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Journal articles on the topic 'AromaScan'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

DU, WEN-XIAN, JEONGMOK KIM, JOHN A. CORNELL, TUNG-SHI HUANG, MAURICE R. MARSHALL, and CHENG-I. WEI. "Microbiological, Sensory, and Electronic Nose Evaluation of Yellowfin Tuna under Various Storage Conditions†." Journal of Food Protection 64, no. 12 (December 1, 2001): 2027–36. http://dx.doi.org/10.4315/0362-028x-64.12.2027.

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Microbiological assessment, sensory evaluation, and electronic nose (AromaScan) analysis were performed on yellowfin tuna stored at 0, 4, 10, and 22°C for 0, 1, 3, 5, and 9 days. Fish color, texture, appearance, and odor were evaluated by a trained sensory panel, while aroma-odor properties were evaluated using an AromaScan. Bacterial enumeration was performed using plate count agar containing 1.5% NaCl. Tuna fillets stored at 22°C for 3 days or longer had a bacterial load of over 107 CFU/g and were rated not acceptable for consumption (grade C) by the sensory panel. Tuna fillets stored at 4°C for 9 days or 10°C for over 5 days were rated as grade C products and also had a bacterial load of over 107 CFU/g. The change in fish quality as determined by AromaScan followed increases in microbiological counts in tuna fillets, indicating that bacterial load can serve as a useful and objective indicator of gross spoilage. Electronic nose devices can be used in conjunction with microbial counts and sensory panels to evaluate the degree of decomposition in tuna during storage.

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2

Du, Wen-Xian, Tung-shi Huang, Jeongmok Kim, Maurice R. Marshall, and Cheng-i. Wei. "Chemical, Microbiological, and AromaScan Evaluation of Mahi-mahi Fillets under Various Storage Conditions." Journal of Agricultural and Food Chemistry 49, no. 1 (January 2001): 527–34. http://dx.doi.org/10.1021/jf0011135.

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3

Shen, N., S. Duvick, P. White, and L. Pollak. "Oxidative stability and AromaScan analyses of corn oils with altered fatty acid content." Journal of the American Oil Chemists' Society 76, no. 12 (December 1999): 1425–29. http://dx.doi.org/10.1007/s11746-999-0179-z.

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4

VISSER, FRANS ROBERT, and MARCUS TAYLOR. "IMPROVED PERFORMANCE OF THE AROMASCAN A32S ELECTRONIC NOSE AND ITS POTENTIAL FOR DETECTING AROMA DIFFERENCES IN DAIRY PRODUCTS." Journal of Sensory Studies 13, no. 1 (April 1998): 95–120. http://dx.doi.org/10.1111/j.1745-459x.1998.tb00077.x.

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5

Hoc, Siegfried. "Mammakarzinom: Mit Exemestan die Therapie optimieren." Onkologische Welt 01, no. 03 (2010): 120. http://dx.doi.org/10.1055/s-0038-1630959.

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Ziel jeder Hormontherapie des Mammakarzinoms ist die Ausschaltung der Östrogenbedingten Wachstumsstimulation. Die dazu neben Antiöstrogenen eingesetzten Aromatase- Inhibitoren vermindern die Östrogen-Produktion, indem sie die Umwandlung (Aromatisierung) von Androgenen in Östrogen unterdrücken. Die Aromatase-Hemmer der dritten Generation wie das steroidale Exemestan (Aromasin®) wirken sehr effektiv und hoch selektiv, sodass deutlich weniger unerwünschte Nebenwirkungen wie etwa Arthralgien und Knochendichteverluste mit der Folge von Frakturen auftreten, erläuterte Prof. Marc Sütterlin, Mannheim.

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6

Hoc, Siegfried. "Mammakarzinom: Mit Exemestan die Therapie optimieren." Onkologische Welt 01, no. 03 (2010): 120. http://dx.doi.org/10.1055/s-0038-1631004.

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Ziel jeder Hormontherapie des Mammakarzinoms ist die Ausschaltung der ÖstrogenbedingtenWachstumsstimulation. Die dazu neben Antiöstrogenen eingesetzten Aromatase- Inhibitoren vermindern die Östrogen-Produktion, indem sie die Umwandlung (Aromatisierung) von Androgenen in Östrogen unterdrücken. Die Aromatase-Hemmer der dritten Generation wie das steroidale Exemestan (Aromasin®) wirken sehr effektiv und hoch selektiv, sodass deutlich weniger unerwünschte Nebenwirkungen wie etwa Arthralgien und Knochendichteverluste mit der Folge von Frakturen auftreten, erläuterte Prof. Marc Sütterlin, Mannheim.

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7

Hoc, Siegfried. "Mammakarzinom: Mit Exemestan die Therapie optimieren." Onkologische Welt 01, no. 03 (2010): 120. http://dx.doi.org/10.1055/s-0038-1631010.

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Ziel jeder Hormontherapie des Mammakarzinoms ist die Ausschaltung der ÖstrogenbedingtenWachstumsstimulation. Die dazu neben Antiöstrogenen eingesetzten Aromatase- Inhibitoren vermindern die Östrogen-Produktion, indem sie die Umwandlung (Aromatisierung) von Androgenen in Östrogen unterdrücken. Die Aromatase-Hemmer der dritten Generation wie das steroidale Exemestan (Aromasin®) wirken sehr effektiv und hoch selektiv, sodass deutlich weniger unerwünschte Nebenwirkungen wie etwa Arthralgien und Knochendichteverluste mit der Folge von Frakturen auftreten, erläuterte Prof. Marc Sütterlin, Mannheim.

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8

Dank, Magdolna. "The role of aromasin in the hormonal therapy of breast cancer." Pathology & Oncology Research 8, no. 2 (June 2002): 87–92. http://dx.doi.org/10.1007/bf03033716.

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9

Dogan, Esma Eryilmaz. "Computational Bioactivity Analysis and Bioisosteric Investigation of the Approved Breast Cancer Drugs Proposed New Design Drug Compounds: Increased Bioactivity Coming with Silicon and Boron." Letters in Drug Design & Discovery 18, no. 6 (August 10, 2021): 551–61. http://dx.doi.org/10.2174/1570180818666210114115415.

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Background: The breast cancer takes the first place among women cancer diagnosed worldwide. Objective: Based on the preferential multi-targeted approach on cancer therapy, we, in this study, aimed to design in silico drug candidates possessing multi-targeted bioactivity to cope with multi-drug resistance using the known drug structures, molecular modeling, and ADME parameters. Materials and Methods: We first evaluated the bioactivity score of the approved breast cancer drugs across the top-three drug targets GPCR, kinase, and nuclear receptors and calculated their physicochemical properties to see their drug-likeness profiles. Among 29 approved drugs, Aromasin and Capecitabine showed the broadest bioactivity across the targets listed. By using molecular modeling and bioisosteric modifications, and applying two filtering approaches, we investigated thirty-one analogues of Aromasin and Capecitabine. Results : Software prediction resulted in that the compounds A14, C4, and C13 replaced with B(OH)2 and/or Si(CH3)3 showed a broader spectrum of biological activity with a multi-targeted manner than even the approved analogs. Conclusion: The interesting point of these new design molecules is to have either silicon and/or boron incorporation. The increased bioactivity effect of Silicon and Boron incorporation is also seen in the recently approved drug list of FDA and in clinical trials ongoing. Our new design boron and silicon-based molecules appeared to be promising candidates for breast cancer treatment to be tested in vitro, in vivo, and in the clinic for further pharmacological investigations.

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10

TAHARA, Makoto, Shunji NOMURA, and Munehiro HASHIMOTO. "Pharmacological and clinical profile of exemestane (Aromasin), a novel irreversible aromatase inhibitor." Folia Pharmacologica Japonica 122, no. 4 (2003): 345–54. http://dx.doi.org/10.1254/fpj.122.345.

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11

Velu, K. S. "Study showing the efficacy of aromasin in metastatic CA breast in postmenopausal women." Journal of Clinical Oncology 26, no. 15_suppl (May 20, 2008): 12023. http://dx.doi.org/10.1200/jco.2008.26.15_suppl.12023.

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12

Mahboobeh Kian and Elham Tazikeh-Lemeski. "Adsorption Behavior of Aromasin onto C20 and C24 Nano-Cages: Density Functional Theory Study." Russian Journal of Inorganic Chemistry 65, no. 12 (December 2020): 1848–53. http://dx.doi.org/10.1134/s0036023620120074.

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13

Mauras, Nelly, John Lima, Deval Patel, Annie Rini, Enrico di Salle, Ambrose Kwok, and Barbara Lippe. "Pharmacokinetics and Dose Finding of a Potent Aromatase Inhibitor, Aromasin (Exemestane), in Young Males." Journal of Clinical Endocrinology & Metabolism 88, no. 12 (December 1, 2003): 5951–56. http://dx.doi.org/10.1210/jc.2003-031279.

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Abstract Suppression of estrogen, via estrogen receptor or aromatase blockade, is being investigated in the treatment of different conditions. Exemestane (Aromasin) is a potent and selective irreversible aromatase inhibitor. To characterize its suppression of estrogen and its pharmacokinetic (PK) properties in males, healthy eugonadal subjects (14–26 yr of age) were recruited. In a cross-over study, 12 were randomly assigned to 25 and 50 mg exemestane daily, orally, for 10 d with a 14-d washout period. Blood was withdrawn before and 24 h after the last dose of each treatment period. A PK study was performed (n = 10) using a 25-mg dose. Exemestane suppressed plasma estradiol comparably with either dose [25 mg, 38% (P ≤ 0.002); 50 mg, 32% (P ≤ 0.008)], with a reciprocal increase in testosterone concentrations (60% and 56%; P ≤ 0.003 for both). Plasma lipids and IGF-I concentrations were unaffected by treatment. The PK properties of the 25-mg dose showed the highest exemestane concentrations 1 h after administration, indicating rapid absorption. The terminal half-life was 8.9 h. Maximal estradiol suppression of 62 ± 14% was observed at 12 h. The drug was well tolerated. In conclusion, exemestane is a potent aromatase inhibitor in men and an alternative to the choice of available inhibitors. Long-term efficacy and safety will need further study.

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14

Bahrami, Nazli, Torill Sauer, Siri Engebretsen, Belal Aljabri, Vahid Bemanian, Jonas Lindstrøm, Torben Lüders, et al. "The NEOLETEXE trial: a neoadjuvant cross-over study exploring the lack of cross resistance between aromatase inhibitors." Future Oncology 15, no. 32 (November 2019): 3675–82. http://dx.doi.org/10.2217/fon-2019-0258.

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The aromatase inhibitor letrozole (Femar®/Femara®) and the aromatase inactivator exemestane (Aromasin®) differ in their biochemical effect on the aromatase enzyme. Letrozole is a competitive aromatase inhibitor while exemestane binds irreversibly to the aromatase enzyme. This pharmacological difference is of clinical interest since a lack of cross-resistance has been documented. It has been demonstrated in several clinical trials that exemestane may cause a disease regression following resistance to nonsteroidal aromatase inhibitors. The exact mechanism(s) behind this phenomenon is yet unknown. Here, we present the NEOLETEXE trial with the aim of exploring the individual mechanisms involved behind the observed lack of cross resistance. Clinical trial registration: The trial has been approved by the Regional Ethics Committee of South-East Norway (project number 2015/84).

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15

&NA;. "Pfizer Canada's exemestane [Aromasin] tablets have been granted a Notice of Compliance with Conditions by Health Canada." Inpharma Weekly &NA;, no. 1539 (May 2006): 23. http://dx.doi.org/10.2165/00128413-200615390-00062.

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16

Jannuzzo, M. G., R. Spinelli, I. Poggesi, P. Cicioni, Y. Böttiger, and L. Bertilsson. "Inhibition of CYP3A4 does not influence Aromasin® (exemestane, EXE) pharmacokinetics (PK) in healthy postmenopausal volunteers (HPV)." European Journal of Cancer 35 (September 1999): S294. http://dx.doi.org/10.1016/s0959-8049(99)81604-9.

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17

Spinelli, R., M. G. Jannuzzo, I. Poggesi, L. Frevola, F. Broutin, P. Cicioni, P. Marrari, and F. Le Coz. "Pharmacokinetics (PK) of Aromasin® (exemestane, EXE) after single and repeated doses in healthy postmenopausal volunteers (HPV)." European Journal of Cancer 35 (September 1999): S295. http://dx.doi.org/10.1016/s0959-8049(99)81605-0.

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18

Jones, S., C. Vogel, A. Arkhipov, L. Fehrenbacher, P. Eisenberg, B. Cooper, S. Honig, et al. "Multicenter, Phase II Trial of Exemestane as Third-Line Hormonal Therapy of Postmenopausal Women With Metastatic Breast Cancer." Journal of Clinical Oncology 17, no. 11 (November 1999): 3418–25. http://dx.doi.org/10.1200/jco.1999.17.11.3418.

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PURPOSE: To assess the antitumor activity, safety, and hormone-suppressive effects of the irreversible aromatase inactivator, exemestane (Aromasin, Pharmacia & Upjohn, Kalamazoo, MI), administered as third-line hormone therapy to postmenopausal women with metastatic breast cancer that is refractory to tamoxifen and megestrol acetate. PATIENTS AND METHODS: Exemestane was administered at a dose of 25 mg/d orally until patients experienced disease progression. The efficacy and safety of exemestane were clinically and radiographically evaluated. The impact of exemestane treatment on tumor-related signs and symptoms was assessed. The effect of exemestane on serum levels of estrogens and other steroidal hormones was determined. RESULTS: Ninety-one patients were treated. There were four complete responses (CR) and eight partial responses (PR), for an objective response rate of 13% in the entire treated population. The overall success rate (CR, PR, or stable disease [SD] ≥ 24 weeks) was 30%. The median duration of response and overall success was 9 months and 8 months, respectively. Most patients with CR/PR (83%; 10 of 12 patients) and SD ≥ 24 weeks (80%; 12 of 15 patients) had improved or stable tumor-related signs and symptoms. Mean levels of circulating estrone (E1), estradiol (E2), and estrone sulfate decreased to 11%, 22%, and 13% of baseline levels, respectively (at week 8 or 16 of treatment). One half of the patients had undetectable E1 and E2 levels during treatment, including at the time of disease progression. Mild nausea (20% of patients) and hot flashes (20%) were the most common drug-related adverse events and were generally grade 1. CONCLUSION: Exemestane is an active and well-tolerated third-line hormonal therapy that represents a new treatment option for postmenopausal patients with advanced breast cancer that has become refractory to standard first- and second-line hormonal therapies.

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19

Tedeschi, M., S. Kvinnsland, S. E. Jones, M. Kaufmann, A. Polli, C. Fowst, and G. Massimini. "Hormonal therapy in breast cancer and predominant visceral disease: effectiveness of the new oral aromatase inactivator, Aromasin® (exemestane), in advanced breast cancer patients having progressed on antiestrogens." European Journal of Cancer 35 (September 1999): S316. http://dx.doi.org/10.1016/s0959-8049(99)81686-4.

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20

Bajetta, E., L. Y. Dirix, L. E. Fein, S. E. Jones, J. Cervek, M. Kaufmann, C. Fowst, A. Polli, E. di Salle, and G. Massimini. "Survival advantage of exemestane (EXE, Aromasin®) over megestrol acetate (MA) in postmenopausal women with advanced breast cancer (ABC) refractory to tamoxifen (TAM): results of a phase III randomized double-blind study." European Journal of Cancer 35 (September 1999): S84. http://dx.doi.org/10.1016/s0959-8049(99)80705-9.

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21

Wolf, C. J., G. Raab, W. Eiermann, and I. Grammatikakis. "An open label, randomized phase II trial of primary systemic therapy with exemestane (EXE 25 mg/d) plus epirubicin (EPI, 20 vs 30 mg/m2 q1w × 8–12) in breast cancer: An interim analysis of the German Neoadjuvant Aromasin Initiative (GENARI-3)." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 826. http://dx.doi.org/10.1200/jco.2004.22.14_suppl.826.

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22

Wolf, C. J., G. Raab, W. Eiermann, and I. Grammatikakis. "An open label, randomized phase II trial of primary systemic therapy with exemestane (EXE 25 mg/d) plus epirubicin (EPI, 20 vs 30 mg/m2 q1w × 8–12) in breast cancer: An interim analysis of the German Neoadjuvant Aromasin Initiative (GENARI-3)." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 826. http://dx.doi.org/10.1200/jco.2004.22.90140.826.

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23

Fuhr, R., MG Jannuzzo, I. Poggesi, N. Sarapa, A. Polli, R. Spinelli, Karl Ludwig Rost, and G. Golor. "Influence of a Two-Week Rifampicin Treatment on the Pharmacokinetics of Exemestane (Aromasin®)." BMC News and views 2, S1 (April 4, 2002). http://dx.doi.org/10.1186/2048-4623-2-s1-p0001.

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24

"National Cancer Institute of Canada – Clinical Trials Group (NCIC CTG)." Breast Cancer Online 9, S1 (December 2006): 373–401. http://dx.doi.org/10.1017/s1470903106009308.

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This section provides current contact details and a summary of recent or ongoing clinical trials being coordinated by National Cancer Institute of Canada – Clinical Trials Group (NCIC CTG). Clinical trials include: Double-blind randomized trial of tamoxifen versus placebo in patients with node-positive or high-risk node-negative (tumor ≥ 1 cm and either higher histological grade (poorly differentiated, or SBR grade III or MSBR grade V) or lymphatic/vascular invasion or both) breast cancer who have completed CMF, CEF or AC adjuvant chemotherapy. NCIC CTG Trial MA.12A randomized trial of antiestrogen therapy versus combined antiestrogen and octreotide LAR therapy in the adjuvant treatment of breast cancer in postmenopausal women. NCIC CTG Trial MA.14A phase III randomized double blind study of letrozole versus placebo in women with primary breast cancer completing five or more years of adjuvant tamoxifen. BIG 01-97/NCIC CTG MA.17NCIC CTG MA.17 Companion study (2): The influence of letrozole on bone mineral density in women with primary breast cancer completing five or more years of adjuvant tamoxifen. BIG 01-97/NCIC MA.17BNCIC CTG MA.17 Companion study (1): The influence of letrozole on serum lipid concentrations in women with primary breast cancer who have completed 5 years of adjuvant tamoxifen. BIG 01-97/NCIC CTG MA.17LNCIC CTG MA.17R A double blind re-randomization to letrozole or placebo for women completing 5 years of adjuvant letrozole in the MA.17 study.A phase III study of regional radiation therapy in early breast cancer. NCIC CTG trial MA.20A phase III adjuvant trial of sequenced EC + GCSF Taxol versus sequenced AC → Taxol versus CEF as therapy for premenopausal women and early postmenopausal women who have had potentially curative surgery for node positive or high-risk node negative breast cancer. NCIC CTG Trial MA.21A phase I/II study of increasing doses of epirubicin and docetaxel + pegfilgrastim for locally advanced or inflammatory breast cancer. NCIC CTG Trial MA.22A randomized phase III trial of exemestane versus anastrozole with or without celecoxib in postmenopausal women with receptor positive primary breast cancer. NCIC CTG Trial MA.27A randomized feasibility study of letrozole in postmenopausal women at increased risk for development of breast cancer as evidenced by high breast density. NCIC CTG Trial MAP.1A randomized study of the effect of exemestane (Aromasin) versus placebo on breast density in postmenopausal women at increased risk for development of breast cancer. NCIC CTG Trial: MAP.2A phase III randomized study of exemestane versus placebo in postmenopausal women at increased risk of developing breast cancer. NCIC CTG Trial: MAP.3

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