Prognostic implication of smoking history in patients with non-small cell lung cancer (NSCLC)

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 7699-7699
Author(s):  
I. Oze ◽  
Y. Segawa ◽  
N. Nogami ◽  
E. Komori ◽  
S. Sawada ◽  
...  

7699 Background: The AJCC disease stage, performance status (PS), and weight loss are established and important prognostic factors in patients with NSCLC. However, it is controversial whether smoking history affects the prognosis or not. We therefore assessed prognostic implication of smoking in patients with NSCLC. Methods: This retrospective study was performed using an institutional database for 1,440 NSCLC patients between 1995 and 2005. The characteristics of these patients were as follows: median age, 68 years (range,19–93); male/female, 947/493 patients; smokers/never-smokers, 897/543 patients; ECOG PS 0–1/2–4, 1319/121 patients; AJCC disease stage I-II/III-IV, 715/725 patients; squamous cell/non-squamous cell histologies, 391/1,049 patients; and weight loss > 5%/0–5%, 229/1,211 patients. Results: At a median follow-up time of 17 months (range, 1–59.7 months), the median survival time in smokers was 25 months, and significantly shorter than that in never-smokers (52 months, P < 0.0001). In a multivariate analysis using a Cox regression model, significance of the risk of death in smoking was confirmed when adjusted for age, sex, AJCC disease stage, ECOG PS, weight loss, and histologic subtypes (HR = 1.227, 95% CI 1.018–1.478, P = 0.032). Conclusions: Smoking history was considered to be a possible prognostic factor in patients with NSCLC. No significant financial relationships to disclose.

2007 ◽  
Vol 25 (18_suppl) ◽  
pp. 9021-9021 ◽  
Author(s):  
I. D. Schnadig ◽  
E. K. Fromme ◽  
C. L. Loprinzi ◽  
J. A. Sloan ◽  
M. Mori ◽  
...  

9021 Background: Physician-reported performance status (PS) is an important prognostic factor in advanced malignancies and is a commonly used stratification variable in cancer clinical trials. However, the extent, predictors, and prognostic importance of disagreement in PS assessment between physicians and patients have not been examined. Methods: Using NCCTG clinical trials from 1987–1990 (J Clin Oncol 19(15):3539–3546, 2001), we analyzed the difference and agreement of PS (ECOG and Karnofsky [KPS]) and nutritional status assessments reported by physicians and patients individually. The degree of disagreement was analyzed using paired t-test. Overall mortality was estimated by Kaplan-Meier method. The effect of disagreement on overall survival was analyzed by Cox regression. Independent predictors of disagreement were identified by logistic regression. Results: 1,636 patients with advanced lung and colorectal cancer had a median survival of 9.8 months (95% CI, 9.4 to 10.4). Percent agreement between patients and physicians about KPS, ECOG PS, and appetite/nutritional status was 32.9%, 43.4% and 42.0% respectively. Physicians were more likely to rate patients better than individual patients were to rate themselves: ECOG (Mean 0.91 vs 1.30, p<.0001), KPS (Mean 83.3 vs. 81.7, p<0.0001), appetite/nutritional status (Mean 1.6 vs. 2.1, p<0.0001). Inability to work, depression and less than a high school education were independently associated with disagreement. An increased risk of death was observed for patient and physician disagreement on KPS (HR=1.15, 95% CI, 1.03 to 1.27 p=0.01) and appetite/nutritional status (HR=1.39, 95% CI, 1.26 to 1.54 p<0.0001). Conclusions: Patients and physicians frequently disagree about patient PS, with physicians tending to rate patients higher than patients do themselves. Baseline patient demographic factors that independently predict disagreement have been identified. Disagreement confers an increased risk of death in the setting of advanced malignancies. These findings illustrate limitations of physician-only assessed PS. No significant financial relationships to disclose.


2006 ◽  
Vol 24 (15) ◽  
pp. 2245-2251 ◽  
Author(s):  
Chee-Keong Toh ◽  
Fei Gao ◽  
Wan-Teck Lim ◽  
Swan-Swan Leong ◽  
Kam-Weng Fong ◽  
...  

Purpose Tobacco smoke is a definite causative agent for lung cancer. It is increasingly being recognized that never-smokers can be afflicted with non–small-cell lung cancer (NSCLC). We aim to assess survival differences between smokers and never-smokers with NSCLC. Patients and Methods We analyzed 975 NSCLC patients who presented from January 1999 to December 2002. Clinical characteristics among current-, former- and never-smokers were tested using χ2 or Kruskal-Wallis test. The hazard ratio (HR) for death and its 95% CI were calculated by Cox regression. Results Of 975 patients, 59 had no smoking history and 33 had no quit time recorded. Of 883 patients analyzed, 286 patients (32.4%) were never-smokers. One hundred ninety-six never-smokers (68.5%) were females compared with 12% among current- and 13% among former-smokers (P < .001). There was a significant difference in histologic subtype between never-smokers and smokers: 69.9% with adenocarcinoma versus 39.9% (current-smokers) versus 47.3% (former-smokers); 5.9% with squamous cell carcinoma versus 35.7% (current-smokers) versus 28% (former-smokers; P < .001). Smokers had significantly poorer performance status (P = .002) and higher median age at diagnosis (P < .001) while more never-smokers presented with advanced disease (P = .002). Eight hundred and five patients (82.6%) died by May 30, 2005. The HR for smokers was significantly higher on both univariate and multivariate analysis (HR, 1.297; 95% CI, 1.040 to 1.619). Conclusion Never-smokers comprised a high proportion of NSCLC patients in Singapore. Definite epidemiologic differences exist between never-smokers and smokers. Differences in survival outcome further suggest that the biology underlying the pathogenesis and behavior of the disease may be different for never-smokers.


Blood ◽  
2017 ◽  
Vol 130 (Suppl_1) ◽  
pp. 915-915
Author(s):  
Qian Wang ◽  
Changchuan Jiang ◽  
Yaning Zhang ◽  
Stuthi Perimbeti ◽  
Prateeth Pati ◽  
...  

Abstract Introduction: Previous studies have shown that uninsured and Medicaid patients had higher morbidity and mortality due to limited access to healthcare. Disparities in cancer-related treatment and survival outcome by different insurance have been well established (Celie et al. J Surg Oncol.,2017). There are approximately 8,260 newly diagnosed HL cases in the US yearly (Master et al. Anticancer Res.2017). Therefore, we aim to investigate the variation of survival outcome and insurance status among HL patients. Methods: We extracted data from the US National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) 18 program. HL patients who were diagnosed from 2007-2014 were included. Demographic information including age, sex, race, annual household income, education and insurance were also collected. Insurance includes uninsured, insured and any Medicaid. Race/ethnicity includes white, black and other (including American Indian/AK native, Asian/Pacific Islander). HL is categorized by using International Classification of Disease for Oncology (ICD-O-3) into classical HL NOS (CHL NOS), nodular lymphocyte predominant HL (NLP), lymphocyte rich (LR), mixed cellularity (MC), lymphocyte depleted (LD), and nodular sclerosis (NS). Treatment modality included RT alone, CT alone, RT and CT combined, and no RT or CT. Survival time was estimated by using the date of diagnosis and one of the following dates: date of death, date last known to be alive or date of the study cutoff (December 31, 2014). Chi-square test and multivariate Cox regression were performed by using SAS 9.4 (SAS Institute Inc., Cary, NC, USA). Exclusion criteria include: 1) patients with unknown or unspecified race; 2) patients who survived less than 6 months because time of radiotherapy/chemotherapy was not known to the time of diagnosis; 3) patients with any other type of cancer prior to the diagnosis of HL; 4) patients with second or later primaries, and who were not actively followed. Results: A total of 14.286 HL patients were included in the analysis. Table 1 indicates the insurance status and demographic and tumor characteristics among HL patients diagnosed between 2007 and 2014. Patients with black race, male sex, and B symptoms were more likely to be uninsured and on any Medicaid compared to other races, female sex and without B symptoms (p&lt;0.01). As stage of disease increased, the percentage of insured patients decreased from 82.0% to 71.7%, (p&lt;0.01). As with year of diagnosis advanced, the percentage of uninsured did not appear to be changed however the proportion of both those with insurance and any Medicaid decreased slightly by 2.4% (p&lt;0.01). Those who received RT only were most likely to have insurance (89.6%) followed by combination modality (80.1%). As expected, uninsured status was associated with lower income and education level (p&lt;0.01). Table 2 shows the insurance and hazard ratio among HL patients by year of diagnosis adjusting for race, sex, histology type, income, education, and year of diagnosis. Any Medicaid patients had the highest HR of death from 2007-2010 compared to insured patients. Without insurance was also associated with increased risk of death but only significant in 2008, HR=2.26, 95% CI (1.35, 3.80). The survival outcomes comparing different insurance status by age groups (&lt;=29 and 30-64) were demonstrated in Kaplan-Meier Curve. In the age 29 or less group, insured patient showed has the best survival outcome followed by any Medicaid and then the uninsured. In the age 30-64 group, Medicaid patients had the worst survival outcome compared to those with or without insurance. Conclusion: Insurance status is one of the most important contributors of health disparity, especially in malignancy given the significant financial toxicity of therapies. We found that the proportion of the uninsured was trending up before the Affordable Care Act (ACA). Regarding the HL outcome, insured patients had the best survival across all age groups even though not significantly while Medicaid patients had the worst outcomes in almost all age groups, even worse than the uninsured after adjusting for the disease stage at diagnosis and sociodemographic factors. It would be of interest to explore the reason behind Medicaid patients' relatively poor outcomes. Future studies may also investigate how ACA, Medicaid expansion, and the possible upcoming republican healthcare reform influence HL outcome. Disclosures No relevant conflicts of interest to declare.


2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 188-189
Author(s):  
Pei Yu ◽  
Su Zhang ◽  
Ming Wang ◽  
He Liang ◽  
Hu Fan ◽  
...  

Abstract Background Several studies have suggested an association between poor oral health and esophageal squamous cell carcinoma (ESCC). We conduct this study to further examine the association between oral hygiene and ESCC risk in Linxian, the high risk area of China. Methods We recruit 29,553 healthy and 3318 esophageal squamous dysplasia participants aged between 40 and 69 in 1985 and then followed up until April, 2015. Basic characteristics were collected and oral related diseases were examined by trained doctors. Cox regression models were used to calculate hazard rations (HRs) and 95% confidence intervals (CIs). Results In general group, 2577 participants’ dead for ESCC and the cumulative rate of ESCC death was 12.9%. Teeth loss more than 20, before age of 40, bleeding of teeth, chapped lips, oral leukoplakia were significantly associated with risk of death from ESCC, and with 1.28 (95% CI: 1.18–1.38), 1.12 (95% CI: 1.03–1.23), 1.28 (95% CI: 1.13–1.45), 1.14 (95% CI: 1.04–1.25), 1.23 (95% CI: 1.12–1.35) fold increased risk of death from ESCC respectively in models adjusted for potential confounders. In dysplasia group, 540 participants’ dead for ESCC and the cumulative rate was 24.7%. Those who loss teeth more than 20, before age of 40, bleeding of teeth, have 1.24 (95% CI: 1.02–1.51), 1.25 (95%CI: 1.02–1.52), 1.35(95%CI: 1.06–1.70) fold increased risk after adjustment. Association between chapped lips and ESCC death was not found. Conclusion Severe teeth loss, early age teeth loss and teeth bleeding were associated with ESCC death and excess risk increased as dysplasia occurred. Chapped lips loss association with ESCC death in dysplasia group, it may reveals that it react before dysplasia change. Further studies are warranted to find the mechanism association and improvements of protecting oral health should be done. Disclosure All authors have declared no conflicts of interest.


Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3790-3790 ◽  
Author(s):  
Rami S. Komrokji ◽  
Dana E Rollison ◽  
Najla H Al Ali ◽  
Maria Corrales-Yepez ◽  
Pearlie K Epling-Burnette ◽  
...  

Abstract Abstract 3790 Background: Several epidemiologic studies suggest a linkage between smoking history and risk of myelodysplastic syndromes (MDS). Only one study addressed the potential impact of cigarette smoking on survival in lower risk MDS. We investigated the effect of smoking on disease outcome among MDS patients treated at the Moffitt Cancer Center (MCC). Methods: MDS patients were identified through the MCC database, followed by individual chart review. Tobacco use was obtained through patient self reported questionnaire. Chi square test and t-test were used to compare baseline characteristics. Kaplan Meier estimates were used to calculate overall survival (OS); log rank test was used for comparison between the different groups and Cox regression analysis was used for multivariable analysis. All analyses were conducted using SPSS version 19.0 software. Results: We identified 743 MDS patients evaluated at MCC with known tobacco smoking history (Data on tobacco use was only missing in 24 patients in the MDS database). Two hundred and fifty six patients never smoked (never-smoker group) and 487 patients were current or former smokers (ever smoker group). Tobacco use included current cigarettes smokers (n=70), former tobacco use (n=399), Cigar/pipe (n=16), Snuff/chew (n=2). The baseline characteristics compared between the 2 groups included age, WHO subtype, International Prognostic system (IPSS), MD Anderson risk model, karyotype, RBC transfusion dependence (RBC TD), serum ferritin, and treatment with hypomethylating agents. No statistically significant differences were observed between the 2 groups. (Table-1) In low and int-1 risk IPSS, a significantly greater proportion of poor risk karyotypes was observed in ever smokers (8.8%) versus never smokers (2.4%) (p=0.003). With a median duration of follow up of 55 months (95%CI 50.5–59.6), median OS for never smokers was 48 months (95%CI=36.9–59.1) compared to 35 months (95%CI =28.7–41.3) in ever smokers (p=0.01). The adverse effect of smoking was greatest in low and intermediate-1 IPSS risk groups where median OS was 69 months (95%CI= 42–96) in never smokers compared to 48 months (95%CI= 41–55) in smokers (p=0.006). The median OS was 69 mo (95%CI =42–96), 50 mo (95%CI= 43–57), and 38 mo (95%CI= 23–53) respectively in never-smoker, former-smoker, and current smoker groups in lower risk MDS (p=0.01). No difference was observed in int-2 and high risk IPSS groups with a median OS of 22 months (95%CI =11.75–32.2) in never smokers and 18 months (95%CI =14.3–21.7) in the ever smoker group. (p=0.89). An adverse impact of smoking was observed in good and intermediate risk karyotypes but not in poor risk karyotypes. Among low/int-1 risk IPSS, the rate of AML transformation was 18.2% in ever smokers compared to 9.5% in non-smokers (p=0.04) while no difference in rate of AML transformation was observed in int-2/high risk IPSS MDS between the 2 groups. In Cox regression analysis tobacco use in lower risk MDS predicted inferior OS (Hazard ratio (HR) 1.52 (95%CI 1.06–2.2) after adjustment for age >60, MD Anderson risk group, serum ferritin, RBC-TD, and use of hypomethylating agents. Conclusions: Our study confirms a negative impact of tobacco use on disease natural history and OS in a large cohort of MDS patients. The higher frequency of poor risk karyotype and AML progression among smoking, lower risk patients suggests that tobacco exposure influences disease biologic potential and behavioral modification to discontinue tobacco use may improve outcome. Disclosures: No relevant conflicts of interest to declare.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 7161-7161 ◽  
Author(s):  
M. Florescu ◽  
B. Hasan ◽  
F. A. Shepherd ◽  
L. Seymour ◽  
K. Ding ◽  
...  

7161 Background: Despite a 9% response rate, BR.21 demonstrated significant survival benefit for patients receiving erlotinib as 2nd/3rd line therapy for NSCLC. We undertook to characterize, by exploratory subset analysis, patients less likely to benefit from erlotinib. To identify factors for consideration, we first identified baseline characteristics associated with early progression by eight wks and early death by 3 mos. Methods: Using stratification factors and potential prognostic factors from BR.21, the Cox regression model with stepwise selection was used to establish a prognostic model to separate erlotinib patients into 4 risk categories based on the 10th, 50th & 90th percentiles of prognostic index scores. 7 variables (smoking history, PS, weight loss, anemia, high LDH, response to prior chemo and time from diagnosis to randomization) were used in the final model. The hypothesis was that the characteristics of the treated patients in the highest risk group would also be predictive of lack of benefit from erlotinib when erlotinib and placebo patients with the same characteristics were compared. Results: Factors associated with PD by 8 wks were: PS2–3 (p = 0.009), weight loss (p = 0.0004), anemia (p = 0.008), PD to prior chemo (p = 0.006), non-Asian (p = 0.047), EGFR IHC-negative (p = 0.005), Factors associated with survival < 3 mos were: PS2–3 (p < 0.0001), weight loss (p < 0.0001), anemia (p < 0.0001), PD to prior chemo (p < 0.0001), non-Asian (p = 0.008), high LDH (p < 0.0001), time to randomization <12 mos (p = 0.0003). Comparison of overall survival for the 4 risk groups derived from prognostic index score as follows: high benefit (HR = 0.41, p = 0.007), 2 intermediate benefit (HR 0.79, p = 0.09; HR 0.80; p = 0.09); no benefit (HR 1.23; p = 0.42). Median survivals for erlotinib (placebo) patients in each group were 17.3 (8.3), 9.7 (7.5), 4.1 (3.7), 1.9 (2.7) mos. Conclusions: By establishing a prognostic model, we identified a small group of patients who are unlikely to benefit from 2nd/3rd line erlotinib therapy. This model requires prospective validation to confirm that it is both prognostic and predictive of outcome from treatment. [Table: see text]


2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 210-210
Author(s):  
T. J. Huang ◽  
D. Li ◽  
Y. Li ◽  
S. P. Kar ◽  
S. Krishnan ◽  
...  

210 Background: The plasma membrane xCT cystine-specific subunit of the cystine/glutamate transporter contributes to chemotherapy resistance in pancreatic cancer by regulating intracellular glutathione levels and protecting cancer cells against oxidative stress. We previously noted that the rs7674870 single nucleotide polymorphism (SNP) of xCT correlated with overall survival in pancreatic cancer and may be predictive of platinum resistance. There are no data regarding xCT protein expression in pancreatic cancer or the functional significance of this SNP. Methods: Paraffin-embedded core and surgical biopsy tumor specimens from 49 patients with metastatic pancreatic adenocarcinoma were analyzed by immunohistochemistry (IHC) using an xCT specific antibody (Novus Biologicals). xCT protein IHC expression scores (product of intensity and percentage of staining cells) were analyzed in relation to overall survival and genotype of the patients using the one factor ANOVA test, Kaplan-Meier plot, log-rank test, and Cox regression analysis. Overall survival was measured from the date of diagnosis to the date of death or last follow-up. Results: Positive xCT expression was detected in 38 (78%) of the 49 samples, and 9 (18%) patients had high levels of expression. High xCT expression was associated with lower overall survival as compared with low expression (5.1 months versus 8.8 months; p = 0.119). In a multivariate Cox regression model with adjustment for prognostic parameters of age, sex, performance status and CA19-9 level, high xCT expression was associated with a 2.1-fold increased risk of death (p = 0.096). Performance status also correlated with overall survival (p = 0.027). Preliminary analysis on the genotype-phenotype association (n = 12) indicated that xCT expression was higher with the TT genotype than the TC/CC genotype (p = 0.115), which is consistent with the previous observation that the TT genotype was associated with reduced survival. Conclusions: These data provide supporting evidence for a possible role of cystine/glutamate transporter xCT subunit in pancreatic cancer progression and survival. Further pharmacogenomic and clinicopathologic studies are ongoing. No significant financial relationships to disclose.


2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 5037-5037 ◽  
Author(s):  
Fred Saad ◽  
Karim Fizazi ◽  
Matthew R. Smith ◽  
Thomas W. Griffin ◽  
Anil Londhe ◽  
...  

5037 Background: BTT can delay symptomatic progression in cancer pts with bone metastases. In a post hoc analysis, we assessed the impact of concomitant BTT on outcomes in a recent large, multinational study in mCRPC pts without prior ctx. Methods: COU-AA-302 was a phase III trial in asymptomatic/mildly symptomatic pts with progressive mCRPC and no prior ctx. 1,088 pts were stratified by ECOG performance status (ECOG-PS, 0 vs 1) and randomized 1:1 to AA 1 g or placebo QD, plus prednisone 5 mg BID. Radiographic progression-free survival (rPFS) and overall survival (OS) were primary end points; secondary end points were times to opiate use, ctx, ECOG-PS deterioration, and PSA progression. The effect of concomitant use of BTT on all end points was assessed retrospectively using a stratified Cox regression model with factors for treatment, concomitant BTT, interaction of treatment and BTT, and baseline covariates. All data were obtained from a prespecified interim analysis at 55% OS events. Results: Median follow-up at the time of analysis was 27.1 mos. Among intent-to-treat (ITT) pts, 184/546 AA and 169/542 P pts received concomitant BTT for treatment of bone metastases, either zoledronic acid (n = 330), other bisphosphonates (n = 16), denosumab (n = 22), and/or other BTT (n = 5). In these pts, concomitant BTT use was associated with improved OS, time to opiate use for cancer pain, and time to ECOG-PS deterioration (Table). Results were similar in a sensitivity analysis including only ITT pts with bone metastases at baseline. Conclusions: In this post hoc, exploratory analysis, concomitant BTT use was associated with delayed symptomatic progression in asymptomatic/mildly symptomatic mCRPC pts. This potential clinical benefit should be investigated in prospective studies. Clinical trial information: NCT00887198. [Table: see text]


2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 298-298
Author(s):  
Kei Saito ◽  
Yousuke Nakai ◽  
Hiroyuki Isayama ◽  
Takashi Sasaki ◽  
Naminatsu Takahara ◽  
...  

298 Background: Smoking is recognized as a risk factor for pancreatic cancer, but its associations with prognosis are not fully elucidated. Smoking was associated with poor outcomes in colon cancer, especially in patients with K-ras mutation (J Clin Oncol. 2013;31:2016-23). Therefore, we conducted this retrospective analysis of the associations of K-ras mutation, smoking and prognosis in patients with pancreatic cancer. Methods: Patients with pancreatic cancer who received surgery or chemotherapy at the University of Tokyo Hospital were retrospectively studied. The prognosis of patients with mutant and wild K-ras were compared. Overall survival was evaluated using Kaplan-Meier methods and compared by long-rank test. Cox regression models were used to calculate hazard ratios (HRs) to evaluate the prognostic factors in patients with pancreatic cancer with mutant K-ras or wild K-ras. Results: Between January 2009 and August 2013, K-ras mutation analysis was evaluated in 187 patients (47 surgical resection and 140 chemotherapy). K-ras mutation was detected in 74.3%. The rates of current-, ex- and never-smokers were 18.2%, 31.6% and 50.3%, respectively. In patients with mutant K-ras, the rate of male gender (46.0% vs. 29.0%), presence of distant metastasis (50.4% vs. 31.3%) and median CA19-9 (374 U/mL vs. 136 U/mL) were significantly higher than that in patients with wild K-ras. The rate of ever smokers (current- and ex-smokers) did not differ significantly (48.2% in mutant K-ras vs. 56.3% in wild K-ras, p=0.403). Median survival time (MST) was 16.7 (95%CI, 11.9-21.8) months in patients with mutant K-ras, compared with 20.3 (95%CI, 15.8-34.6) in patients with wild K-ras (p=0.193). Meanwhile, MST was 22.2 (95%CI, 16.9-27.9) vs. 14.8 (95%CI, 9.1-19.4) months in patients with and without smoking (p=0.024). After adjustment by age, gender, performance status, CA19-9 and treatment, HRs of smoking were 1.96 (95%CI, 1.06-3.68, p=0.032) in patients with mutant K-ras, but the association was not significant in patients with wild-K-ras (HR 1.35 [95%CI, 0.37-5.28], p=0.653). Conclusions: As previously reported in colon cancer, smoking was associated with poor prognosis in pancreatic cancer with K-ras mutation.


2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e17530-e17530
Author(s):  
Carlo Resteghini ◽  
Stefano Cavalieri ◽  
Alessandro Rametta ◽  
Salvatore Alfieri ◽  
Donata Galbiati ◽  
...  

e17530 Background: Immunotherapy (IT) provides advantages in a small proportion of recurrent / metastatic head and neck squamous cell carcinoma (RM HNSCC) patients (pts). Predictive biomarkers are still an unmet need. We aimed to determine if known prognostic clinical factors in RM HNSCC as well as new variables hold prognostic value in the IT era. Methods: We conducted a retrospective analysis of a cohort of 106 RM HNSCC pts enrolled into IT trials at National Cancer Institute of Milan-Italy between Oct 2014 - Jul 2018. Using Log Rank test and Cox proportional hazard model we computed univariate and multivariate analysis (UVA; MVA) of demographics, clinical and biological data to assess their prognostic value for progression free survival (PFS) and overall survival (OS). Results: Ninety-three pts (M 75; F: 18) were included in the final analysis with a median follow up of 20.8 months. The majority (96%) were treated in platinum-refractory setting. Approximately half of pts received anti-PD-1 or anti-PDL-1 monotherapy while the remaining 52% received them in combination with other IT agents. Median OS and PFS were 6.5 (CI 95%: 4.6-10.4) and 2.1 months (CI 95%: 1.8-2.2), respectively. Statistically significant factors at UVA for PFS were smoking history - both pos vs neg and < vs ≥ 30 PY, disease subsite, weight loss > 5%, Karnosfky performance status (PSK), occurrence of any and G3-G4 drug related (DR) toxicities, neutrophil to lymphocytes ratio (NLR). Without stratification for disease subsite, MVA showed independent predictive value of prolonged PFS for positive smoking history (HR 0.5, p 0.02) and any DR toxicities (HR 0.43, p < 0.01). Several factors reached significance for OS in UVA (smoking history and PY, weight loss > 5%, ECOG PS, PSK, occurrence of any toxicities, CRP, baseline C-reactive protein, antibiotic use, steroid use in the 30 days before IT). Of these, PSK (HR 0.95, p 0.01) and any DR toxicities (HR 0.3, p < 0.01) resulted to be predictive in the MVA. Conclusions: Clinical parameters, especially pretreatment PSK, smoking history and occurrence of any DR toxicities, appear to be strong predictors of outcome in RM HNSCC pts treated with IT. These results should be validated in an independent cohort.


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