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• W4238604577 abstract "Primary lung cancer is the most common malignancy after non-melanocytic skin cancer with deaths from lung cancer exceeding those from any other type of malignancy worldwide [1.Jemal A. Bray F. Center M.M. et al.Global cancer statistics.CA Cancer J Clin. 2011; 61: 69-90Crossref PubMed Scopus (29831) Google Scholar]. While it has been the most important cause of cancer mortality in men since the 1960s, it has equalled breast cancer as a cause of mortality in women since the 1990s. To date, prevention and smoking cessation are still the main methods to reduce the death toll [2.Field J.K. Oudkerk M. Pedersen J.H. Duffy S.W. Prospects for population screening and diagnosis of lung cancer.Lancet. 2013; 382: 732-741Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar]. Lung cancer is still increasing both in incidence and mortality worldwide. In countries with effective tobacco control measures, the incidence of new lung cancer has begun to decline in men and is reaching a plateau for women [3.Malvezzi M. Bertuccio P. Levi F. et al.European cancer mortality predictions for the year 2012.Ann Oncol. 2012; 23: 1044-1052Abstract Full Text Full Text PDF PubMed Scopus (131) Google Scholar, 4.International Agency for Research on Cancer (IARC)http://www.iarc.fr/ (23 May 2014, date last accessed)Google Scholar]. In the European Union in 2013, lung cancer mortality fell in men (-6%) compared with 2009 while cancer death rates in women are increasing (+7%) and approaching those of men [5.Malvezzi M. Bertuccio P. Levi F. et al.European cancer mortality predictions for the year 2013.Ann Oncol. 2013; 24: 792-800Abstract Full Text Full Text PDF PubMed Scopus (284) Google Scholar]. Non-small-cell lung cancers (NSCLC) account for 85%–90% of lung cancers, while small-cell lung cancer (SCLC) has been decreasing in frequency in many countries over the last two decades [1.Jemal A. Bray F. Center M.M. et al.Global cancer statistics.CA Cancer J Clin. 2011; 61: 69-90Crossref PubMed Scopus (29831) Google Scholar]. Smoking is the main cause of lung cancer, responsible for more than 80% of cases. The observed variations in lung cancer rates across countries largely reflect differences in the stage and degree of the tobacco epidemic with reported crude incidence rates between 2/100 000–80/100 000 and 1/100 000–39/100 000 for men and women, respectively. There are several other known risk factors including exposure to asbestos, arsenic, radon, and non-tobacco-related polycyclic aromatic hydrocarbons, and interesting hypotheses about indoor air pollution (e.g. coal-fuelled stoves and cooking fumes) suspected to contribute to the relatively high burden of non-smoking-related lung cancer in women in some countries. Prevalence of lung cancer in females without a history of tobacco smoking is estimated to represent 19% compared with 9% of male lung carcinoma in the United States [6.Wakelee H.A. Chang E.T. Gomez S.L. et al.Lung cancer incidence in never smokers.J Clin Oncol. 2007; 25: 472-478Crossref PubMed Scopus (404) Google Scholar]. Women are over-represented among younger patients, raising the question of gender-specific differences in the susceptibility to lung carcinogens [7.Edwards B.K. Brown M.L. Wingo P.A. et al.Annual report to the nation on the status of cancer, 1975–2002, featuring population-based trends in cancer treatment.J Natl Cancer Inst. 2005; 97: 1407-1427Crossref PubMed Scopus (832) Google Scholar]. In recent times, an increase in the proportion of NSCLC patients who are never smokers has been observed, especially in Asian countries [8.Toh C.K. Gao F. Lim W.T. et al.Never-smokers with lung cancer: epidemiologic evidence of a distinct disease entity.J Clin Oncol. 2006; 24: 2245-2251Crossref PubMed Scopus (290) Google Scholar]. These new epidemiological data have resulted in ‘non-smoking-associated lung cancer’ being considered a distinct disease entity, where specific molecular and genetic tumour characteristics are being recognised. Therapeutic decisions for NSCLC patients rely on tumour subtype definition. Immunohistochemistry (IHC) should be used to reduce the NSCLC-NOS (not otherwise specified) rate to under 10% of cases diagnosed [9.Travis W.D. Brambilla E. Noguchi M. et al.International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society: international multidisciplinary classification of lung adenocarcinoma: executive summary.Proc Am Thorac Soc. 2011; 8: 381-385Crossref PubMed Scopus (391) Google Scholar]. Obtaining adequate tissue material for histological diagnosis and molecular testing is important in order to allow individual treatment decisions. Re-biopsy at disease progression may be considered [10.Sequist L.V. Waltman B.A. Dias-Santagata D. et al.Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors.Sci Transl Med. 2011; 3: 75ra26Crossref PubMed Scopus (2602) Google Scholar, 11.Kerr K.M. Bubendorf L. Edelman M.J. et al.2nd ESMO Consensus Conference on Lung Cancer: pathology and molecular biomarkers for non-small-cell lung cancer.Ann Oncol. 2014; 25: 1681-1690Abstract Full Text Full Text PDF PubMed Scopus (222) Google Scholar]. Pathological diagnosis should generally be made according to the World Health Organisation (WHO) classification. The International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society (IASLC/ATS/ERS) classification document on adenocarcinoma, however, provides new recommendations and also addresses important issues not covered by the current WHO classification concerning small biopsy samples and cytology. Adoption of these recommendations is strongly advised [9.Travis W.D. Brambilla E. Noguchi M. et al.International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society: international multidisciplinary classification of lung adenocarcinoma: executive summary.Proc Am Thorac Soc. 2011; 8: 381-385Crossref PubMed Scopus (391) Google Scholar], and will be integrated into the revised 2015 WHO classification. Genetic alterations which are key oncogenic events have been identified in numerous small subsets of NSCLC. Two of these alterations have been validated as reliable targets for selective pathway directed systemic therapy. The opportunity of applying systemic molecular-based targeted approaches for other driver alterations (such as ROS1, BRAF, HER2, and RET) is currently under evaluation [11.Kerr K.M. Bubendorf L. Edelman M.J. et al.2nd ESMO Consensus Conference on Lung Cancer: pathology and molecular biomarkers for non-small-cell lung cancer.Ann Oncol. 2014; 25: 1681-1690Abstract Full Text Full Text PDF PubMed Scopus (222) Google Scholar, 12.Besse B. Adjei A. Baas P. et al.2nd ESMO Consensus Conference on Lung Cancer: non-small-cell lung cancer first-line/second and further lines of treatment in advanced disease.Ann Oncol. 2014; 25: 1475-1484Abstract Full Text Full Text PDF PubMed Scopus (189) Google Scholar]. Activating (sensitising) epidermal growth factor receptor (EGFR) mutations are predictive for response to the EGFR tyrosine kinase inhibitors (TKIs) gefitinib, erlotinib, and afatinib resulting, in this context, in an improved response rate (RR), progression-free survival (PFS), and quality of life (QoL) as well as a better tolerability when compared with first-line chemotherapy, as demonstrated in several phase III randomised trials. The incidence of EGFR mutations in the Caucasian population is about 10% and is higher in never smokers, adenocarcinoma subtype, and women. Prevalence has also been shown to be higher in East-Asian patients. EGFR mutation testing is recommended in all patients with advanced NSCLC of a non-squamous subtype [I, A]. Testing is not recommended in patients with a confident diagnosis of squamous cell carcinoma, except in never/former light smokers (<15 packs per year) [IV, A] [13.Rekhtman N. Paik P.K. Arcila M.E. et al.Clarifying the spectrum of driver oncogene mutations in biomarker-verified squamous carcinoma of lung: lack of EGFR/KRAS and presence of PIK3CA/AKT1 mutations.Clin Cancer Res. 2012; 18: 1167-1176Crossref PubMed Scopus (308) Google Scholar]. It should be systematically analysed—with a validated mutation detection platform in a laboratory participating in an external quality assurance scheme—in all such patient subgroups [V, A]. Choice of methodology will vary but should provide the test sensitivity required for the tumour content of the sample, and provide an adequate coverage of all clinically relevant mutations [11.Kerr K.M. Bubendorf L. Edelman M.J. et al.2nd ESMO Consensus Conference on Lung Cancer: pathology and molecular biomarkers for non-small-cell lung cancer.Ann Oncol. 2014; 25: 1681-1690Abstract Full Text Full Text PDF PubMed Scopus (222) Google Scholar]. Laboratories should validate their practice internally and through external quality assurance programmes. The anaplastic lymphoma kinase (ALK) fusion genes have been identified as important oncogenic drivers [14.Kwak E.L. Bang Y.J. Camidge D.R. et al.Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer.N Engl J Med. 2010; 363: 1693-1703Crossref PubMed Scopus (3743) Google Scholar]. ALK fusion is encountered more frequently in never smokers, the adenocarcinoma subtype, and in younger patients, representing an incidence of around 5% in adenocarcinomas [15.Shaw A.T. Yeap B.Y. Mino-Kenudson M. et al.Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.J Clin Oncol. 2009; 27: 4247-4253Crossref PubMed Scopus (1588) Google Scholar]. ALK activity can be effectively targeted by the ALK TKIs, and routine testing for ALK rearrangements is now a standard of care. Testing should focus on the same group of patients selected as for EGFR mutation [II, A]. Testing should be carried out, if at all possible, in parallel with EGFR mutation analysis. Currently, the standard test for detecting ALK fusion remains the break-apart fluorescence in situ hybridisation (FISH) test. A multiplex polymerase chain reaction (PCR) approach may be successful but requires an adequate coverage of the many possible fusion genes now recognised and is challenged by the availability of adequate quality nucleic acid from typical samples, and by the methodology itself. High sensitivity IHC has been shown to have a high positive and negative predictive value for the presence and absence, respectively, of ALK fusion and, while not a recognised primary biomarker for ALK TKI therapy, it is widely used to screen patients for possible ALK FISH testing. Next-generation sequencing approaches for detecting fusion genes are in development. A complete history including smoking history and comorbidities, weight loss, performance status (PS), and physical examination must be recorded. Standard tests include routine haematology, renal and hepatic function, and bone biochemistry tests. Routine use of serum markers—such as carcinoembryonic antigen (CEA)—is not recommended. Contrast-enhanced computed tomography (CT) scan of the chest and upper abdomen should be carried out.•Imaging of the central nervous system (CNS) is reserved for patients with neurological symptoms or signs. Magnetic resonance imaging (MRI) is more sensitive than CT scan.•If metastatic disease has been shown on the CT scan of the chest and upper abdomen or on brain imaging, other imaging is only necessary when it might impact treatment.•If bone metastases are clinically suspected, bone imaging is required. Positron emission tomography (PET), CT, and bone scan are helpful for the systemic screening for bone metastasis with a slightly higher sensitivity for PET [16.Wu Y. Li P. Zhang H. et al.Diagnostic value of fluorine 18 fluorodeoxyglucose positron emission tomography/computed tomography for the detection of metastases in non-small-cell lung cancer patients.Int J Cancer. 2013; 132: E37-E47Crossref PubMed Scopus (71) Google Scholar]. MRI might be useful to document and describe a localised bone metastasis.•Fluorodeoxyglucose (FDG)–PET-CT scan offers the highest sensitivity for mediastinal lymph nodes and distant metastasis assessment. NSCLC is staged according to the American Joint Committee on Cancer (AJCC)/Union for International Cancer Control (UICC) system (7th edition) and is grouped into the stage categories shown in Tables 1 and 2. Measurement of lesions should follow Response Evaluation Criteria in Solid Tumors (RECIST) criteria v1.1 [17.Eisenhauer E.A. Therasse P. Bogaerts J. et al.New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1).Eur J Cancer. 2009; 45: 228-247Abstract Full Text Full Text PDF PubMed Scopus (16946) Google Scholar].Table 1AJCC/UICC TNM staging system, 7th edition (from Edge SB, Byrd DR, Compton CC, eds. AJCC Cancer Staging Handbook. 7th ed. New York, NY.: Springer, 2010)Primary Tumor (T)TXPrimary tumor cannot be assessed, or tumor proven by the presence of malignant cells in sputum or bronchial washings but not visualized by imaging or bronchoscopyT0No evidence of primary tumorTisCarcinoma in situT1Tumor 3 cm or less in greatest dimension, surrounded by lung or visceral pleura, without bronchoscopic evidence of invasion more proximal than the lobar bronchus (i.e., not in the main bronchus)*The uncommon superficial spreading tumor of any size with its invasive component limited to the bronchial wall, which may extend proximally to the main bronchus, is also classified as T1a. T1aTumor 2 cm or less in greatest dimension T1bTumor more than 2 cm but 3 cm or less in greatest dimensionT2Tumor more than 3 cm but 7 cm or less or tumor with any of the following features (T2 tumors with these features are classified T2a if 5 cm or less); Involves main bronchus, 2 cm or more distal to the carina; Invades visceral pleura (PL1 or PL2); Associated with atelectasis or obstructive pneumonitis that extends to the hilar region but does not involve the entire lung T2aTumor more than 3 cm but 5 cm or less in greatest dimension T2bTumor more than 5 cm but 7 cm or less in greatest dimensionT3Tumor more than 7 cm or one that directly invades any of the following: parietal pleural (PL3) chest wall (including superior sulcus tumors), diaphragm, phrenic nerve, mediastinal pleura, parietal pericardium; or tumor in the main bronchus (less than 2 cm distal to the carina*The uncommon superficial spreading tumor of any size with its invasive component limited to the bronchial wall, which may extend proximally to the main bronchus, is also classified as T1a. but without involvement of the carina; or associated atelectasis or obstructive pneumonitis of the entire lung or separate tumor nodule(s) in the same lobeT4Tumor of any size that invades any of the following: mediastinum, heart, great vessels, trachea, recurrent laryngeal nerve, esophagus, vertebral body, carina, separate tumor nodule(s) in a different ipsilateral lobeRegional Lymph Nodes (N)NXRegional lymph nodes cannot be assessedN0No regional lymph node metastasesN1Metastasis in ipsilateral peribronchial and/or ipsilateral hilar lymph nodes and intrapulmonary nodes, including involvement by direct extensionN2Metastasis in ipsilateral mediastinal and/or subcarinal lymph node(s)N3Metastasis in contralateral mediastinal, contralateral hilar, ipsilateral or contralateral scalene, or supraclavicular lymph node(s)Distant Metastasis (M)M0No distant metastasisM1Distant metastasisM1aSeparate tumour nodule(s) in a contralateral tumor with pleural nodules or malignant pleural (or pericardial) effusion**Most pleural (and pericardial) effusions with lung cancer are due to tumor. In a few patients, however, multiple cytopathologic examinations of pleural (pericardial) fluid are negative for tumor, and the fluid is nonbloody and is not an exudate. Where these elements and clinical judgment dictate that the effusion is not related to the tumor, the effusion should be excluded as a staging element and the patient should be classified as M0.M1bDistant metastasisUsed with the permission of the American Joint Committee on Cancer (AJCC), Chicago, Illinois. The original source for this material is the AJCC Cancer Staging Handbook, Seventh Edition (2010) published by Springer Science and Business Media LLC, www.springerlink.com.* The uncommon superficial spreading tumor of any size with its invasive component limited to the bronchial wall, which may extend proximally to the main bronchus, is also classified as T1a.** Most pleural (and pericardial) effusions with lung cancer are due to tumor. In a few patients, however, multiple cytopathologic examinations of pleural (pericardial) fluid are negative for tumor, and the fluid is nonbloody and is not an exudate. Where these elements and clinical judgment dictate that the effusion is not related to the tumor, the effusion should be excluded as a staging element and the patient should be classified as M0. Open table in a new tab Table 2Anatomic stage/prognostic groups accoding to the AJCC/UICC TNM staging system, 7th edition (from Edge SB, Byrd DR, Compton CC, eds. AJCC Cancer Staging Handbook. 7th ed. New York, NY.: Springer, 2010)Anatomic stage/prognostic groupsOccult carcinomaTXN0M0Stage 0TisN0M0Stage IATla,bN0M0Stage IBT2aN0M0Stage IIAT2bN0M0Tla,bN1M0T2aN1M0Stage IIBT2bN1M0T3N0M0Stage IIIATla,b, T2a,bN2M0T3N1, N2M0T4N0, N1M0Stage IIIBT4N2M0Any TN3M0Stage IVAny TAny NMlUsed with the permission of the American Joint Committee on Cancer (AJCC), Chicago, Illinois. The original source for this material is the AJCC Cancer Staging Handbook, Seventh Edition (2010) published by Springer Science and Business Media LLC, http://www.springerlink.com. Open table in a new tab Used with the permission of the American Joint Committee on Cancer (AJCC), Chicago, Illinois. The original source for this material is the AJCC Cancer Staging Handbook, Seventh Edition (2010) published by Springer Science and Business Media LLC, www.springerlink.com. Used with the permission of the American Joint Committee on Cancer (AJCC), Chicago, Illinois. The original source for this material is the AJCC Cancer Staging Handbook, Seventh Edition (2010) published by Springer Science and Business Media LLC, http://www.springerlink.com. In the presence of a solitary metastatic lesion on imaging studies, including pleural and pericardial effusion, efforts should be made to obtain a cytological or histological confirmation of stage IV disease. An evaluation of resectability or the suitability of high-dose radiotherapy with curative intent should be made at least in the context of a solitary brain or adrenal lesion or oligometastatic disease confined to the lungs. The treatment strategy should take into account histology, molecular pathology, age, PS, comorbidities, and patient's preferences. Treatment decisions should ideally be discussed within a multidisciplinary tumour board. Systemic therapy should be offered to all stage IV NSCLC patients with a PS 0–2 [I, A]. In any stage of NSCLC, smoking cessation should be highly encouraged because it improves outcome, and as smoking may interact with systemic therapy [II, A] [18.Baser S. Shannon V.R. Eapen G.A. et al.Smoking cessation after diagnosis of lung cancer is associated with a beneficial effect on performance status.Chest. 2006; 130: 1784-1790Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar]. For example, smoking reduces erlotinib bioavailability [19.Hughes A.N. O'Brien M.E. Petty W.J. et al.Overcoming CYP1A1/1A2 mediated induction of metabolism by escalating erlotinib dose in current smokers.J Clin Oncol. 2009; 27: 1220-1226Crossref PubMed Scopus (134) Google Scholar]. Platinum-based doublet chemotherapy prolongs survival and improves QoL in patients with PS 0–2 [I, A]. Chemotherapy should be initiated while the patient maintains a good PS. For most patients, four cycles of chemotherapy are recommended, notably when maintenance treatment is considered, with a maximum of six cycles [20.Park J.O. Kim S.W. Ahn J.S. et al.Phase III trial of two versus four additional cycles in patients who are nonprogressive after two cycles of platinum-based chemotherapy in non small-cell lung cancer.J Clin Oncol. 2007; 25: 5233-5239Crossref PubMed Scopus (175) Google Scholar] [II, B]. Several regimens have shown comparable efficacy [21.Schiller J.H. Harrington D. Belani C.P. et al.Comparison of four chemotherapy regimens for advanced non-small-cell lung cancer.N Engl J Med. 2002; 346: 92-98Crossref PubMed Scopus (4735) Google Scholar]. The expected toxicity profile should contribute to the selection of the chemotherapy regimen, taking into account that:•Meta-analyses have shown higher RRs for cisplatin combinations when compared with carboplatin combinations. The overall survival (OS) was significantly superior for cisplatin in the subgroup of non-squamous tumours and in patients treated with third-generation regimens, including gemcitabine and taxanes in one meta-analysis [I, B] [22.Ardizzoni A. Boni L. Tiseo M. et al.Cisplatin- versus carboplatin-based chemotherapy in first-line treatment of advanced non-small-cell lung cancer: an individual patient data meta-analysis.J Natl Cancer Inst. 2007; 99: 847-857Crossref PubMed Scopus (547) Google Scholar]. Cisplatin-based chemotherapy is associated with more digestive, neuro-, and nephrotoxicity, while hematotoxicity is more often observed with carboplatin.•Pemetrexed-based combination chemotherapy represents a therapeutic option in patients with advanced non-squamous NSCLC based on the results of a recent meta-analysis that showed a slight but significant survival benefit compared with gemcitabine- or docetaxel-based combinations and of a pre-planned subgroup analysis of a large randomised phase III trial [II, A] [23.Li M. Zhang Q. Fu P. et al.Pemetrexed plus platinum as the first-line treatment option for advanced non-small cell lung cancer: a meta-analysis of randomized controlled trials.PLoS One. 2012; 7: e37229Crossref PubMed Scopus (50) Google Scholar, 24.Scagliotti G.V. Parikh P. von Pawel J. et al.Phase III study comparing cisplatin plus gemcitabine with cisplatin plus pemetrexed in chemotherapy-naive patients with advanced-stage non-small-cell lung cancer.J Clin Oncol. 2008; 26: 3543-3551Crossref PubMed Scopus (2831) Google Scholar]. Pemetrexed use should be restricted to non-squamous NSCLC in any line of treatment [I, A] [25.Scagliotti G. Hanna N. Fossella F. et al.The differential efficacy of pemetrexed according to NSCLC histology: a review of two phase III studies.Oncologist. 2009; 14: 253-263Crossref PubMed Scopus (637) Google Scholar, 26.Ciuleanu T. Brodowicz T. Zielinski C. et al.Maintenance pemetrexed plus best supportive care versus placebo plus best supportive care for non-small-cell lung cancer: a randomised, double-blind, phase 3 study.Lancet. 2009; 374: 1432-1440Abstract Full Text Full Text PDF PubMed Scopus (1027) Google Scholar].•The survival benefit of carboplatin in combination with pemetrexed has been investigated in an exploratory subgroup analysis of a recent meta-analysis, where the survival benefit for pemetrexed plus platinum held true for cisplatin-containing regimens but not carboplatin-based regimens [23.Li M. Zhang Q. Fu P. et al.Pemetrexed plus platinum as the first-line treatment option for advanced non-small cell lung cancer: a meta-analysis of randomized controlled trials.PLoS One. 2012; 7: e37229Crossref PubMed Scopus (50) Google Scholar]. However, there is no prospective randomised study available investigating this question.•According to a randomised clinical trial, bevacizumab improves OS when combined with paclitaxel–carboplatin regimens in patients with non-squamous histology and PS 0–1, and may be offered after exclusion of contraindications [I, A] [27.Sandler A. Gray R. Perry M.C. et al.Paclitaxel-carboplatin alone or with bevacizumab for non-small-cell lung cancer.N Engl J Med. 2006; 355: 2542-2550Crossref PubMed Scopus (5143) Google Scholar]. Recently, adding bevacizumab to carboplatin and paclitaxel chemotherapy significantly improved PFS in 276 Chinese patients with non-squamous NSCLC, while OS data are pending [28.Zhou C. Chen G. Liu X. et al.A randomized, double-blind, placebo controlled, multicentre, phase III study of first-line carboplatin/paclitaxel (CP) plus bevacizumab(Bv) or placebo (Pl) in Chinese patients with advanced or recurrent non-squamous non-small cell lung cancer (NSCLC).J Thorac Oncol. 2013; 8 (abstr MO06.13)Google Scholar]. While one trial of cisplatin–gemcitabine with/without bevacizumab demonstrated an objective RR (ORR), and modest PFS advantage, but no OS benefit [AVAiL], two meta-analyses showed a consistent significant improvement of RR, PFS, and OS for the combination of bevacizumab and platinum-based chemotherapy compared with platinum-based chemotherapy in eligible patients with non-squamous NSCLC [29.Lima A.B. Macedo L.T. Sasse A.D. Addition of bevacizumab to chemotherapy in advanced non-small cell lung cancer: a systematic review and meta-analysis.PLoS One. 2011; 6: e22681Crossref PubMed Scopus (81) Google Scholar, 30.Soria J.C. Mauguen A. Reck M. et al.Systematic review and meta-analysis of randomised, phase II/III trials adding bevacizumab to platinum-based chemotherapy as first-line treatment in patients with advanced non-small-cell lung cancer.Ann Oncol. 2013; 24: 20-30Abstract Full Text Full Text PDF PubMed Scopus (253) Google Scholar]. Therefore, the combination of bevacizumab and other platinum-based chemotherapies may be considered in eligible patients [I, A] [1.Jemal A. Bray F. Center M.M. et al.Global cancer statistics.CA Cancer J Clin. 2011; 61: 69-90Crossref PubMed Scopus (29831) Google Scholar].•Non-platinum-based combination chemotherapy with third-generation agents should be considered only if platinum therapy is contraindicated. Several meta-analyses show lower RRs for non-platinum combinations with one of them showing inferior survival [31.Pujol J.L. Barlesi F. Daures J.P. Should chemotherapy combinations for advanced non-small cell lung cancer be platinum-based? A meta-analysis of phase III randomized trials.Lung Cancer. 2006; 51: 335-345Abstract Full Text Full Text PDF PubMed Scopus (108) Google Scholar] [I, A]. Chemotherapy prolongs survival and possibly improves QoL [32.Gridelli C. Ardizzoni A. Le Chevalier T. et al.Treatment of advanced non-small-cell lung cancer patients with ECOG performance status 2: results of an European Experts Panel.Ann Oncol. 2004; 15: 419-426Abstract Full Text Full Text PDF PubMed Scopus (138) Google Scholar] in NSCLC patients with PS 2, when compared with best supportive care (BSC) [I, B]. Single-agent chemotherapy with gemcitabine, vinorelbine, and taxanes represents an option [I, B] [33.Gridelli C. Effects of vinorelbine on quality of life and survival of elderly patients with advanced non-small-cell lung cancer. The Elderly Lung Cancer Vinorelbine Italian Study Group.J Natl Cancer Inst. 1999; 91: 66-72Crossref PubMed Scopus (897) Google Scholar]. Superiority of carboplatin-based combinations over monotherapy has been identified in a subgroup analysis within large phase III trials, with an acceptable toxicity profile [34.Lilenbaum R. Villaflor V.M. Langer C. et al.Single-agent versus combination chemotherapy in patients with advanced non-small cell lung cancer and a performance status of 2: prognostic factors and treatment selection based on two large randomized clinical trials.J Thorac Oncol. 2009; 4: 869-874Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar, 35.Quoix E. Zalcman G. Oster J.P. et al.Carboplatin and weekly paclitaxel doublet chemotherapy compared with monotherapy in elderly patients with advanced non-small-cell lung cancer: IFCT-0501 randomised, phase 3 trial.Lancet. 2011; 378: 1079-1088Abstract Full Text Full Text PDF PubMed Scopus (450) Google Scholar]. Moreover, combination chemotherapy with carboplatin significantly improved survival compared with monotherapy alone in 205 NSCLC patients with Eastern Cooperative Oncology Group (ECOG) PS 2. Carboplatin-based combination chemotherapy should be considered in eligible PS 2 patients [II, A] [36.Zukin M. Barrios C.H. Pereira J.R. et al.Randomized phase III trial of single-agent pemetrexed versus carboplatin and pemetrexed in patients with advanced non-small-cell lung cancer and Eastern Cooperative Oncology Group performance status of 2.J Clin Oncol. 2013; 31: 2849-2853Crossref PubMed Scopus (170) Google Scholar]. Poor PS (3–4) patients should be offered BSC [II, B] in the absence of documented activating (sensitising) EGFR mutations. Two randomised phase III trials established single-agent chemotherapy as the standard of care for first-line therapy for clinically unselected elderly advanced NSCLC patients [33.Gridelli C. Effects of vinorelbine on quality of life and survival of elderly patients with advanced non-small-cell lung cancer. The Elderly Lung Cancer Vinorelbine Italian Study Group.J Natl Cancer Inst. 1999; 91: 66-72Crossref PubMed Scopus (897) Google Scholar, 37.Gridelli C. Perrone F. Gallo C. et al.Chemotherapy for elderly patients with advanced non-small-cell lung cancer: the Multicenter Italian Lung Cancer in the Elderly Study (MILES) phase III randomized trial.J Natl Cancer Inst. 2003; 95: 362-372Crossref PubMed Scopus (771) Google Scholar]. A recent prospective randomised trial comparing monthly carboplatin plus weekly paclitaxel versus single-agent vinorelbine or gemcitabine in patients aged 70–89 years with PS 0–2 has reported a survival advantage for combination therapy [35.Quoix E. Zalcman G. Oster J.P. et al.Carboplatin and weekly paclitaxel doublet chemotherapy compared with monotherapy in elderly patients with advanced non-small-cell lung cancer: IFCT-05" @default.
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• W4238604577 title "Metastatic non-small-cell lung cancer (NSCLC): ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up" @default.
• W4238604577 cites W1523764380 @default.
• W4238604577 cites W1963495497 @default.
• W4238604577 cites W1974820090 @default.
• W4238604577 cites W1980497534 @default.
• W4238604577 cites W1987288037 @default.
• W4238604577 cites W1996589664 @default.
• W4238604577 cites W1997087602 @default.
• W4238604577 cites W2019607817 @default.
• W4238604577 cites W2021499674 @default.
• W4238604577 cites W2026951990 @default.
• W4238604577 cites W2032332769 @default.
• W4238604577 cites W2037139573 @default.
• W4238604577 cites W2037791152 @default.
• W4238604577 cites W2050249255 @default.
• W4238604577 cites W2058188403 @default.
• W4238604577 cites W2087281307 @default.
• W4238604577 cites W2087769940 @default.
• W4238604577 cites W2088088880 @default.
• W4238604577 cites W2097026987 @default.
• W4238604577 cites W2097268198 @default.
• W4238604577 cites W2099556905 @default.
• W4238604577 cites W2099725888 @default.
• W4238604577 cites W2099904227 @default.
• W4238604577 cites W2100912832 @default.
• W4238604577 cites W2104830962 @default.
• W4238604577 cites W2105022277 @default.
• W4238604577 cites W2106787323 @default.
• W4238604577 cites W2108824619 @default.
• W4238604577 cites W2110675408 @default.
• W4238604577 cites W2110697049 @default.
• W4238604577 cites W2111662961 @default.
• W4238604577 cites W2112621029 @default.
• W4238604577 cites W2113003672 @default.
• W4238604577 cites W2118019849 @default.
• W4238604577 cites W2120031407 @default.
• W4238604577 cites W2121095198 @default.
• W4238604577 cites W2122553809 @default.
• W4238604577 cites W2122798232 @default.
• W4238604577 cites W2125760261 @default.
• W4238604577 cites W2128278369 @default.
• W4238604577 cites W2130629599 @default.
• W4238604577 cites W2130652363 @default.
• W4238604577 cites W2132000516 @default.
• W4238604577 cites W2132542518 @default.
• W4238604577 cites W2134667653 @default.
• W4238604577 cites W2134693386 @default.
• W4238604577 cites W2137009016 @default.
• W4238604577 cites W2137510882 @default.
• W4238604577 cites W2138297714 @default.
• W4238604577 cites W2139110945 @default.
• W4238604577 cites W2139939379 @default.
• W4238604577 cites W2140617449 @default.
• W4238604577 cites W2145835533 @default.
• W4238604577 cites W2147016542 @default.
• W4238604577 cites W2147481343 @default.
• W4238604577 cites W2149603665 @default.
• W4238604577 cites W2149775776 @default.
• W4238604577 cites W2153550440 @default.
• W4238604577 cites W2154442955 @default.
• W4238604577 cites W2161650275 @default.
• W4238604577 cites W2166084034 @default.
• W4238604577 cites W2166696317 @default.
• W4238604577 cites W2167191456 @default.
• W4238604577 cites W2170744484 @default.
• W4238604577 cites W2185481272 @default.
• W4238604577 cites W2607182122 @default.
• W4238604577 cites W2912163165 @default.
• W4238604577 cites W2916080668 @default.
• W4238604577 doi "https://doi.org/10.1093/annonc/mdu199" @default.
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