PMID- 17457280 OWN - NLM STAT- MEDLINE DCOM- 20070618 LR - 20191110 IS - 0761-8417 (Print) IS - 0761-8417 (Linking) VI - 63 IP - 1 DP - 2007 Feb TI - [New biological treatments for lung cancer]. PG - 20-8 AB - Therapies targeted on cell signal pathways that control cell division and tumor angiogenesis have been developed over the last five years for non small cell lung cancer (NSCLC) with some amazing results, in subgroups of selected patients, predicting more significant success in the upcoming years. Compounds targeted on EGF tyrosine kinase receptor have been tested in large clinical phase 2 and 3 trials including thousands of patients. Their efficacy has been proved, in second and third line trials, after first line cisplatin-based chemotherapy for non-mucinous adenocarcinoma in non-smokers, women and Asian patients. Response rates vary from 10% in non selected Caucasian patients to 40% in non-smoking Asian patients with long survivals. Therapeutic targeting improves success rates, either relying on EGFR gene amplification detection by FISH, or search for EGFR tyrosine kinase domain mutations. Commercial kits are available for routine molecular diagnosis of domain mutations potentially enabling molecular targeting in addition to clinical targeting. Angiogenesis inhibitors, especially monoclonal antibody to VEGF, bevacizumab, have also been developed in the last few years. Bevacizumab associated with classical cytotoxic chemotherapy led, in selected patients (with non squamous cell lung cancer and no past history of cardiovascular disease) to an increase of median survival to more than 12 months with tolerable toxicity. Other drugs that have both anti-EGFR activity and anti-angiogenic properties will be soon developed, since future bioactive anti-cancer drugs will probably be multi-targeted drugs. FAU - Zalcman, G AU - Zalcman G AD - Service de Pneumologie, UFR de Medecine Caen-Basse Normandie, CHU de Caen, avenue de la Cote-de-Nacre, 14033 Caen Cedex 05. zalcman-g@chu-caen.fr FAU - Richard, N AU - Richard N FAU - Bergot, E AU - Bergot E LA - fre PT - Journal Article PT - Review TT - Les nouvelles therapeutiques biologiques du cancer bronchique. PL - France TA - Rev Pneumol Clin JT - Revue de pneumologie clinique JID - 8406312 RN - 0 (Angiogenesis Inhibitors) RN - 0 (Antibodies, Monoclonal) RN - 0 (Antibodies, Monoclonal, Humanized) RN - 0 (Antineoplastic Agents) RN - 0 (Protein Kinase Inhibitors) RN - 0 (Quinazolines) RN - 0 (Vascular Endothelial Growth Factor A) RN - 2S9ZZM9Q9V (Bevacizumab) RN - DA87705X9K (Erlotinib Hydrochloride) RN - EC 2.7.10.1 (ErbB Receptors) RN - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases) RN - S65743JHBS (Gefitinib) SB - IM MH - Angiogenesis Inhibitors/*therapeutic use MH - Antibodies, Monoclonal/administration & dosage/*therapeutic use MH - Antibodies, Monoclonal, Humanized MH - Antineoplastic Agents/administration & dosage/*therapeutic use MH - Bevacizumab MH - Biopsy MH - Clinical Trials as Topic MH - Clinical Trials, Phase II as Topic MH - Clinical Trials, Phase III as Topic MH - ErbB Receptors/*antagonists & inhibitors/genetics MH - Erlotinib Hydrochloride MH - Female MH - Forecasting MH - Gefitinib MH - Humans MH - Lung/pathology MH - Lung Neoplasms/*drug therapy/genetics/mortality/pathology MH - Male MH - Mutation MH - Patient Selection MH - Polymerase Chain Reaction MH - Prospective Studies MH - Protein Kinase Inhibitors/administration & dosage/*therapeutic use MH - Quinazolines/administration & dosage/therapeutic use MH - Receptor Protein-Tyrosine Kinases/antagonists & inhibitors MH - Survival Analysis MH - Treatment Outcome MH - Vascular Endothelial Growth Factor A/*antagonists & inhibitors RF - 40 EDAT- 2007/04/26 09:00 MHDA- 2007/06/19 09:00 CRDT- 2007/04/26 09:00 PHST- 2007/04/26 09:00 [pubmed] PHST- 2007/06/19 09:00 [medline] PHST- 2007/04/26 09:00 [entrez] AID - MDOI-RPC-02-2007-63-1-0761-8417-101019-200520001 [pii] AID - 10.1016/s0761-8417(07)90085-1 [doi] PST - ppublish SO - Rev Pneumol Clin. 2007 Feb;63(1):20-8. doi: 10.1016/s0761-8417(07)90085-1.