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  • 1
    Electronic Resource
    Electronic Resource
    Control of emsis by intravenous granisetron in breast cancer patients treated with 5-FU, epirubicin and cyclophosphamide (1994)
    Springer
    Supportive care in cancer 2 (1994), S. 197-200 
    Details
    ISSN: 1433-7339
    Keywords: Granisetron ; Anti-emesis ; Emesis control in chemotherapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Granisetron, a potent and selective 5-hydroxytryptamine receptor (5-HT3) antagonist was reported to be an effective antiemetic agent both in animal studies and in patients given highly emetogenic chemotherapy. A sample of 43 patients with breast cancer was accrued from September to November 1992 in a phase II study to assess the efficacy of granisetron in patients receiving FEC (5-FU, epirubicin, cyclophosphamide). Each patient received 3 mg intravenous granisetron as a single dose just prior to chemotherapy. Oral metoclopromide was prescribed to each patient as a rescue anti-emetic. The emetic episodes and degree of nausea were evaluated on a daily basis. Good control of emesis (0–2 episodes of vomiting) and nausea (mild or no nausea) was in the range 77%–98% and 77%–93% respectively. There was a complete response (no emetic episodes throughout the 6-day period) in 16 patients (37.2%). Onset of emesis tends to occur on day 1 and tend to subside after day 3; 85% of patients had onset of emesis in the first 2 days after chemotherapy. Control of emesis and nausea tends to improve after day 3, which could be the result of the reduced emetogenicity of the combination FEC with time. Altogether, 77% had good control of acute emesis; control of delayed emesis was better with 84% achieving a major response on day 2 after chemotherapy, which improved to more than 90% after day 4. Granisetron was generally tolerated with headache being the most common side-effect folloed by constipation and flushing. This study suggests that granisetron is an effective and well-tolerated anti-emetic agent, which deserves randomised trials to elucidate its efficacy further.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417481
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  • 2
    Electronic Resource
    Electronic Resource
    Activity of paclitaxel by three-hour infusion in Asian patients with metastatic undifferentiated nasopharyngeal cancer (1998)
    Springer
    Annals of oncology 9 (1998), S. 327-329 
    Details
    ISSN: 1569-8041
    Keywords: nasopharyngeal cancer ; paclitaxel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background: Despite its moderate anti-tumour activity in head and neck cancers there have been no reports on the activity of paclitaxel in patients with nasopharyngeal cancer, a highly chemosensitive tumour. A phase II study was thus initiated to determine the objective response rate and toxicity of paclitaxel in patients with previously untreated metastatic nasopharyngeal cancer. Patients and methods: Twenty-four patients with previously untreated measurable metastatic nasopharyngeal carcinoma were accrued, one of them ineligible because of concomitant beta-blocker usage. Male : female ratio was 19 : 5, with a median age of 46 years. All had previously received radiotherapy but were chemotherapy-naïve. The great majority (20 of 24) had undifferentiated carcinoma. Paclitaxel (Anzatax, Faulding Pharmaceuticals) 175 mg/m2 was given intravenously over three hours every 21 days after premedication with oral dexamethasone and intravenous diphenhydramine and cimetidine. Results: There were five (21.7%) partial responses while eight patients remained stable. Median response duration was 7.5 months and median survival was 12 months. The main toxicity was haematological, with grade 1–2 neutropenia in 19% and grade 3–4 neutropenia in 4.5% of cycles. Three cycles were complicated by grade 3–4 anaemia and one patient required a blood transfusion. No thrombocytopenia was seen. Peripheral neuropathy was frequent (20 of 23 patients) but mild. Alopecia was complete in 14 patients. There were no cardiac toxicity or hypersensitivity reactions. Conclusions: Paclitaxel is well tolerated even in previously irradiated patients with metastatic nasopharyngeal cancer. Single-agent activity was 22% and its inclusion into combination chemotherapy regimens should be studied.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008255220284
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  • 3
    Electronic Resource
    Electronic Resource
    Phase II trial of a paclitaxel and carboplatin combination in Asian patients with metastatic nasopharyngeal carcinoma (1999)
    Springer
    Annals of oncology 10 (1999), S. 235-237 
    Details
    ISSN: 1569-8041
    Keywords: carboplatin ; metastatic nasopharyngeal carcinoma ; paclitaxel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: An earlier phase II trial of paclitaxel in patients with metastatic nasopharyngeal carcinoma (NPC) demonstrated a response rate of 22%. Hence we proceeded to study the combination of paclitaxel and carboplatin in these patients. Patients and methods: The 21-day regimen was as follows: i.v. paclitaxel 175 mg/m2 over three hours preceded by standard premedications, followed by i.v. carboplatin dosed at AUC of six infused over one hour. Only chemotherapy-naïve patients with histological diagnoses of undifferentiated carcinoma of the nasopharynx, systemic metastases and radiologically measurable lesions were eligible. Results: Thirty-two patients were accrued to this study. Twenty patients (62%) had at least two sites of metastasis. The main grade 3–4 toxicity was neutropenia (31%). Nine patients (28%) developed neutropenic sepsis, which caused the demise of one of them. Twenty-four patients (75%) responded to treatment, with one (3%) attaining a complete response. The median time to progression of disease was seven months and the median survival was 12 months. At one year, 52% of the patients were alive. Conclusions: The combination of paclitaxel and carboplatin is an active regimen in NPC. Its convenience of administration and good tolerability make it an attractive alternative regimen to consider for patients with metastatic disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1008390929826
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  • 4
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    Impact of EGFR Inhibitor in Non-Small Cell Lung Cancer on Progression-Free and Overall Survival: A Meta-Analysis (2013)
    Oxford University Press
    Details
    Publication Date: 2013-05-01
    Description: Background The epidermal growth factor receptor (EGFR) signaling pathway is crucial for regulating tumorigenesis and cell survival and may be important in the development and progression of non–small cell lung cancer (NSCLC). We examined the impact of EGFR–tyrosine kinase inhibitors (TKIs) on progression-free survival (PFS) and overall survival (OS) in advanced NSCLC patients with and without EGFR mutations. Methods Randomized trials that compared EGFR-TKIs monotherapy or combination EGFR-TKIs-chemotherapy with chemotherapy or placebo were included. We used published hazard ratios (HRs), if available, or derived treatment estimates from other survival data. Pooled estimates of treatment efficacy of EGFR-TKIs for the EGFR mutation–positive (EGFRmut + ) and EGFR mutation–negative (EGFRmut – ) subgroups were calculated with the fixed-effects inverse variance weighted method. All statistical tests were two-sided. Results We included 23 eligible trials (13 front-line, 7 second-line, 3 maintenance; n = 14570). EGFR mutation status was known in 31% of patients. EGFR-TKIs treatment prolonged PFS in EGFRmut + patients, and EGFR mutation was predictive of PFS in all settings: The front-line hazard ratio for EGFRmut + was 0.43 (95% confidence interval [CI] = 0.38 to 0.49; P 〈 .001), and the front-line hazard ratio for EGFRmut – was 1.06 (95% CI = 0.94 to 1.19; P = .35; P interaction 〈 .001). The second-line hazard ratio for EGFRmut + was 0.34 (95% CI = 0.20 to 0.60; P 〈 .001), and the second-line hazard ratio for EGFRmut – was 1.23 (95% CI = 1.05 to 1.46; P = .01; P interaction 〈 .001). The maintenance hazard ratio for EGFRmut + was 0.15 (95% CI = 0.08 to 0.27; P 〈 .001), and the maintenance hazard ratio for EGFRmut – was 0.81 (95% CI = 0.68 to 0.97; P = .02; P interaction 〈 .001). EGFR-TKIs treatment had no impact on OS for EGFRmut + and EGFRmut – patients. Conclusions EGFR-TKIs therapy statistically significantly delays disease progression in EGFRmut + patients but has no demonstrable impact on OS. EGFR mutation is a predictive biomarker of PFS benefit with EGFR-TKIs treatment in all settings. These findings support EGFR mutation assessment before initiation of treatment. EGFR-TKIs should be considered as front-line therapy in EGFRmut + advanced NSCLC patients.
    Electronic ISSN: 1460-2105
    Topics: Medicine
    Published by Oxford University Press
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  • 5
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    Mutation of Arabidopsis SMC4 identifies condensin as a corepressor of pericentromeric transposons and conditionally expressed genes [Research Papers] (2017)
    Cold Spring Harbor Laboratory Press
    Details
    Publication Date: 2017-09-15
    Description: In eukaryotes, transcriptionally inactive loci are enriched within highly condensed heterochromatin. In plants, as in mammals, the DNA of heterochromatin is densely methylated and wrapped by histones displaying a characteristic subset of post-translational modifications. Growing evidence indicates that these chromatin modifications are not sufficient for silencing. Instead, they are prerequisites for further assembly of higher-order chromatin structures that are refractory to transcription but not fully understood. We show that silencing of transposons in the pericentromeric heterochromatin of Arabidopsis thaliana requires SMC4, a core subunit of condensins I and II, acting in conjunction with CG methylation by MET1 (DNA METHYLTRANSFERASE 1), CHG methylation by CMT3 (CHROMOMETHYLASE 3), the chromatin remodeler DDM1 (DECREASE IN DNA METHYLATION 1), and histone modifications, including histone H3 Lys 27 monomethylation (H3K27me1), imparted by ATXR5 and ATXR6. SMC4/condensin also acts within the mostly euchromatic chromosome arms to suppress conditionally expressed genes involved in flowering or DNA repair, including the DNA glycosylase ROS1, which facilitates DNA demethylation. Collectively, our genome-wide analyses implicate condensin in the suppression of hundreds of loci, acting in both DNA methylation-dependent and methylation-independent pathways.
    Print ISSN: 0890-9369
    Topics: Biology
    Published by Cold Spring Harbor Laboratory Press
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  • 6
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    PPARG in CaP [Medical Sciences] (2016)
    National Academy of Sciences
    Details
    Publication Date: 2016-07-21
    Description: Prostate cancer (CaP) is the most common adult male cancer in the developed world. The paucity of biomarkers to predict prostate tumor biology makes it important to identify key pathways that confer poor prognosis and guide potential targeted therapy. Using a murine forward mutagenesis screen in a Pten-null background, we...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 7
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    SMAD3 Deficiency Promotes Inflammatory Aortic Aneurysms in Angiotensin II-Infused Mice Via Activation of iNOS [Hypertension] (2013)
    American Heart Association (AHA)
    Details
    Publication Date: 2013-06-27
    Description: Background Ninety percent of the patients carrying distinct SMAD3 mutations develop aortic aneurysms and dissections, called aneurysms-osteoarthritis syndrome (AOS). However, the etiology and molecular events downstream of SMAD3 leading to the pathogenesis of aortic aneurysms in these patients still remain elusive. Therefore, we aimed to investigate the vascular phenotypes of SMAD 3-knockout mice. Methods and Results We have shown that angiotensin II–induced vascular inflammation, but not hypertension, leads to aortic aneurysms and dissections, ultimately causing aortic rupture and death in mice. Lipopolysaccharide-triggered inflammation confirmed that enhanced aortic macrophage recruitment was essential for aneurysm formation in angiotensin II–infused SMAD3 -knockout mice. In contrast, phenylephrine-triggered hypertension alone was insufficient to induce aortic aneurysms in mice. Using uniaxial tensile and contractility tests, we showed that SMAD3 deficiency resulted in defective aortic biomechanics and physiological functions, which caused weakening of the aortic wall and predisposed the mice to aortic aneurysms. Chromatin immunoprecipitation (ChIP) and re-ChIP assays revealed that the underlying mechanism involved aberrant upregulation of inducible nitric oxide synthase (iNOS)–derived nitric oxide production and activation of elastolytic matrix metalloproteinases 2 and 9. Administration of clodronate-liposomes and iNOS inhibitor completely abrogated these aortic conditions, thereby identifying iNOS-mediated nitric oxide secretion from macrophages as the downstream event of SMAD3 that drives this severe pathology. Conclusions Macrophage depletion and iNOS antagonism represent 2 promising approaches for preventing aortic aneurysms related to SMAD3 mutations and merit further investigation as adjunctive strategies for the life-threatening manifestations of AOS.
    Electronic ISSN: 2047-9980
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 8
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    Gefitinib, cisplatin, and concurrent radiotherapy for locally advanced head and neck cancer: EGFR FISH, protein expression, and mutational status are not predictive biomarkers (2012)
    Oxford University Press
    Details
    Publication Date: 2012-04-03
    Description: Background: Gefitinib was demonstrated to be synergistic with cisplatin and radiotherapy (RT) in in vitro studies. Biomarkers predictive of response to gefitinib in squamous cell head and neck cancer is still lacking. Methods: Thirty-one patients with locally advanced and easily accessible primary tumor sites for biopsies were recruited. Gefitinib was started 3 weeks before the start of cisplatin/concurrent radiotherapy (CTRT) and continued during the CTRT phase and thereafter for 4 months as consolidation phase. Two baselines and a repeat tumor sample were taken after 2 weeks of gefitinib alone to study its impact on tumor gene expression. Epidermal growth factor receptor (EGFR) protein expression, FISH and mutational status, and matrix metallopeptidase 11 (MMP11) protein expression were correlated with response and survival outcome. Results: The overall response rate to gefitinib alone was 9.7%. The survival outcome is as follows: median disease free 1.3 years, median survival time 2.4 years, 3-year disease free 42.9%, and 3-year overall survival 48.4%. EGFR FISH, protein expression, and mutational status did not predict for response nor survival outcome of patients. Although MMP11 overexpression did not predict for response, it predicted significantly for a poorer survival outcome. Conclusions: Gefitinib can be combined safely with cisplatin/RT. More studies are needed to uncover predictive biomarkers of benefit to gefitinib.
    Print ISSN: 0923-7534
    Electronic ISSN: 1569-8041
    Topics: Medicine
    Published by Oxford University Press
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  • 9
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    A phase II study evaluating the safety and efficacy of an adenovirus-{Delta}LMP1-LMP2 transduced dendritic cell vaccine in patients with advanced metastatic nasopharyngeal carcinoma (2012)
    Oxford University Press
    Details
    Publication Date: 2012-04-03
    Description: Background: Individuals with metastatic Epstein–Barr virus (EBV)-positive nasopharyngeal carcinoma (NPC) continue to have poor outcomes. To evaluate the ability of a dendritic cell (DC) vaccine to target subdominant EBV antigens LMP1 and LMP2 expressed by NPC cells, we vaccinated patients using autologous DCs transduced with an adenovirus encoding a truncated LMP1 (LMP1) and full-length LMP2 (Ad-LMP1-LMP2). Materials and methods: Sixteen subjects with metastatic NPC received Ad-LMP1-LMP2 DC vaccines i.d. biweekly for up to five doses. Toxicity, immune responses and clinical responses were determined. Results: Most patients had extensive disease, with a median of three visceral sites of involvement (range 1–7). No significant toxicity was observed. Ad-LMP1-LMP2 DCs induced delayed type hypersensitivity responses in 9 out of 12 patients, but although these DCs activated LMP1/2-specific T cells in vitro , no such increase in the frequency of peripheral LMP1/2-specific T cells was detected. Three patients had clinical responses including one with partial response (for 71/2 months) and two with stable disease (for 61/2 and 71/2 months). Conclusions: Ad-LMP1-LMP2 transduced DCs can be successfully generated and safely administered to patients with advanced NPC. Since efficacy was limited, future studies should focus on DC vaccines with greater potency administered to subjects with less tumor burden.
    Print ISSN: 0923-7534
    Electronic ISSN: 1569-8041
    Topics: Medicine
    Published by Oxford University Press
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