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19% of the erlotinib group needed dose reductions due to drug related toxic effects, compared to 2% of the placebo group. These effects were mainly rash 12% ; and diarrhoea 5% ; placebo was 0% for both. 5% discontinued erlotinib due to drug-related toxic effects compared to 2% on placebo.
The information about response to treatment with statins was analyzed after careful retrospective assessment of medical case notes of all affected individuals. The serum total cholesterol values on treatment for each patient have been derived as a mean of 2 measurements 3 months apart after the patient had been on treatment with the same statin and dose for 3 months and when no physiological or other pathological causes that might have interfered with lipid levels had been identified.
Abramov, I., Gordon, J., & Chan, H. 1991 ; . Color appearance across the retina: Effects of stimulus size. Journal of the Optical Society of America, 8, 404-414. Alpern, M., & Torii, S. 1968a ; . The luminosity curve of the protanomalus fovea. Journal of General Physiology, 52, 717737. Alpern, M., & Torii, S. 1968b ; . The luminosity curve of the deuteranomalous fovea. Journal of General Physiology, 52, 738-749. Berlin, B., & Kay, P. 1969 ; . Basic color terms: Their universality and evolution. Berkeley, CA: University of California Press. Birch, J. 1993 ; . Diagnosis of defective color vision. Oxford, UK: Oxford University Press. Boynton, R.M., & Scheibner, H.M.O. 1967 ; . On the perception of red by red-blind observers. Acta Chromatic, 1, 205-220. Boynton, R.M., & Olson, C.X. 1987 ; . Locating basic colors in the OSA space. Color Research and Application, 12, 94-105. Boynton, R.M., & Olson, C.X. 1990 ; . Salience of chromatic basic color terms confirmed by three measures. Vision Research, 30, 1311-1317. Commission Internationale de l'Eclairage 1931 ; . CIE proceedings 1931. Cambridge, UK: Cambridge University Press. Corbett, G.G., & Davies, I.R.L. 1997 ; . Establishing basic color terms: Measures and techniques. In C.L. Hardin & L. Maffi Eds. ; , Color categories in thought and language pp. 197223 ; . Cambridge, MA: Cambridge University Press. Coren, S., Ward, L., & Enns, J.T. 1994 ; . Sensation and perception 4th ed. ; . London: Harcourt Brace. Crawford, T.D. 1982 ; . Defining "basic colour terms." Anthroplogical Linguistics, 24, 338-343. Davies, I.R.L., & Corbett, G.G. 1994 ; . The basic color terms of Russian. Linguistics, 32, 65-89. De Marco, P., Pokorny, J., & Smith, V.C. 1992 ; . Full-spectrum cone sensitivity functions for X-chromosome-linked anomalous trichromats. Journal of the Optical Society of America, 9, 14651476. Fletcher, R. 1980 ; . The City University Colour Vision Test 2nd ed. ; . London: Keeler. Fletcher, R., & Voke, J. 1985 ; . Defective colour vision. Bristol, UK: Adam Hilger.
TK Inhibitors: Mechanism of Action Inhibitors of TK phosphorylation TK inhibitors [TKIs] ; are small-molecule agents that block EGFR activity by interfering with the adenosine triphosphate-binding site on the intracellular region of the receptor.24 A variety of TKIs have been developed for advanced NSCLC. Gefitinib was the first of the class of EGFR-TKIs to be approved by the FDA for treatment in patients with advanced NSCLC. Gefitinib has been shown to induce radiographic tumor responses, improve symptoms, and improve quality of life in those patients who have failed to respond to previous cancer therapies.25, 26 In addition, in the compassionate-use program for gefitinib, which enrolled 21, 000 patients with NSCLC in the United States, the 1-year survival rate was 30%, which is comparable to that of single-agent chemotherapy.27 Several other small-molecule reversible TKIs, including erlotinib, are also being investigated in clinical trials for patients with end-stage NSCLC. Erlotinib has proven efficacy as a second-line or third-line treatment for patients with advanced NSCLC. In a recent phase III trial, 28 erlotinib treatment increased survival, decreased symptoms, and improved the overall quality of life in patients with advanced NSCLC compared with placebo. Erlotinib has recently been approved by the FDA as a second-line agent for use in patients with advanced NSCLC.
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Three trials compared monthly with 2-dose IPT with sulfadoxine-pyrimethamine during pregnancy D. H. Hamer, MD, unpublished data, 2006 ; .17, 32 Two trials included both HIV-positive and.
The state-system argument has been advanced from quite different directions of approach, each version carrying its own implications and anchored in different analytical perspectives Immanuel Wallerstein's 1974 ; emphasis on the `Failure of Empire', and on the dynamic consequences ensuing when the scale of economic reproduction moved up to a level beyond the spatial grasp of political power. Perry Anderson's descriptive220 1974 ; definition of European feudalism, stressing its composite, polystructural, and variable character, and rooting its dynamics not only in the struggle over the and ertapenem.
M * rHre Baserda J a n Polhamuai Benjamin, to Merlsm H Millar, b o t h -~-L - : 1MT, J a n . Hlnea, H a r r Co., N , J t o Co, 1I81 O c t , Conoly, Minister 911 ; T h o 9rh t Hammell, Upper Freehold , 1166, D a e , 2 L.ydta Q. Haley, Upper Fraenold : ; , iS6f, i a p t , Oonnely, Minister G r e - Woallay, Ocean T o w .81 Curtli, M r , A b Miaa B a r Grtin, Wall Township 1667, J a n , 1 Aider Freeman, Minister 336 ; M o r boy, N , J t o 1167, J a n , g Hawkins Abraham, to Mary E , H o both, of M a t IMT, M a r , S ; Badle, Juatio * Seamones, McCharles, t o B-lan Morton -- iiiT, t-ab. B By W . Vanleer, Minister W a i BJliia V a n 1866, S i c . 221 ; Ti\Mor -is - Jeradera o f - , N ii?.T, . M o n row, o f R i 1|66, D e o , 1 .-- lies, Oct. M S m.
443454, 1990. 17. Manohar M, Hutchens E, and Coney E. Pulmonary haemodynamics in the exercising horse and their relationship to exercise-induced pulmonary haemorrhage. British Veterinary Journal 149: 419-428, 1993. Manohar M, and Goetz TE. Pulmonary vascular pressures of exercising Thoroughbred horses with and without endoscopic evidence of EIPH. Journal of Applied Physiology 81: 1589-1593, 1996. Manohar M, and Goetz TE and esmolol
Composed of an extracellular ligand-binding domain, a transmembrane domain, and an intracellular domain with a TK region.Altered or increased expression of EGFR has been observed in 6080% of patients with lung cancer and has been linked to disease progression, poor survival, poor response to therapy, development of resistance to cytotoxic agents, advanced tumor stage, and increased risk for metastasis.19 Overexpression of EGFR is most commonly found in squamous cell 84% ; , followed by large cell 68% ; and adenocarcinoma 65% ; .20 The inhibition of EGFR can therefore be accomplished upstream by blocking the ligand-binding domain with monoclonal antibodies i.e. cetuximab ; or downstream by interfering with signal transduction via TK by using small molecule TKIs i.e. erlotinib and gefitinib
Break PLENARY SESSION: Emerging Issues Regarding the Diagnostic Utility of Ballroom A Gene Expression Profiles in Breast Cancer Moderator: Ngina Lythcott Consumer Perspective Helen Schiff Molecular Profiling Guides Treatment of Breast Cancer Laura van't Veer A 21 Gene Assay to Predict Recurrence of Tamoxifen-Treated, Node-Negative Breast Cancer Steven Shak Stratification of Human Breast Cancer by mRNA Expression Profiling Cindy A. Wilson Gene Expression Markers Are "Continuous or Quantitative Variables" Gottfried E. Konecny An Epidemiologist Perspective: Rules of Evidence for Cancer Molecular-Marker Discovery David F. Ransohoff Break CONCURRENT SYMPOSIA SESSIONS III Symposium 14 - Estrogen as an Initiator of Breast Cancer and estramustine.
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Combined Celecoxib and Erlotinib in Advanced NSCLC After mixing, the sample was loaded on a diatomaceous earth extraction cartridge Argonaut, Redwood City, CA ; . The loaded cartridge was allowed to incubate 30 minutes, and the sample was eluted with t-butyl methyl ether. The organic fraction was evaporated to dryness under nitrogen at 35jC. Extracts were reconstituted in 150 AL of mobile phase, and 20 AL were injected. The high-performance liquid chromatography system consisted of a Leap CTC Pal autosampler and an Agilent 1100 series binary pump. Chromatographic separation of extracted plasma samples was done using a Waters, Symmetry C18 column 4.6 50 mm inner diameter, 3.5-Am particle size ; in isocratic mode at ambient temperature. The mobile phase consisted of 70% methanol, 30% 20 mmol L ammonium formate pH 4.8 ; , and was delivered at a flow rate of 1.0 mL min. Mass spectrometric detection was carried out using an Applied Biosystems MDS Sciex API 3000 triple quadrupole mass spectrometer Concord, Ontario, Canada ; , equipped with an atmospheric pressure chemical ionization source operating in positive ion mode under multiple reaction monitoring. The following transitions were monitored: m z 394.3 278.0 for OSI-774 and m z 408.4 292.0 for internal standard. Peak area ratios erlotinib peak area internal standard ; versus concentration were fitted to a linear regression equation, with 1 x 2 weighting. The regression equation was used to calculate concentrations of OSI-774 in the samples. The range of the assay was from 1.00 to 600 ng mL. EGFR mutation analysis. EGFR mutational analysis was done at the CLIA certified laboratory at the City of Hope Medical Center Duarte, CA ; . The laboratory routinely performs mutational analysis for a number of cancer predisposition syndromes. For this assay, tumor blocks or slides were submitted. Slides were reviewed by a board-certified pathologist who demarcated areas of tumor for dissection. Needle microdissection was done under a microscope, taking two representative areas from the region demarcated by the pathologist. These areas were digested overnight. Each dissected area was analyzed independently. Exons 18 to 21 the EGFR gene were amplified from the digested products by PCR. Negative controls were included to rule out contamination. The amplified products were directly sequenced using ABI's automated fluorescent sequencing kit and sequencer. The chromatogram data were then reviewed for changes and reported.
1. Ullrich A, Coussens L, Hayflick JS, et al. Human epidermal growth factor receptor cDNA sequence and aberrant expression of the amplified gene in A431 epidermoid carcinoma cells. Nature 1984; 309: 418 Ullrich A, Schlessinger J. Signal transduction by receptors with tyrosine kinase activity. Cell 1990; 61: 203 Faivre S, Djelloul S, Raymond E. New paradigms in anticancer therapy: targeting multiple signaling pathways with kinase inhibitors. Semin Oncol 2006; 33: 407 Gschwind A, Fischer OM, Ullrich A. The discovery of receptor tyrosine kinases: targets for cancer therapy. Nat Rev Cancer 2004; 4: 361 Perona R. Cell signalling: growth factors and tyrosine kinase receptors. Clin Transl Oncol 2006; 8: 77 Slamon DJ, Leyland-Jones B, Shak S, et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. N Engl J Med 2001; 344: 783 Romond EH, Perez EA, Bryant J, et al. Trastuzumab plus adjuvant chemotherapy for operable HER2-positive breast cancer. N Engl J Med 2005; 353: 1673 Piccart-Gebhart MJ, Procter M, Leyland-Jones B, et al. Trastuzumab after adjuvant chemotherapy in HER2-positive breast cancer. N Engl J Med 2005; 353: 1659 Reynolds NA, Wagstaff AJ. Cetuximab: in the treatment of metastatic colorectal cancer. Drugs 2004; 64: 109 discussion 19 21. 10. Perez-Soler R. Phase II clinical trial data with the epidermal growth factor receptor tyrosine kinase inhibitor erlotinib OSI-774 ; in non-smallcell lung cancer. Clin Lung Cancer 2004; 6 Suppl 1: S20 3. 11. Pollak MN. Insulin-like growth factors and neoplasia. Novartis Found Symp 2004; 262: 84 discussion 107. 12. Baserga R. Targeting the IGF-1 receptor: from rags to riches. Eur J Cancer 2004; 40: 2013 Bohula EA, Playford MP, Macaulay VM. Targeting the type 1 insulinlike growth factor receptor as anti-cancer treatment. Anticancer Drugs 2003; 14: 669 Sciacca L, Costantino A, Pandini G, et al. Insulin receptor activation by IGF-II in breast cancers: evidence for a new autocrine paracrine mechanism. Oncogene 1999; 18: 2471 Ullrich A, Gray A, Tam AW, et al. Insulin-like growth factor I receptor primary structure: comparison with insulin receptor suggests structural determinants that define hormonal specificity. EMBO J 1986; 5: 2503 Demeyts P, Wallach B, Christoffersen CT, et al. The insulin-like growth factor-I receptor--structure, ligand-binding mechanism and signal transduction. Horm Res 1994; 42: 152 and eszopiclone.
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Tyrosine kinase activity [7]. Among the most extensively investigated new drugs are gefitinib ZD 1839, Iressa, AstraZeneca, UK ; and erlotinib OSI 774, Tarceva, Genentech, USA ; , which are orally active selective EGFR tyrosine-kinase inhibitors EGFR-TKI ; that demonstrated antitumor activity in approximately 10% of unselected NSCLC [810]. Biological mechanisms underlying EGFR-TKI sensitivity and resistance have recently been identified. EGFR gene gain and activating EGFR gene mutations, particularly deletions in exon 19, were demonstrated to confer a sensitive phenotype [1113] and recent findings demonstrated that EGFR overexpressing patients are sensitive to the inhibitory effects of both gefitinib or erlotinib [11, 14]. Conversely, mutations in the KRAS gene or in exon 20 of the EGFR gene were demonstrated to be responsible for intrinsic or acquired TKI resistance, respectively [1517]. It is feasible that intrinsic or acquired resistance to TKIs may be related to the ability of tumor cells to utilize alternative.
At the May Pharmacy and Therapeutics Committee meeting, the following medications were added to the PDL: P.11 Antineoplastic Agents: Antineoplastic Agents Tarceva Erlotinib HCL ; 25, 150 and 200 mg. tablets. PA required. For oncologists only and ethionamide
[Chpt 4] But in the latter days it will come to pass, that the hill of the Lords house shall be set up higher then any mountains or hills: Yee the people shall praise unto it, and the multitude of the Gentiles shall hast them thither, saying: Come, let us go up the hill of the Lord, and to the house of the God of Jacob: that he may teach us his way, and that we may walk in his paths. For the law shall come out of Sion, and the word of God from Jerusalem, And shall give sentence among the multitude of the Heathen and reform the people of far countries: so that of their swords they shall make plowshares, and scythes of their spears. One people shall not lift up a sword against another, yee they shall no more learn to fight: but every man shall sit under his vineyard and under his fig tree, and no man to * fraie him away: for the mouth of the Lord of hosts hath spoken it. Therefore, whereas all the people have walked every man in the name of his own God, we will walk in the name of our God for ever.
Roleptics. For typical neuroleptics, mean 9.05 dose years SD 6.89, range 0.6019.36, median 6.74 for atypical neuroleptics, mean 0.93 dose years SD 1.53; range 04.77, median 0 ; . The remaining 10 patients had been exposed mostly to atypical drugs over the previous 2 years. Six of these 10 patients were treated exclusively with atypical neuroleptics clozapine, olanzapine, or risperidone ; during the follow-up period, while four had minimal exposure to typical neuroleptics primarily haloperidol this exposure occurred during the early part of the follow-up period in all cases. For atypical neuroleptics, mean 10.96 dose years SD 9.14, range 1.2527.76, median 7.18 ; , and for typical neuroleptics, mean 1.14 dose years SD 1.45, range 03.28, median 0 ; . When viewed as two separate groups in this manner, exposure to neuroleptics at intake for the two groups was as follows: group 1: N 13, typical neuroleptic mean 4.38 dose years SD 10.11, range 037.25, median 1.25 ; , atypical neuroleptic mean 0.25 dose years SD 0.88, range 03.17, median 0 group 2: N 10, typical neuroleptic mean 4.08 dose years SD 5.17, range 0.0915.00, median 1.61 ; , atypical neuroleptic mean 1.53 dose years SD 4.76, range 0 15.07, median 0 ; . There was no significant difference between the mean ages of patients in the two groups. Age at intake was as follows: group 1: N 13, age at first scan, mean 25.77 years SD 5.80, range 19.00 38.00, median 24.00 group 2: N 10, age at first scan, mean 25.30 years SD 6.98, range 18.00 41.00, median 23.50 ; . There was also no significant difference in the length of the time interval between the time 1 and time 2 scans across groups: group 1: N 13, time interval between first and follow-up scans, mean 2.12 years SD 0.54, range 1.183.67, median 2.12 group 2: N 10, time interval between first and followup scans, mean 2.21 years SD 0.18, range 2.00 2.61, median 2.17 ; . Change in basal ganglia volume over the 2-year interval was compared in these two groups by using a simple repeated measures analysis of variance. There was a significant group-by-time interaction F 12.92, df 1, 21, p 0.002 ; . This indicates that the changes over time differ for the two groups table 1 ; . Follow-up t tests showed a significant mean decrease in basal gan1202 and ethosuximide.
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Harper ME, Goddard L, Glynne-Jones E, Assender J, Dutkowski CM, Barrow D, Dewhurst OL, Wakelinh AE, Nicholson RI. Multiple responses to EGF receptor activation and their abrogation by a specific EGF receptor tyrosine kinase inhibitor. Prostate 2002; 52: 59-68. Herbst RS, Giaccone G, Schiller JH, Natale RB, Miller V, Manegold C, Scagliotti G, Rosell R, Oliff I, Reeves JA, Wolf MK, Krebs AD, Averbuch SD, Ochs JS, Grous J, Fandi A, Johnson DH. Gefitinib in combination with paclitaxel and carboplatin in advanced nonsmall-cell lung cancer: a Phase III trial-INTACT 2. J Clin Oncol 2004; 22: 785-794. Herbst RS, Prager D, Hermann R, Fehrenbacher L, Johnson BE, Sandler A, Kris MG, Tran HT, Klein P, Li X, Ramies D, Johnson DH, Miller VA. TRIBUTE: A phase III trial of erlotinib hydrochloride OSI-774 ; combined with carboplatin and paclitaxel chemotherapy in advanced non-small-cell lung cancer. J Clin Oncol 2005; 23: 5892-5899. Hofmann F, Garca-Echeverra C. Blocking insulin-like growth factor-I receptor as a strategy for targeting cancer. Drug Discov Today 2005; 10: 1041-1047. Hpfner M, Sutter AP, Beck NI, Barthel B, Maaser K, Jockers-Scherbl MC, Zeitz M, Scherbl H. Meta-iodobenzylguanidine induces growth inhibition and apoptosis of neuroendocrine gastrointestinal tumor cells. Int J Cancer 2002; 101: 210-216. Huang S, Armstrong EA, Benavente S, Chinnaiyan P, Harari PM. Dual-agent molecular targeting of the epidermal growth factor receptor EGFR ; : Combining anti-EGFR antibody with tyrosine kinase inhibitor. Cancer Res 2004; 64: 5355-5362. Huang SM, Bock JM, Harari PM. Epidermal growth factor receptor blockade with C225 modulates proliferation, apoptosis, and radiosensitivity in squamous cell carcinomas of the head and neck. Cancer Res 1999; 59: 1935-1940. Huang SM, Harari PM. Epidermal growth factor receptor inhibition in cancer therapy: Biology, rationale and preliminary clinical results. Invest New Drugs 1999; 17: 259-269. Hui AM, Makuuchi M, Li X. Cell cycle regulators and human hepatocarcinogenesis. Hepatogastroenterology 1998; 45: 1635-1642. Jakobisiak M, Golab J. Potential antitumor effects of statins. Int J Oncol 2003; 23: 1055-1069. Jiang Y, Rom WN, Yie TA, Chi CX, Tchou-Wong KM. Induction of tumor suppression and glandular differentiation of A549 lung carcinoma cells by dominant-negative IGF-I receptor. Oncogene 1999; 28: 60716077. Johnson GL, Lapadat R. Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases. Science 2002; 298: 1911-1912 and erlotinib.
1. Fukuoka M, Yano S, Giaccone G, et al. Multiinstitutional randomized phase II trial of gefitinib for previously treated patients with advanced non-smallcell lung cancer. J Clin Oncol 2003; 21: 2237 Kris MG, Natale RB, Herbst RS, et al. Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial. JAMA 2003; 290: 2149 Miller VA, Kris MG, Shah N, et al. Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer. J Clin Oncol 2004; 22: 1103 Janne PA, Gurubhagavatula S, Yeap BY, et al. Outcomes of patients with advanced non-small cell lung cancer treated with gefitinib ZD1839, `Iressa' ; on an expanded access study. Lung Cancer 2004; 44: 221 Haringhuizen A, van Tinteren H, Vaessen HF, Baas P, van Zandwijk N. Gefitinib as a last treatment option for non-small-cell lung cancer: durable disease control in a subset of patients. Ann Oncol 2004; 15: 786 Simon GR, Ruckdeschel JC, Williams C, et al. Gefitinib ZD1839 ; in previously treated advanced non-smallcell lung cancer: experience from a single institution. Cancer Control 2003; 10: 388 Argiris A, Mittal N. Gefitinib as first-line, compassionate use therapy in patients with advanced non-smallcell lung cancer. Lung Cancer 2004; 43: 317 Park J, Park BB, Kim JY, et al. Gefitinib ZD1839 ; monotherapy as a salvage regimen for previously treated advanced non-small cell lung cancer. Clin Cancer Res 2004; 10: 4383 Shepherd FA, Rodrigues Pereira J, Ciuleanu T, et al. Erlotinib in previously treated non-small-cell lung cancer. N Engl J Med 2005; 353: 123 Thatcher N, Chang A, Parikh P, et al. Gefitinib plus best supportive care in previously treated patients with refractory advanced non-small-cell lung cancer: results from a randomised, placebo-controlled, multicentre study Iressa Survival Evaluation in Lung Cancer ; . Lancet 2005; 366: 1527 Herbst RS, Prager D, Hermann R, et al. TRIBUTE: a phase III trial of erlotinib hydrochloride OSI-774 ; combined with carboplatin and paclitaxel chemotherapy in advanced non-small-cell lung cancer. J Clin Oncol 2005; 23: 5892 Paez JG, Janne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 2004; 304: 1497 Lynch TJ, Bell DW, Sordella R, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med 2004; 350: 2129 Pao W, Miller V, Zakowski M, et al. EGF receptor gene mutations are common in lung cancers from ``never smokers'' and are associated with sensitivity of tumors to gefitinib and erlotinib. Proc Natl Acad Sci U S A 2004; 101: 13306 Shigematsu H, Lin L, Takahashi T, et al. Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers. J Natl Cancer Inst 2005; 97: 339 Mitsudomi T, KosakaT, Endoh H, et al. Mutations of the epidermal growth factor receptor gene predict prolonged survival after gefitinib treatment in patients with non-small-cell lung cancer with postoperative recurrence. J Clin Oncol 2005; 23: 2513 Han SW, Kim TY, Hwang PG, et al. Predictive and prognostic impact of epidermal growth factor receptor mutation in non-small-cell lung cancer patients treated with gefitinib. J Clin Oncol 2005; 23: 2493 Marchetti A, Martella C, Felicioni L, et al. EGFR mutations in non-small-cell lung cancer: analysis of a large series of cases and development of a rapid and sensitive method for diagnostic screening with potential implications on pharmacologic treatment. J Clin Oncol 2005; 23: 857 Huang SF, Liu HP, Li LH, et al. High frequency of epidermal growth factor receptor mutations with complex patterns in non-small cell lung cancers related to gefitinib responsiveness in Taiwan. Clin Cancer Res 2004; 10: 8195 KosakaT, Yatabe Y, Endoh H, et al. Mutations of the epidermal growth factor receptor gene in lung cancer: biological and clinical implications. Cancer Res 2004; 64: 8919 Janne PA, Engelman JA, Johnson BE. Epidermal growth factor receptor mutations in non-small-cell lung cancer: implications for treatment and tumor biology. J Clin Oncol 2005; 23: 3227 Tsao MS, Sakurada A, Cutz JC, et al. Erlotinib in lung cancer: molecular and clinical predictors of outcome. N Engl J Med 2005; 353: 133 Cappuzzo F, Hirsch FR, Rossi E, et al. Epidermal growth factor receptor gene and protein and gefitinib sensitivity in non-small-cell lung cancer. J Natl Cancer Inst 2005; 97: 643 Wong C, DiCioccio RA, Allen HJ, Werness BA, Piver MS. Mutations in BRCA1 from fixed, paraffinembedded tissue can be artifacts of preservation. Cancer Genet Cytogenet 1998; 107: 21 Bernstein JL, Thompson WD, Casey G, et al. Comparison of techniques for the successful detection of BRCA1 mutations in fixed paraffin-embedded tissue. Cancer Epidemiol Biomarkers Prev 2002; 11: 809 Kobayashi S, Boggon TJ, Dayaram T, et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med 2005; 352: 786 Pao W, Miller VA, Politi KA, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005; 2: 1 Greulich H, Chen TH, Feng W, et al. Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants. PLoS Med 2005; 2: e313. 29. Hirsch FR, Varella-Garcia M, McCoy J, et al. Increased epidermal growth factor receptor gene copy number detected by fluorescence in situ hybridization associates with increased sensitivity to gefitinib in patients with bronchioloalveolar carcinoma subtypes: A Southwest Oncology Group Study. J Clin Oncol 2005; 23: 6838 Takano T, Ohe Y, Sakamoto H, et al. Epidermal growth factor receptor gene mutations and increased copy numbers predict gefitinib sensitivity in patients with recurrent non-small-cell lung cancer. J Clin Oncol 2005; 23: 6829 Cappuzzo F, Varella-Garcia M, Shigematsu H, et al. Increased HER2 gene copy number is associated with response to gefitinib therapy in epidermal growth factor receptor-positive non-small-cell lung cancer patients. J Clin Oncol 2005; 23: 5007 Engelman JA, Janne PA, Mermel C, et al. ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines. Proc Natl Acad Sci U S A 2005; 102: 3788 Fujimoto N, Wislez M, Zhang J, et al. High expression of ErbB family members and their ligands in lung adenocarcinomas that are sensitive to inhibition of epidermal growth factor receptor. Cancer Res 2005; 65: 11478 Sasaki H, Endo K, Konishi A, et al. EGFR Mutation status in Japanese lung cancer patients: genotyping analysis using LightCycler. Clin Cancer Res 2005; 11: 2924 Nagai Y, Miyazawa H, Huqun T, et al. Genetic heterogeneity of the epidermal growth factor receptor in non-small cell lung cancer cell lines revealed by a rapid and sensitive detection system, the peptide nucleic acid-locked nucleic acid PCR clamp. Cancer Res 2005; 65: 7276 Pan Q, Pao W, Ladanyi M. Rapid polymerase chain reaction-based detection of epidermal growth factor receptor gene mutations in lung adenocarcinomas. J Mol Diagn 2005; 7: 396 Janne PA, Borras AM, Kuang Y, et al. A rapid and sensitive enzymatic method for EGFR mutation screening. Clin Cancer Res 2006; 12: 751 Cortes-Funes H, Gomez C, Rosell R, et al. Epidermal growth factor receptor activating mutations in Spanish gefitinib-treated non-small-cell lung cancer patients. Ann Oncol 2005; 16: 1081 Taron M, Ichinose Y, Rosell R, et al. Activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor are associated with improved survival in gefitinib-treated chemorefractory lung adenocarcinomas. Clin Cancer Res 2005; 11: 5878 and etidronate.
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We did a phase II study of single-agent erlotinib as firstline therapy in patients with advanced NSCLC. We also did biological studies on tumor samples of patients entered in the study to identify patients who benefited most from treatment and etodolac
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