National Office and pages and or links will be made available to all branches and SIGs. The National Office is working very hard and the staff are doing a great job; we have had a very successful membership drive, the finances are now back in the black and the conference organisation is going really well. done Chris, Janette, Meg and Lena. I have just finished a national lecture tour organised by ASM and sponsored by Novartis it was great to be able to visit all the branches. I see an opportunity for ASM to repeat this exercise with other Australian speakers. It would be ideal if we could set up a national speaker The March issue of Microbiology Australia contained important information about the various awards and prizes available to ASM members. The closing date for most of these is 1 June 2004. I would like to encourage members to either apply for or to nominate a colleague for one of these awards for full details see theasm .au. The Annual Scientific Meeting and Exhibition offers an exciting programme covering all aspects of microbiology and registrations are now well advanced. Early bird registrations close on 30 June 2004 so don't be late. Abstract submissions should be made online and are due by 14 May 2004, so you may still have a chance to get one in. biochemical ID, mycology The and workshops on antibiotic resistance, parasitology will be of major interest to many laboratories. All details regarding the Sydney meeting are on the website asm2004 .au. While on websites, the ASM site is currently undergoing a major revision. A special thank you to Tom Riley who has recently stepped down from both the Editorial Board and as coordinator of our International Visitor Programme. Tom has unselfishly served the ASM in these roles for at least 15 years and has made a major contribution to the society. John MacKenzie is also standing down as a long term member of the Editorial Board and I also wish to acknowledge his worthwhile contributions. Mary Barton will take over the International Visitor Programme and I also wish to welcome Mary Barton and Bill Rawlinson to the Editorial Board of Microbiology Australia. Finally, I would also like to congratulate the Editorial Board, especially Ailsa Hocking Chair ; and Penny Bishop Editor ; of Microbiology Australia for also doing a great job. I, like many members, have really enjoyed reading MA and the quality and variety of the articles have been excellent. programme using Australian expertise to cover areas of interest to the members. Well Let me know if you have any questions posted: mon mar 27, 2006 5: post subject: tarceva xeloda.
John Crookshank. It was interesting to hear at first hand about the ship's first operational deployment. EGFR mutations in non-small cell lung cancer: Predictive and prognostic implications. Kenneth J. Hillan & David A. Eberhard, Genentech, Inc., South San Francisco CA USA Lung cancer is the most common cause of cancer death worldwide, and the majority of cases are associated with cigarette smoking. Non-small cell lung cancer NSCLC ; arising in smokers has a different spectrum of molecular abnormalities than does NSCLC arising in non-smokers, suggesting differences in molecular etiology, pathogenesis and possibly prognosis. For example, KRAS mutations occur in 20-40% of NSCLC, are strongly associated with smoking, and have been associated with poor prognosis in some studies but not in others. Molecular abnormalities in NSCLC also represent promising therapeutic targets, since present chemotherapies for advanced or metastatic NSCLC have modest efficacy and considerable side effects. The epidermal growth factor receptor EGFR ; is a receptor tyrosine kinase that is expressed in the majority of NSCLC. The efficacy of EGFR inhibitors in preclinical models together with their favorable toxicity profiles, have led to their clinical development in NSCLC and other indications. Erlotinib Tarceva ; and gefitinib Iressa ; are small-molecule inhibitors of the EGFR tyrosine kinase that showed activity in NSCLC as single agents in phase II trials. A US single arm phase II study of erlotinib demonstrated an objective response rate of 12.3%, and gefitinib provided response rates of 10.4% in non-Japanese patients and 27.5% in Japanese patients. Non-smokers have a markedly higher response rate than smokers. However, randomized phase III studies of gefitinib or erlotinib in combination with chemotherapy failed to demonstrate an increase in efficacy for EGFR inhibitors over chemotherapy alone. One suggested explanation for this may be that cytostatic agents could cause a schedule-dependent antagonism of cytotoxic drugs by inhibiting progression through the cell cycle and apoptosis. Alternatively, patients were not selected to enrich for likelihood of response to an EGFR inhibitor in these trials. In contrast to HER2 testing for trastuzumab therapy, EGFR expression does not predict for sensitivity to inhibitors in preclinical models or in tumors from treated patients, and hence there is no molecular method for patient selection. Recent reports have associated somatic mutations in the tyrosine kinase domain of EGFR in a subset of NSCLC with sensitivity of the tumors to gefitinib Lynch et al., 2004; Paez et al., 2004 ; . Paez et al. found tyrosine kinase domain mutations were restricted to EGFR out of the 47 tyrosine kinases tested ; in a panel of 119 lung cancers. The frequency of heterozygous mutations amino acid substitutions and deletions ; was found to be 2% in the American population and 26% in Japanese patients. Lynch et al. reported a prevalence of mutations of 8% 2 25 ; unselected patients. Overall, somatic mutations in EGFR were reported in 13 of patients who responded to gefitinib and in none of 11 patients who were treated and did not respond. Notably, patients with EGFR mutations had negative or remote smoking histories. In functional studies, the mutations resulted in increased activity of EGFR and increased sensitivity to inhibition by gefitinib. Thus, EGFR mutation may define a subset of tumors that are highly dependent on activated EGFR signaling and particularly responsive to EGFR inhibitor therapy. These initial studies did not present data regarding the prognostic significance of these activating EGFR mutations outside the setting of EGFR inhibitor treatment or whether the objective responses in EGFR mutants translate into increased survival. Notably, one of the published gefitinib-responsive patients lacked any mutations in EGFR exons 18-21, indicating that EGFR mutationsre not necessary for patients to derive clinical benefit from EGFR inhibitor therapy. Dr Kenneth Hillan Dr Kenneth Hillan came to Genentech in 1994 to study the role of hepatocyte growth factor in liver regeneration. He joined the Pathology department as a scientist in 1996, was promoted to director of Pathology in 1998, and was named senior director of Research Operations in 2001. In 2002, Hillan was promoted to vice president, Research Operations and Pathology. In July 2003, Dr Hillan was named vice president, Development Sciences. In this position, he is responsible for managing the collaboration between Research and Development as the company moves promising molecules from research into development. In addition, Dr Hillan manages the Research Pathology department and its ongoing work in oncology, immunology, vascular biology and other therapeutic areas. While at Genentech, Hillan's key research contributions have included the study of VEGF and EG-VEGF in experimental models and human disease, and the application of quantitative analysis of molecular markers in-situ in human tissue microarrays. These quantitative technologies have been used extensively as part of the selection of candidate antigens in the company's Tumor Antigen Project and are being applied in the study of molecular markers that might predict response to a number of Genentech's pipeline therapeutics. Dr Hillan is on the editorial advisory board of the Journal of Pathology and is an ad hoc reviewer for the Journal of Clinical Pathology and the American Journal of Pathology and Liver. He has published more than 40 articles in peer-reviewed journals. He also is an Honorary Professor of Molecular and Therapeutic Pathology at the University of Leeds.

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