: Leukemia cells escape BCR-ABL–targeted therapy by developing mutations, such as T315I, in the p210BCR-ABL fusion protein in Philadelphia chromosome–positive chronic myeloid leukemia (CML). Although most effort has been focused on development of new tyrosine kinase inhibitors, enrichment of these small-molecule inhibitors in the tumor tissue can also have a profound impact on treatment outcomes. Here, we report that a 2-hour exposure of the T315I-mutant CML cells to 10 μmol/L of the multikinase inhibitor TG101209 suppressed BCR-ABL–independent signaling and caused cell-cycle arrest at G2–M. Further increase in drug concentration to 17.5 μmol/L blocked phosphorylation of the mutant BCR-ABL kinase and its downstream JAK2 and STAT5. The effective dosage to overcome therapy resistance identified in an in vitro setting serves as a guidance to develop the proper drug formulation for in vivo efficacy. A targeted formulation was developed to achieve sustained bone marrow TG101209 concentration at or above 17.5 μmol/L for effective killing of CML cells in vivo. Potent inhibition of leukemia cell growth and extended survival were observed in two murine models of CML treated with 40 mg/kg intravenously administered targeted TG101209, but not with the untargeted drug at the same dosage. Our finding provides a unique approach to develop treatments for therapy-resistant CML. Mol Cancer Ther; 15(5); 899–910. ©2016 AACR.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 3
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 23, No. 8 ( 2014-08-01), p. 1628-1637
    Abstract: Background: Despite accumulating evidence for the preventive effect of vitamin D on colorectal carcinogenesis, its precise mechanisms remain unclear. We hypothesized that vitamin D was associated with a lower risk of colorectal cancer with high-level vitamin D receptor (VDR) expression, but not with risk of tumor with low-level VDR expression. Methods: Among 140,418 participants followed from 1986 through 2008 in the Nurses' Health Study and the Health Professionals' Follow-up Study, we identified 1,059 incident colorectal cancer cases with tumor molecular data. The predicted 25-hydroxyvitamin D [25(OH)D] score was developed using the known determinants of plasma 25(OH)D. We estimated the HR for cancer subtypes using the duplication method Cox proportional hazards model. Results: A higher predicted 25(OH)D score was associated with a lower risk of colorectal cancer irrespective of VDR expression level (Pheterogeneity for subtypes = 0.75). Multivariate HRs (95% confidence intervals) comparing the highest with the lowest quintile of predicted 25(OH)D scores were 0.48 (0.30–0.78) for VDR-negative tumor and 0.56 (0.42–0.75) for VDR-positive tumor. Similarly, the significant inverse associations of the predicted 25(OH)D score with colorectal cancer risk did not significantly differ by KRAS, BRAF, or PIK3CA status (Pheterogeneity for subtypes ≥ 0.22). Conclusions: A higher predicted vitamin D score was significantly associated with a lower colorectal cancer risk, regardless of VDR status and other molecular features examined. Impact: The preventive effect of vitamin D on colorectal carcinogenesis may not totally depend on tumor factors. Host factors (such as local and systemic immunity) may need to be considered. Cancer Epidemiol Biomarkers Prev; 23(8); 1628–37. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 4
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2009
    In:  Molecular Cancer Therapeutics Vol. 8, No. 5 ( 2009-05-01), p. 1239-1249
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 8, No. 5 ( 2009-05-01), p. 1239-1249
    Abstract: The αvβ6 integrin is an attractive therapeutic target for several cancers due to its role in metastasis and its negligible expression in normal tissues. We previously identified a peptide from a phage-displayed peptide library that binds specifically to αvβ6. The tetrameric version of the peptide has higher affinity for its cellular targets than the corresponding monomers. However, the inefficient synthesis limits its clinical potential. We report here a convergent synthesis producing the tetrameric peptide in high yield and purity. The ease of the synthesis allows for rapid optimization of the peptide. We have optimized this αvβ6 integrin–binding peptide, determining the minimal binding domain and valency. Importantly, the half-maximal binding affinity of the optimal peptide for its target cell is in the 40 to 60 pmol/L range, rivaling the affinity of commonly used antibody-targeting reagents. This peptide mediates cell-specific uptake, is functional in diagnostic formats, is stable in sera, and can home to a tumor in an animal. We anticipate that this high-affinity ligand for αvβ6 will find clinical use as a diagnostic and therapeutic reagent. [Mol Cancer Ther 2009;8(5):1239–49]
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2015
    In:  Molecular Cancer Therapeutics Vol. 14, No. 12 ( 2015-12-01), p. 2864-2873
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 14, No. 12 ( 2015-12-01), p. 2864-2873
    Abstract: DNA methylation, the best known epigenetic marker, can be used as a prognostic biomarker in many cancers. We examined DNA methylation status and survival in nasopharyngeal carcinoma (NPC) patients. Aberrant DNA-methylated genes in 24 NPC tissues and 24 noncancer nasopharyngitis biopsy tissues (NCNBT) were identified using Illumina 450K BeadChip. Correlations between DNA methylation and clinical outcomes were evaluated using bisulfite pyrosequencing in 454 NPC patients. Genome-wide methylation analysis demonstrated that NPC tissues had distinct DNA methylation patterns compared with NCNBT. Among all significant CpG sites, 2,173 CpG sites with β change ≥ 0.2 (1,880 hypermethylated, 293 hypomethylated) were identified (P & lt; 0.05). A methylation gene panel comprising six hypermethylated genes was constructed with the average Z-score method. Patients in the training cohort with high methylation had poorer disease-free survival [DFS, HR, 2.26; 95% confidence interval (CI), 1.28–4.01; P, 0.005] and overall survival (OS, HR, 2.47; 95% CI, 1.30–4.71; P, 0.006) than those with low methylation. There were similar results in the validation (DFS, HR, 2.07; 95% CI, 1.17–3.67; P, 0.013; OS, HR, 1.83; 95% CI, 1.01–3.31; P, 0.046) and independent cohorts (DFS, HR, 1.94; 95% CI, 1.08–3.47; P, 0.026; OS, HR, 2.09; 95% CI, 1.10–3.98; P, 0.022). Analysis indicated that the methylation gene panel was an independent prognostic factor. Furthermore, patients with low methylation had a favorable response to concurrent chemotherapy with an improved DFS (P = 0.045) and OS (P = 0.031), whereas patients with high methylation did not benefit from concurrent chemotherapy. The six–hypermethylated gene panel was associated with poor survival in patients with NPC, demonstrating its potential usefulness as a prognostic biomarker to clinicians in NPC management. Mol Cancer Ther; 14(12); 2864–7 3. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
    detail.hit.zdb_id: 2062135-8
    SSG: 12
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  • 6
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 15, No. 24 ( 2009-12-15), p. 7726-7736
    Abstract: Purpose: We evaluated the clinical benefit of an allogeneic melanoma cell lysate (MCL)–pulsed autologous dendritic cell (DC) vaccine in advanced colorectal cancer patients expressing at least one of six MAGE-A antigens overexpressed by the cell line source of the lysate. Experimental Design: DCs were cultured from peripheral blood mononuclear cells (PBMC), pulsed with the allogeneic MCL, and matured using cytokines that achieved high CD83- and CCR7-expressing DCs. Each patient received up to 10 intradermal vaccinations (3-5 × 106 cells per dose) at biweekly intervals. Results: Twenty patients received a total of 161 vaccinations. Treatment was well tolerated and quality of life measurements did not vary much across time. One patient experienced partial response [5%; 95% confidence interval (CI), 1-24%] and seven achieved stable disease (35%; 95% CI, 18-57%), one of whom also achieved late tumor regression, yielding a clinical benefit response rate of 40% (95% CI, 22-61%). Although overall median progression-free survival was 2.4 months (95% CI, 1.9-4.1 months), five patients (25%) experienced prolonged progression-free survival ( & gt;6 months), two of whom (10%) remain progression-free for & gt;27 and & gt;37 months, respectively. This result is particularly meaningful as all patients had progressive disease before treatment. Overall, DC vaccination was associated with a serial decline in regulatory T cells. Using an antibody array, we characterized plasma protein profiles in responding patients that may correlate with vaccine activity and report a prevaccination protein signature distinguishing responders from nonresponders. Conclusion: This phase II vaccine study using mature, MCL-pulsed DCs has shown promising results and warrants further evaluation in a prospective randomized setting. (Clin Cancer Res 2009;15(24):7726–36)
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 7
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 81, No. 5 ( 2021-03-01), p. 1413-1425
    Abstract: Novel strategies to treat late-stage nasopharyngeal carcinoma that often develop resistance to chemotherapy remains an unmet clinical demand. In this study, we identify the multi-kinase inhibitor pacritinib as capable of resensitizing the response to paclitaxel in an acquired resistance model. Transcriptome analysis of paclitaxel-sensitive and -resistant cell lines, as well as chemorefractory clinical samples, identified S100A9 as the top candidate gene suppressed by pacritinib and whose overexpression was significantly associated with paclitaxel resistance and poor clinical outcome. Moreover, both paclitaxel-resistant nasopharyngeal carcinoma cells and relapsed/metastatic clinical samples exhibited increased IRAK1 phosphorylation and demonstrated that pacritinib could abolish the IRAK1 phosphorylation to suppress S100A9 expression. Functional studies in both in vitro and in vivo models showed that genetic or pharmacologic blockade of IRAK1 overcame the resistance to paclitaxel, and combined treatment of pacritinib with paclitaxel exhibited superior antitumor effect. Together, these findings demonstrate an important role for the IRAK1–S100A9 axis in mediating resistance to paclitaxel. Furthermore, targeting of IRAK1 by pacritinib may provide a novel therapeutic strategy to overcome chemoresistance in nasopharyngeal carcinoma. Significance: Deregulation of the IRAK1–S100A9 axis correlates with poor prognosis, contributes to chemoresistance in nasopharyngeal carcinoma, and can be targeted by pacritinib to overcome chemoresistance in nasopharyngeal carcinoma.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 82, No. 4_Supplement ( 2022-02-15), p. PD5-03-PD5-03
    Abstract: Purpose: Endocrine therapy is associated with cardiovascular disease among breast cancer (BC) survivors, with observed opposing effects between aromatase inhibitors (AIs) and tamoxifen. AIs deplete endogenous estrogen levels, while tamoxifen has mixed estrogenic and antiestrogenic activity. Yet, observational studies comparing AI vs. tamoxifen use may be confounded by indication and few have tested their associations with cardiometabolic risk factors. Therefore, we examined the association of AI or tamoxifen use on the incidence of newly diagnosed hypertension, diabetes, and dyslipidemia in a cohort of BC survivors within Kaiser Permanente Northern California (KPNC). Methods: The Pathways Heart Study is an ongoing cohort study within KPNC examining incident CVD outcomes and risk factors in 14,942 women with history of BC. Eligibility was: 1) stage I-IV invasive BC diagnosis between Nov 2005 and Mar 2013; 2) & ge;21 years; and 3) active KPNC membership & ge;12 months at diagnosis. KPNC records were used to collect demographic, socioeconomic, and health characteristics. Endocrine therapy was collected from outpatient pharmacy data. Incident hypertension, diabetes, and dyslipidemia were identified from ICD-9/10 codes, laboratory results, and/or medication use. Hazard ratios (HR) and 95% confidence intervals (CI) from Cox proportional models were used to determine whether AI and tamoxifen use were associated with incident hypertension, diabetes, and dyslipidemia compared to BC survivors not receiving either of these therapies. For each cardiometabolic risk factor, models adjusted for demographic, socioeconomic, and health characteristics and excluded women with the cardiometabolic risk factor at baseline. Results: Among 14,942 women with a history of BC, mean age at baseline was 61.2±12.8 years and mean follow-up time was 7.0±3.5 years (range 1-13.4). The frequency of use was: AI, n=6,070 (40.6%); tamoxifen, n=1,755 (11.8%); and neither, n=7,117 (47.6%). Regression models showed AI use was associated with increased risk of incident hypertension (HR: 1.1, 95% CI: 1.00-1.21) and increased risk of incident dyslipidemia (HR: 1.18, 95% CI: 1.07-1.3) relative to BC survivors who did not use endocrine therapy. (Table). In contrast, tamoxifen use was associated with decreased risk of dyslipidemia (HR: 0.8, 95% CI: 0.68-0.94) relative to BC survivors who did not use endocrine therapy. Neither AI nor tamoxifen use was associated with risk of incident diabetes. Conclusion: Compared to BC survivors who did not use endocrine therapy, women treated with AIs had a higher risk of incident hypertension and dyslipidemia, while women treated with tamoxifen had a lower risk of dyslipidemia. AIs reduce endogenous estrogen levels, which can alter lipid profiles, although prior studies have been inconsistent, possibly due to differences in steroidal and non-steroidal AIs. More work is needed to understand the implications of these associations on long-term cardiovascular health and how to best manage cardiometabolic risk factors in BC survivors with a history of endocrine therapy use. Table. Adjusted1 hazard ratios (95% confidence intervals) of incident cardiometabolic risk factors among women with a history of breast cancer, by endocrine therapy useNo Endocrine Therapy(n=7,117)Endocrine TherapyAromatase inhibitor(n=6,070)Tamoxifen(n=1,755)Incident HypertensionRef1.10 (1.00, 1.21)0.98 (0.85, 1.14)Incident DiabetesRef0.99 (0.87, 1.13)0.98 (0.80, 1.20)Incident DyslipidemiaRef1.18 (1.07, 1.30)0.80 (0.68, 0.94)1Adjusted for age, race/ethnicity, baseline body mass index, AJCC stage, menopausal status, smoking status, education level, income, chemotherapy, radiation therapy, and prevalent cardiovascular disease. Citation Format: Heather Greenlee, Eileen Rillamas-Sun, Carlos Iribarren, Richard Cheng, Romain Neugebauer, Jamal S. Rana, Mai Nguyen-Huynh, Zaixing Shi, Cecile A. Laurent, Valerie S. Lee, Janise M. Roh, Hanjie Shen, Dawn L. Hershman, Lawrence H. Kushi, Marilyn L. Kwan. Development of cardiometabolic risk factors following endocrine therapy: The pathways heart study [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr PD5-03.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2022
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 9
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2062-2062
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2062-2062
    Abstract: MicroRNAs (miRNAs) represent an endogenous, post-transcriptional gene expression regulatory mechanism that is mediated by small, non-coding double-stranded RNAs (dsRNA) which target discrete messenger RNAs (mRNAs) resulting in their degradation or translational repression. Current computational methodologies predict that an average of 200 unique genes may be targeted by a single miRNA with the vast majority remaining, as yet, experimentally unvalidated. Furthermore, as miRNAs regulate their gene targets post-transcriptionally, the application of global, quantitative proteomic analysis to miRNA target discovery will yield a more comprehensive assessment of miRNA activity than gene expression analysis alone. Several miRNAs have been shown to be robustly downregulated in breast cancer, including microRNA-145 (miR-145). Recent investigations of miR-145 in breast cancer have revealed tumor suppressor activities for this miRNA and that loss of miR-145 expression may be associated with early stages of breast cancer pathogenesis. To elucidate targets of miR-145 and its role in breast cancer, we restored expression in the human breast cancer cell lines MDA-MB-231 and SKBR3 and conducted both phenotypic and global, quantitative protein expression analysis utilizing mass spectrometry-based proteomics. Phenotypic analyses indicated that MDA-MB-231 and SKBR3 cells stably expressing miR-145 exhibit a growth advantage relative to control cells. In support of this evidence, GO enrichment analysis of significantly differentially expressed proteins in miR-145-expressing MDA-MB-231 (MDA-145) cells revealed modulation of factors associated with cell cycle regulation, such as increased expression of the G2/M-phase regulatory factors anaphase promoting complex subunit 1 (ANAPC1) and cell division cycle 20 homolog (CDC20) expression and decreased expression of DnaJ (Hsp40) homolog (DNAJA3). Investigation of miR-145-specific effects via sequence analysis of 3’ untranslated regions derived from genes corresponding to proteins which were decreased in abundance in MDA-145 cells revealed 33 target candidates that contained a miR-145 “seed” motif. Of these 33 candidates, 21 have been previously predicted as miR-145 targets (miRNAMap). Target candidates are associated with cell cycle regulation and mitochondrial function and include integrin linked kinase (ILK), the cytokine growth factor chromosome 19 open reading frame 10 (C19ORF10) and microsomal glutathione S-transferase 1 (MGST1). Validation of target candidates and exploration of their role in the miR-145-mediated growth advantage phenotype are currently underway. In conclusion, these results indicate that restoration of stable miR-145 expression in breast cancer cells confers a growth advantage which is underscored by modulation of proteins associated with cell cycle regulation and mitochondrial activity. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2062.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 27, No. 15 ( 2021-08-01), p. 4186-4194
    Abstract: Previous studies suggest that a cumulative cisplatin dose of 200 mg/m2 might be adequate in the intensity-modulated radiation therapy (IMRT) era for locoregionally advanced nasopharyngeal carcinoma (LANPC). However, two cycles of once-every-3-weeks cisplatin at 100 mg/m2 has never been prospectively compared with standard once-a-week cisplatin regimen. Patients and Methods: This trial was conducted at three hospitals from 2011 to 2016. Patients who met the eligibility criteria were recruited (ChiCTR-TRC-12001979) and randomly assigned (1:1) via a computer-generated sequence to receive once-every-3-weeks cisplatin at 100 mg/m2 for two cycles or once-a-week cisplatin at 40 mg/m2 for six cycles concurrently with IMRT. Primary endpoint was failure-free survival and between-group absolute difference of 10% as the noninferiority margin. Results: A total of 510 patients were enrolled. Median follow-up time was 58.3 months with 85.4% of 3-year failure-free survival in the once-every-3-weeks group and 85.6% in the once-a-week group. An absolute difference of −0.2% (95% confidence interval, −6.3 to 5.9; Pnoninferiority = 0.0016). Acute toxicities of grade 3 or higher occurred in 55.8% in the once-every-3-weeks group and 66.3% in the once-a-week group (P = 0.015). The most common acute toxicities were hematologic abnormalities, including leukopenia (16% vs. 27%; P = 0.0022) and thrombocytopenia (1% vs. 5%; P = 0.015). The late grade 3–4 auditory loss rate was significantly lower in the once-every-3-weeks group than the once-a-week group (6% vs. 13%; P = 0.0039). Conclusions: Once-every-3-weeks cisplatin as concurrent chemoradiotherapy is noninferior to once-a-week cisplatin in the treatment efficacy in the LANPC. Although both regimens are well tolerated, severe acute toxicities and late-onset auditory loss are higher in the once-a-week group.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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