***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    ***EXAMPLES*** 
    Input: BACKGROUND Atezolizumab is a humanised antiprogrammed death-lig and 1 ( PD-L1 ) monoclonal antibody that inhibits PD-L1 and programmed death-1 ( PD-1 ) and PD-L1 and B7 - 1 interactions , reinvigorating anticancer immunity . We assessed its efficacy and safety versus docetaxel in previously treated patients with non-small-cell lung cancer . METHODS We did a r and omised , open-label , phase 3 trial ( OAK ) in 194 academic or community oncology centres in 31 countries . We enrolled patients who had squamous or non-squamous non-small-cell lung cancer , were 18 years or older , had measurable disease per Response Evaluation Criteria in Solid Tumors , and had an Eastern Cooperative Oncology Group performance status of 0 or 1 . Patients had received one to two previous cytotoxic chemotherapy regimens ( one or more platinum based combination therapies ) for stage IIIB or IV non-small-cell lung cancer . Patients with a history of autoimmune disease and those who had received previous treatments with docetaxel , CD137 agonists , anti-CTLA4 , or therapies targeting the PD-L1 and PD-1 pathway were excluded . Patients were r and omly assigned ( 1:1 ) to intravenously receive either atezolizumab 1200 mg or docetaxel 75 mg/m2 every 3 weeks by permuted block r and omisation ( block size of eight ) via an interactive voice or web response system . Co primary endpoints were overall survival in the intention-to-treat ( ITT ) and PD-L1-expression population TC1/2/3 or IC1/2/3 ( ≥1 % PD-L1 on tumour cells or tumour-infiltrating immune cells ) . The primary efficacy analysis was done in the first 850 of 1225 enrolled patients . This study is registered with Clinical Trials.gov , number NCT02008227 . FINDINGS Between March 11 , 2014 , and April 29 , 2015 , 1225 patients were recruited . In the primary population , 425 patients were r and omly assigned to receive atezolizumab and 425 patients were assigned to  receive  docetaxel  .  Overall survival was significantly longer with atezolizumab in the ITT and PD-L1-expression population s. In the ITT population , overall survival was improved with atezolizumab compared with docetaxel ( median overall survival was 13·8 months [ 95 % CI 11·8 - 15·7 ] vs 9·6 months [ 8·6 - 11·2 ] ; hazard ratio [ HR ] 0·73 [ 95 % CI 0·62 - 0·87 ] , p=0·0003 ) . Overall survival in the TC1/2/3 or IC1/2/3 population was improved with atezolizumab ( n=241 ) compared with docetaxel ( n=222 ; median overall survival was 15·7 months [ 95 % CI 12·6 - 18·0 ] with atezolizumab vs 10·3 months [ 8·8 - 12·0 ] with docetaxel ; HR 0·74 [ 95 % CI 0·58 - 0·93 ] ; p=0·0102 ) . Patients in the PD-L1 low or undetectable subgroup ( TC0 and IC0 ) also had improved survival with atezolizumab ( median overall survival 12·6 months vs 8·9 months ; HR 0·75 [ 95 % CI 0·59 - 0·96 ] ) . Overall survival improvement was similar in patients with squamous ( HR 0·73 [ 95 % CI 0·54 - 0·98 ] ; n=112 in the atezolizumab group and n=110 in the docetaxel group ) or non-squamous ( 0·73 [ 0·60 - 0·89 ] ; n=313 and n=315 ) histology . Fewer patients had treatment-related grade 3 or 4 adverse events with atezolizumab ( 90 [ 15 % ] of 609 patients ) versus docetaxel ( 247 [ 43 % ] of 578 patients ) . One treatment-related death from a respiratory tract infection was reported in the docetaxel group . INTERPRETATION To our knowledge , OAK is the first r and omised phase 3 study to report results of a PD-L1-targeted therapy , with atezolizumab treatment result ing in a clinical ly relevant improvement of overall survival versus docetaxel in previously treated non-small-cell lung cancer , regardless of PD-L1 expression or histology , with a favourable safety profile . FUNDING F. Hoffmann-La Roche Ltd , Genentech , Background Kidney and renal pelvis cancers account for 4 % of all new cancer cases in the United States , among which 85 % are renal cell carcinomas ( RCC ) . While cigarette smoking is an established risk factor for RCC , little is known about the contribution of environmental tobacco smoke ( ETS ) to RCC incidence . This study assesses the role of smoking and ETS on RCC incidence using a population -based case-control design in Florida and Georgia . Methods Incident cases ( n = 335 ) were identified from hospital records and the Florida cancer registry , and population controls ( n = 337 ) frequency-matched by age ( + /- 5 years ) , gender , and race were identified through r and om-digit dialing . In-person interviews assessed smoking history and lifetime exposure to ETS at home , work , and public spaces .  Home ETS  was measured in both years and hours of exposure . Odds ratios and 95 % confidence intervals were calculated using logistic regression , controlled for age , gender , race , and BMI . Results Cases were more likely to have smoked 20 or more pack-years , compared with never-smokers ( OR : 1.35 , 95 % CI : 0.93 – 1.95 ) . A protective effect was found for smoking cessation , beginning with 11–20 years of cessation ( OR : 0.39 , 95 % CI : 0.18–0.85 ) and ending with 51 or more years of cessation ( OR : 0.11 , 95 % CI : 0.03–0.39 ) in comparison with those having quit for 1–10 years . Among never-smokers , cases were more likely to report home ETS exposure of greater than 20 years , compared with those never exposed to home ETS ( OR : 2.18 ; 95 % CI : 1.14–4.18 ) . Home ETS associations were comparable when measured in lifetime hours of exposure , with cases more likely to report 30,000 or more hours of home ETS exposure ( OR : 2.37 ; 95 % CI : 1.20–4.69 ) . Highest quartiles of combined home/work ETS exposure among never-smokers , especially with public ETS exposure , increased RCC risk by 2 to 4 times . Conclusion These findings confirm known associations between smoking and RCC and establish a potential etiologic role for ETS , particularly in the home . Differences in methods of retrospective measurement of lifetime smoking and ETS exposure may contribute to discrepancies in measures of associations across studies , and should be addressed in future research Purpose Nivolumab , a programmed death-1 inhibitor , prolonged overall survival compared with docetaxel in two independent phase III studies in previously treated patients with advanced squamous ( CheckMate 017 ; Clinical Trials.gov identifier : NCT01642004 ) or nonsquamous ( CheckMate 057 ; Clinical Trials.gov identifier : NCT01673867 ) non-small-cell lung cancer ( NSCLC ) . We report up date d results , including a pooled analysis of the two studies . Methods Patients with stage IIIB/IV squamous ( N = 272 ) or nonsquamous ( N = 582 ) NSCLC and disease progression during or after prior platinum-based chemotherapy were r and omly assigned 1:1 to nivolumab ( 3 mg/kg every 2 weeks ) or docetaxel ( 75 mg/m2 every 3 weeks ) . Minimum follow-up for survival was 24.2 months . Results Two-year overall survival rates with nivolumab versus docetaxel were 23 % ( 95 % CI , 16 % to 30 % ) versus 8 % ( 95 % CI , 4 % to 13 % ) in squamous NSCLC and 29 % ( 95 % CI , 24 % to 34 % ) versus 16 % ( 95 % CI , 12 % to 20 % ) in nonsquamous NSCLC ; relative reductions in the risk of death with nivolumab versus docetaxel remained similar to those reported in the primary analyses . Durable responses were observed with nivolumab ; 10 ( 37 % ) of 27 confirmed responders with squamous NSCLC and 19 ( 34 % ) of 56 with nonsquamous NSCLC had ongoing responses after 2 years ' minimum follow-up . No patient in either docetaxel group had an ongoing response . In the pooled analysis , the relative reduction in the risk of death with nivolumab versus docetaxel was 28 % ( hazard ratio , 0.72 ; 95 % CI , 0.62 to 0.84 ) , and rates of treatment-related adverse events were lower with nivolumab than with docetaxel ( any grade , 68 % v 88 % ; grade 3 to 4 , 10 % v 55 % ) . Conclusion Nivolumab provides long-term clinical benefit and a favorable tolerability profile compared with docetaxel in previously treated patients with advanced NSCLC 
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Conclusions  Higher PD-L1 expression  is more closely associated with poor prognosis and more advanced clinicopathological features in RCC patients than PD-L2 , especially in women and Caucasian patients .
PD-L2 was a weak negative predictor of poor CSS of RCC and was not a prompt for the metastasis of RCC