Mutational analysis of K-RAS and EGFR implicates K-RAS as a resistance marker in the Southwest Oncology Group (SWOG) trial S0126 of bronchioalveolar carcinoma (BAC) patients (pts) treated with gefitinib

Gumerlock, Paul H.; Holland, William; Chen, H.; Franklin, W.; Hirsch, Fred R.; Mack, Philip C.; Davies, Angela M.; McCoy, Jason; West, Howard; Gandara, David R.

doi:10.1200/jco.2005.23.16_suppl.7008

Cited by 28 publications

(20 citation statements)

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“…In addition, a mutation in the K-ras gene, which mediates EGFR signaling, may also confer resistance to TKIs [28,79]. If confirmed, these findings suggest that screening for such mutations may identify patients who are more, or less, likely to respond to gefitinib.…”

Section: Gefitinibmentioning

confidence: 93%

Clinical Implications of EGFR Expression in the Development and Progression of Solid Tumors: Focus on Non-Small Cell Lung Cancer

Ettinger

2006

The Oncologist

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Section: Gefitinibmentioning

confidence: 93%

Clinical Implications of EGFR Expression in the Development and Progression of Solid Tumors: Focus on Non-Small Cell Lung Cancer

Ettinger

2006

The Oncologist

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“…Recent analysis from BR.21 study has suggested that there was an unusually high EGFR mutation rate (23% of the 177 patients for whom tumour tissue was adequate for the study), with a low positive predictive value (16%) and a higher response rate (20% versus 2.4%) in patients with a high versus a low EGFR copy number, respectively [77]. Dr. Paul Gumerlock has also reported a response rate in 23% of patients with an EGFR mutation versus 13% of those with wild-type EGFR, and in 26% of those with a high copy number versus 11% of those with a low one, with k-ras mutations being a possible resistance marker for response [78]. At the same time, higher results (53% to 100%) were reported by other groups regarding the positive predictive role of an EGFR mutation [79][80][81].…”

Section: Other Egfr-tkismentioning

confidence: 94%

Targeted Therapies for Non-Small Cell Lung Cancer

Papaetis

Roussos²,

Syrigos³

2007

CPD

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Conventional therapy for non-small cell lung cancer (NSCLC) has reached a plateau in increasing patient survival and overall prognosis still remains dismal. Advances in the knowledge of molecular events governing oncogenesis has led to a number of novel agents targeting specific pathways critical for tumour growth and survival. In the present paper we have thoroughly reviewed the existing evidence of novel agents currently studied in clinical trials, focusing on epidermal growth factor receptor family inhibitors, angiogenesis inhibitors, cyclooxygenase-2 inhibitors, Bcl-2 targeted agents, protein kinase C inhibitors, proteasome inhibitors, farnesyl transferase inhibitors and retinoids. Although erlotinib monotherapy in the second or third line setting and bevacizumab combined with conventional chemotherapy as a frontline therapy manage to prolong the life of patients with NSCLC, there is still much to be learned about the proper design of clinical trials and the selection of patient population enrolled in them. Multi-targeted therapy still remains the most attractive avenue for future treatment strategies.

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“…Such characteristics are likely to be linked to molecular differences in EGFR or its associated signaling pathways, but these differences have not yet been clearly identified. Relationships between expression of EGFR, pMAPK, and pAkt and response to EGFR TKIs also remain to be firmly established as results have been contradictory [65][66][67][68][69][70][71][72], but there is some evidence that amplification of the EGFR gene may be linked to a higher likelihood of response and extended survival for patients with NSCLC [73,74]. Recent findings also suggest that somatic mutations in the EGFR tyrosine kinase domain may predict for good response to erlotinib and gefitinib treatment [66,73,[75][76][77][78][79], whereas K-ras mutations may be associated with poor clinical outcome for these patients [66,73].…”

Section: Erlotinibmentioning

confidence: 95%

New directions in the management of advanced pancreatic cancer: a review

Rocha-Lima¹

2008

Anti-Cancer Drugs

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Complete surgical resection is the only potentially curative option for pancreatic cancer. However, most patients have advanced/metastatic disease at the time of diagnosis, or will relapse after surgery. Systemic chemotherapy is only palliative. Gemcitabine-based therapy is an acceptable standard for unresectable locally advanced/metastatic pancreatic cancer, but average median survival is only 6 months. The addition of other chemotherapies (including other antimetabolites, platinum, and topoisomerase I inhibitors) or targeted therapies (farnesyl transferase inhibitors, metalloproteinase inhibitors, cetuximab and bevacizumab) to gemcitabine has failed to improve outcome. The combination of gemcitabine and erlotinib, a small-molecule tyrosine kinase inhibitor of the human epidermal growth factor receptor, was recently approved by the US/European authorities for use in advanced disease. In a phase III trial, the combination demonstrated a significant improvement in overall survival compared with gemcitabine monotherapy. Positive efficacy results have also been observed in a phase III trial, favoring the addition of capecitabine to gemcitabine compared with gemcitabine alone. This review focuses on the recent developments in systemic treatment, and discusses how novel agents might be incorporated into future treatment strategies for pancreatic cancer.

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Mutational analysis of K-RAS and EGFR implicates K-RAS as a resistance marker in the Southwest Oncology Group (SWOG) trial S0126 of bronchioalveolar carcinoma (BAC) patients (pts) treated with gefitinib

Cited by 28 publications

References 0 publications

Clinical Implications of EGFR Expression in the Development and Progression of Solid Tumors: Focus on Non-Small Cell Lung Cancer

Clinical Implications of EGFR Expression in the Development and Progression of Solid Tumors: Focus on Non-Small Cell Lung Cancer

Targeted Therapies for Non-Small Cell Lung Cancer

New directions in the management of advanced pancreatic cancer: a review

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