A simplified prevention bundle with dual hand hygiene audit reduces early-onset ventilator-associated pneumonia in cardiovascular surgery units: An interrupted time-series analysis.

BACKGROUND: To investigate the effect of a simplified prevention bundle with alcohol-based, dual hand hygiene (HH) audit on the incidence of early-onset ventilation-associated pneumonia (VAP). METHODS: This 3-year, quasi-experimental study with interrupted time-series analysis was conducted in two cardiovascular surgery intensive care units in a medical center. Unaware external HH audit (eHH) performed by non-unit-based observers was a routine task before and after bundle implementation. Based on the realistic ICU settings, we implemented a 3-component bundle, which included: a compulsory education program, a knowing internal HH audit (iHH) performed by unit-based observers, and a standardized oral care (OC) protocol with 0.1% chlorhexidine gluconate. The study periods comprised 4 phases: 12-month pre-implementation phase 1 (eHH+/education-/iHH-/OC-), 3-month run-in phase 2 (eHH+/education+/iHH+/OC+), 15-month implementation phase 3 (eHH+/education+/iHH+/OC+), and 6-month post-implementation phase 4 (eHH+/education-/iHH+/OC-). RESULTS: A total of 2553 ventilator-days were observed. VAP incidences (events/1000 ventilator days) in phase 1-4 were 39.1, 40.5, 15.9, and 20.4, respectively. VAP was significantly reduced by 59% in phase 3 (vs. phase 1, incidence rate ratio [IRR] 0.41, P = 0.002), but rebounded in phase 4. Moreover, VAP incidence was inversely correlated to compliance of OC (r2 = 0.531, P = 0.001) and eHH (r2 = 0.878, P < 0.001), but not applied for iHH, despite iHH compliance was higher than eHH compliance during phase 2 to 4. Compared to eHH, iHH provided more efficient and faster improvements for standard HH practice. The minimal compliances required for significant VAP reduction were 85% and 75% for OC and eHH (both P < 0.05, IRR 0.28 and 0.42, respectively). CONCLUSIONS: This simplified prevention bundle effectively reduces early-onset VAP incidence. An unaware HH compliance correlates with VAP incidence. A knowing HH audit provides better improvement in HH practice. Accordingly, we suggest dual HH audit and consistent bundle performance does matter in quality-of-care VAP prevention.

Brain metastasis features and association with tumor epidermal growth factor receptor mutation in patients with adenocarcinoma of the lung.

AIM: Epidermal growth factor receptor (EGFR) mutations are frequent in pulmonary adenocarcinoma patients. The association between tumor EGFR mutation and characteristics of brain metastasis (BM) is still unclear. METHODS: We retrospectively reviewed pulmonary adenocarcinoma patients with and without BMs, and characteristics of BM to analyze the association between tumor EGFR mutation and characteristics of BM. RESULTS: Of 374 cases, 239 had EGFR mutations; 69 had BM at initial diagnosis, and 82 with BMs after treatment. All eligible patients received EGFR-tyrosine kinase inhibitors treatment. Older patients (≥70 years old) were less likely to have BMs than younger patients (25.8% vs 48%, P < 0.001). Patients with higher N stage had higher proportion of BMs (P = 0.006). Patients with exon 19 deletion were more likely to have BMs than those without EGFR mutation (48.1% vs 34.1%, P = 0.021). Patients with exon 19 deletion didn't have significantly higher chance of BMs at initial diagnosis but had higher chance to develop BM after treatment than those without EGFR mutation (35.6% vs 21.2%, P = 0.019). Patients with exon 19 deletion survived longer than those without EGFR mutation (1-year survival rate 95.8% vs 78.7%, P = 0.003). Thus, longer survival may lead to higher proportion of BM occurrence in patients with exon 19 deletion than those without EGFR mutation. CONCLUSIONS: In pulmonary adenocarcinoma, there is no significant difference in frequency of BMs at initial diagnosis between patients with EGFR mutation and wild type. However, after treatment, patients with EGFR mutations are significantly more likely to develop BM.

Spectrum of cancer risk among Taiwanese with chronic obstructive pulmonary disease.

BACKGROUND: Patients with chronic obstructive pulmonary disease (COPD) are liable to develop significant comorbidities, including lung cancer. Whether they are at a higher risk for cancer of other types remains debatable, especially for Asians. We studied the risk of incident cancer in COPD patients using a nationwide representative database, the Taiwan National Health Insurance Research Database. METHODS: From 1995 to 2008, 50,875 COPD patients who were free of antecedent malignancy were identified and followed up to development of malignancy, death or end of 2008, whichever came first. The risk of cancer was determined with the standardized incidence ratio (SIR), which is based on comparison to the national cancer incidence among the general population. RESULTS: During a median follow-up period of 5.61 years, 3623 (7.02 %) patients developed cancer and the SIR was 1.2 [95 % confidence interval (CI) 1.16-1.24, p < 0.001]. The risk remained higher at <1, 1-5, and even ≥5 years after the diagnosis of COPD (SIR 1.83, 1.07, and 1.11, respectively). Furthermore, the risk was significantly higher for some specific types of cancer, including head and neck cancer (SIR 1.23, 95 % CI 1.08-1.39, p = 0.002), esophageal cancer (SIR 1.35, 95 % CI 1.08-1.67, p = 0.010), lung and mediastinal cancer (SIR 1.86, 95 % CI 1.74-1.99, p < 0.001), breast cancer (SIR 1.19, 95 % CI 1.01-1.4, p = 0.041), prostate cancer (SIR 1.20, 95 % CI 1.06-1.35, p < 0.001), cancer of the central nervous system (SIR 1.58, 95 % CI 1.05-2.28, p = 0.030), lymphoma (SIR 1.53, 95 % CI 1.22-1.90, p < 0.001), and multiple myeloma (SIR 1.95, 95 % CI 1.31-2.80, p = 0.001). CONCLUSION: COPD patients had increased risk for incident cancers, including lung cancer and several extrapulmonary cancers.

Induced Pluripotent Stem Cell-conditioned Medium Suppressed Melanoma Tumorigenicity Through the Enhancement of Natural-Killer Cellular Immunity.

Induced pluripotent stem cells (iPSCs) can secrete cytokines that are involved in T-cell development and affect cytotoxic activity. To assess the effect of iPSC-conditioned medium on tumorigenicity, we retrieved splenocytes from B6 mice and cocultured them with or without irradiated B16 melanoma cells, mouse interleukin-2 (mIL-2), or iPSC-conditioned medium. Splenocyte cytotoxicity assays against B16 melanoma cells [as cytotoxic T lymphocyte (CTL) activity] and P815 cells [as natural killer (NK) activity] were performed. IL-10 and interferon-γ concentrations were measured. An in vivo subcutaneous B16 melanoma growth model was performed in B6 mice and treated with iPSC-conditioned medium. The lymphocyte subpopulation depletion test was performed to determine effectors against B16 melanoma cells. We found that unstimulated splenocytes had little cytotoxic activity. Without tumor cells, mIL-2 could augment iPSC-conditioned medium-treated CTL and NK activities (P<0.01). With irradiated tumor cells, mIL-2 treatment of splenocytes could not enhance CTL or NK activity, but iPSC-conditioned medium could enhance CTL and NK activity (P<0.001). Irradiated tumor cells induced mice splenocytes to secrete more IL-10, similar to mIL-2 treatment, but not iPSC-conditioned medium treatment. mIL-2 had better efficacy than conditioned medium in inducing splenocyte interferon-γ production. The CTL and NK cell depletion test showed that the immunostimulating effect of iPSC-conditioned medium on splenocytes was through the enhancement of NK cellular activity (P<0.05). The subcutaneous melanoma growth model showed that B16-bearing mice treated with an iPSC-conditioned medium intraperitoneal injection had a decreased tumor growth rate (P<0.01). Our study suggests that iPSC-conditioned medium had a protective effect against tumor-induced immunosuppression through the enhancement of host NK cellular activity.

Erlotinib Salvage Therapy in Pulmonary Adenocarcinoma Patients With Disease Progression After Previous EGFR-TKI Treatment.

BACKGROUND: Erlotinib is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) with promising efficacy in treating pulmonary adenocarcinoma. Treatment choices are few when patients with pulmonary adenocarcinoma have failed both EGFR-TKI and chemotherapy. The purpose of this study was to demonstrate the efficacy of erlotinib as salvage treatment for these nonresponsive patients. METHODS: We retrospectively reviewed the chart records of our stage IV pulmonary adenocarcinoma patients who were diagnosed and treated between July 2004 and June 2013. Clinical data, including type of response to treatment, time to disease progression, duration between the end of first-line EGFR-TKI treatment and starting erlotinib treatment, and overall survival time, were collected. RESULTS: A total of 98 patients were enrolled, and all had been treated with EGFR-TKI, either as a first-line therapy or following platinum-based chemotherapy; of them, 60 patients had a response to initial EGFR-TKI treatment. All received erlotinib as salvage treatment after their disease had progressed following EGFR-TKI treatment. Ninety-three (93.3%) patients had also received previous platinum-based chemotherapy. The median progression-free survival with erlotinib as salvage treatment for patients with and without a response to front-line EGFR-TKI was 4.9 and 3.4 months (P=0.869), respectively. The progression-free survival with erlotinib treatment in the sensitizing EGFR mutation group was 4.3 months, and in the EGFR wild-type group it was 2.6 months (P=0.22). CONCLUSIONS: In pulmonary adenocarcinoma patients who had been heavily treated, erlotinib could still be a choice, regardless of the EGFR mutation status, or whether the patients had responded to previous EGFR-TKI treatment.

Latent TB infection in newly diagnosed lung cancer patients - A multicenter prospective observational study.

OBJECTIVES: Lung cancer and tuberculosis (TB) share common risk factors and are associated with high morbidity and mortality. Coexistence of lung cancer and TB were reported in previous studies, with uncertain pathogenesis. The association between lung cancer and latent TB infection (LTBI) remains to be explored. METHODS: Newly diagnosed, treatment-naïve lung cancer patients were prospectively enrolled from four referral medical centers in Taiwan. The presence of LTBI was determined by QuantiFERON-TB Gold In-Tube (QFT-GIT). Demographic characteristics and cancer-related factors associated with LTBI were investigated. The survival status was also analyzed according to the status of LTBI. RESULTS: A total of 340 lung cancer patients were enrolled, including 96 (28.2%) LTBI, 214 (62.9%) non-LTBI, and 30 (8.8%) QFT-GIT results-indeterminate cases. Non-adenocarcinoma cases had higher proportion of LTBI than those of adenocarcinoma, especially in patients with younger age. In multivariate analysis, COPD (OR 2.41, 95% CI 1.25-4.64), fibrocalcified lesions on chest radiogram (OR 2.73, 95% CI 1.45-5.11), and main tumor located in typical TB areas (OR 2.02, 95% CI 1.15-3.55) were independent clinical predictors for LTBI. Kaplan-Meier survival analysis demonstrated patients with indeterminate QFT-GIT results had significantly higher 1-year all-cause mortality than those with LTBI (p<0.001) and non-LTBI (p=0.003). In multivariate analysis, independent predictors for 1-year all-cause mortality included BMI<18.5 (HR 2.09, 95% CI 1.06-4.14, p=0.033), advanced stage of lung cancer (RR 7.76, 95% CI 1.90-31.78, p=0.004), and indeterminate QFT-GIT results (RR 2.40, 95% CI 1.27-4.54, p=0.007). CONCLUSIONS: More than one-quarter of newly diagnosed lung cancer patients in Taiwan have LTBI. The independent predictors for LTBI include COPD, fibrocalcified lesions on chest radiogram, and main tumor located in typical TB areas. The survival rate is comparable between LTBI and non-LTBI cases. However, indeterminate QFT-GIT result was an independent predictor for all-cause mortality in lung cancer patients.

Circulating free mitochondrial DNA concentration and its association with erlotinib treatment in patients with adenocarcinoma of the lung.

Changes in circulating free DNA concentrations have been correlated with chemotherapeutic effects in solid tumors. The present study was designed to determine and compare the changes in circulating free mitochondrial DNA (mtDNA) concentrations prior to and following erlotinib treatment, as well as the potential prognostic value of plasma mtDNA. Patients with adenocarcinoma of the lung who were to receive erlotinib treatment were enrolled in the present study once informed consent had been obtained. Patient plasma samples were collected immediately prior to starting erlotinib treatment, on days 15 and 29 following the initiation of erlotinib treatment and also when the patient's disease had progressed. The most common erlotinib treatment response was a partial response (PR), achieved in 26 (49.1%) of the 53 enrolled patients, followed by stable disease (SD) in 13 patients (24.5%) and progressive disease (PD) in 14 patients (26.4%). Plasma mtDNA concentrations were significantly decreased on day 15 compared with day 0 in the patients with PD (P=0.028) or in those patients without a response to erlotinib treatment (SD and PD; P=0.007). Plasma mtDNA concentrations were similar or elevated on day 15 compared with day 0 in the patients with a PR (P=0.808). The concentration of plasma mtDNA did not correlate with progression-free survival (PFS). Tumor epidermal growth factor receptor (EGFR) mutation status (activating mutations in 16 patients and wild-type in 14 patients) did not correlate with the concentration of plasma mtDNA (P=0.951). Plasma mtDNA levels did not correlate with the PFS of the patients when they received erlotinib treatment. The plasma mtDNA levels were decreased on day 15 in those patients who had disease progression following erlotinib treatment. These results demonstrate that plasma mtDNA is of weak clinical utility as a screening, diagnostic or prognostic tool in lung cancer patients.

Erlotinib has better efficacy than gefitinib in adenocarcinoma patients without EGFR-activating mutations, but similar efficacy in patients with EGFR-activating mutations.

Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are an effective treatment for advanced non-small cell lung cancer. The objective of the present study was to compare the efficacy of gefitinib and erlotinib in patients with pulmonary adenocarcinoma, whose tumor EGFR mutation status was known. Pulmonary adenocarcinoma patients who began receiving gefitinib or erlotinib treatment from January 2005 to December 2010, and whose tumor EGFR mutation status had been determined, were included. Clinical data, type of treatment response and survival time data were collected. Of the 224 patients enrolled, 124 received gefitinib treatment and 100 received erlotinib treatment. Of these patients, 146 individuals had tumors with EGFR-activating mutations (exon 19 deletions and/point mutation of L858R in exon 21) and 78 did not. There was no difference in treatment response whether or not the patients had tumors with EGFR-activating mutations at the time they received gefitinib or erlotinib treatment. The median progression-free survival (PFS) of the gefitinib and erlotinib groups was 7.6 and 7.9 months, respectively (p=0.4731). PFS was significantly longer for patients without EGFR-activating mutations who received erlotinib treatment (n=48; median, 4.5 months) than for those who received gefitinib treatment (n=30; median, 2.3 months), with a hazard ratio of 0.58 (95% CI, 0.35-0.96; p=0.0339). Patients whose tumors had EGFR-activating mutations displayed no difference in PFS with either gefitinib (n=94; median, 10.5 months) or erlotinib treatment (n=52; median, 10.4 months). In conclusion, PFS showed no difference with either agent in patients whose tumors had EGFR-activating mutations, but was significantly longer in patients whose tumors did not have EGFR-activating mutations when receiving erlotinib treatment.

Plasma epidermal growth factor receptor mutation analysis and possible clinical applications in pulmonary adenocarcinoma patients treated with erlotinib.

Tumor epidermal growth factor receptor (EGFR) mutation analysis is significant for making treatment decisions for metastatic pulmonary adenocarcinoma. However, less than half of patients have adequate tumor samples for mutation analysis. Patients with adenocarcinoma of the lungs who were due to receive erlotinib treatment were included in the present study. Tumor EGFR mutation status was analyzed using DNA sequencing. Plasma specimens from the patients were collected prior to erlotinib treatment. The plasma-free DNA EGFR mutation status was analyzed using the PCR clamp method. A total of 54 consecutive patients were included in the study. The plasma-free DNA EGFR mutation status of the 54 patients was analyzed. Only 30 patients had adequate tumor samples for EGFR analysis, including 15 with activating mutations (exon 19 deletions or L858R). EGFR-activating mutations were detected in the plasma-free DNA in 25 of 54 patients. The response rate was 86.7 and 33.3% in patients with and without tumor activating mutations, respectively (p=0.002). The response rate was 68 and 31% based on the patients' plasma-free DNA EGFR mutation status, respectively (p=0.013). No significant difference in progression-free survival (PFS) was observed between patients with and without EGFR-activating mutations, according to data from tumor tissue or plasma-free DNA analysis, although the median PFS time was longer for those patients with EGFR-activating mutations in plasma samples. Plasma EGFR mutation analysis is useful for adenocarcinoma patients who have no or inadequate tumor samples available for EGFR examination. Patients with plasma EGFR-activating mutations had an improved response rate and a statistically insignificant longer PFS.

Phase II randomized trial of erlotinib or vinorelbine in chemonaive, advanced, non-small cell lung cancer patients aged 70 years or older.

INTRODUCTION: The primary objective of this study was to compare the response rates of elderly, chemonaive patients with advanced non-small cell lung cancer (NSCLC) treated with daily oral erlotinib versus oral vinorelbine. METHODS: Chemonaive Taiwanese patients aged 70 years or older who had advanced NSCLC were randomized to receive either oral erlotinib 150 mg (E) daily or oral vinorelbine 60 mg/m (V) on days 1 and 8 every 3 weeks. RESULTS: From February 2007 to July 2008, 116 patients were enrolled and 113 were included in the intent-to-treat population: 57 patients in the E group and 56 patients in the V group. Objective response rates were 22.8% (13 of 57) in E and 8.9% (5 of 56) in V (p = 0.0388). Median progression-free survival (PFS) was 4.57 months in E and 2.53 months in V (p = 0.0287), with an 80.6% increase in median PFS for E compared with V. Median survival time was 11.67 months in E and 9.3 months in V (p = 0.6975). Toxicities were generally mild in both groups. Median PFS was longest for epidermal growth factor receptor gene (EGFR)-mutated patients in the E group, followed by EGFR-mutated patients in V, EGFR wild type in E, and EGFR wild type in V (p = 0.0034). Overall survival was longer for EGFR-mutated patients than for EGFR wild-type patients (p < 0.0001). CONCLUSIONS: Erlotinib is highly effective compared with oral vinorelbine in elderly, chemonaive, Taiwanese patients with NSCLC. EGFR-mutated patients had better survival than those with EGFR wild-type disease, regardless of the treatment received.

Association between tumor epidermal growth factor receptor mutation and pulmonary tuberculosis in patients with adenocarcinoma of the lungs.

BACKGROUND: The possible association between pulmonary tuberculosis (TB) and lung cancer development has been studied for several decades. However, the association between epidermal growth factor receptor (EGFR) mutation status and pulmonary TB in patients with adenocarcinoma of the lungs is unknown. METHODS: We reviewed the data of our patients with adenocarcinoma of the lungs who had a clinical history of pulmonary TB or old TB lesions shown on chest computed tomography scan and evaluated the association between tumor EGFR mutation status and pulmonary TB. RESULTS: From June 1999 to January 2011, there were 275 patients with pulmonary adenocarcinoma with tumor EGFR mutation data available for analysis. Of them, 191 patients had EGFR mutations, 17 had a clinical history of pulmonary TB infection, 72 had old TB lesions on chest computed tomography scans, and 14 had scar cancer. Patients with old TB lesions had a higher incidence of EGFR mutation than those without (p = 0.018). Exon 19 deletions occurred more frequently in patients with old TB lesions than in patients without (p < 0.001). Those patients with old TB lesions who had EGFR mutations or exon 19 mutations survived longer than those who did not (p = 0.014 and 0.001, respectively). Patients with exon 19 deletions and old TB lesions showed no survival difference compared with those with exon 19 deletions and without old TB lesions (p = 0.271). CONCLUSIONS: Patients with pulmonary adenocarcinoma who had scar cancer or had old TB lesions had a higher probability of having EGFR mutations, especially exon 19 deletions.

Third-line or fourth-line chemotherapy in non-small-cell lung cancer patients with relatively good performance status.

BACKGROUND: Our aim here was to explore treatment efficacy of pemetrexed and docetaxel in non-small-cell lung cancer patients who had failed previous chemotherapy and epidermal growth factor receptor-tyrosine kinase inhibitor therapy. METHODS: We retrospectively reviewed clinical data of our non-small-cell lung cancer patients who received third- or fourth-line chemotherapy with pemetrexed or docetaxel in our institution from January 2006 to December 2009. RESULTS: One hundred and twenty-three patients received treatment, including 85 patients with pemetrexed treatment and 38 patients with docetaxel treatment. There was no difference in tumor response rate and toxicity profiles when using pemetrexed as third- or fourth-line treatment, neither was there difference in docetaxel treatment of third- versus fourth-line treatment. There was also no difference between docetaxel and pemetrexed in response rate and control rate when they were used as fourth-line treatment. However, docetaxel used in fourth-line treatment had higher incidence of neutropenia and more frequent need of granulocyte colony-stimulating factor support compared with pemetrexed in fourth-line treatment. Median progression-free survivals (PFSs) were 2.6 months and 3.8 months when using pemetrexed as third- and fourth-line treatment, respectively (p = 0.417). Median PFSs were 3.8 months and 4.8 months when using docetaxel as third- and fourth-line treatment, respectively (p = 0.882). There was also no difference in PFS between pemetrexed and docetaxel, both in third- and fourth-line treatment. Median survivals were 13.4, 12.2, 13.2, and 13 months for pemetrexed in third-line, fourth-line, and docetaxel in third-line and fourth-line treatment, respectively. CONCLUSION: This retrospective study of pemetrexed and docetaxel showed relatively safe toxicity profile, reasonable response rate, and long survival when used as third- and fourth-line chemotherapy. Thus, it is reasonable to give good performance status patients third- and fourth-line chemotherapy. A phase III randomized trial is needed for better clarification of these issues.

A phase II randomized trial of gefitinib alone or with tegafur/uracil treatment in patients with pulmonary adenocarcinoma who had failed previous chemotherapy.

BACKGROUND: Tegafur/uracil (UFT) is suitable for metronomic chemotherapy because of its underlying antiangiogenesis mechanism. This study aimed to assess the efficacy of adding daily oral UFT to gefitinib treatment in patients with pulmonary adenocarcinoma who had failed previous chemotherapy. METHODS: Taiwanese patients who had adenocarcinoma of the lung and failed previous chemotherapy were randomized into gefitinib 250 mg daily alone (G) or plus daily oral UFT (GU). From November 2005 to August 2009, 115 patients were enrolled. RESULTS: There were 58 patients in the G arm and 57 in the GU arm. One-year progression-free survival (PFS) was 18% in the G arm and 36.7% in the GU arm (p = 0.03). Fifty-four patients had tissue samples available for tumor epidermal growth factor receptor (EGFR) sequence analysis: 16 classical mutations and 8 wild types in the G arm, and 20 classical mutations and 10 wild-types in the GU arm. The addition of UFT significantly improved PFS in patients with EGFR mutations (14.4 versus 7.6 months, p = 0.0061). Forty-three patients underwent tumor tissue microvessel density measurement, and a trend favoring the addition of UFT to gefitinib treatment was found in those with low microvessel density (median PFS: 11.8 versus 2.8 months, p = 0.0536). The median survival time was 18.3 months in the G arm and 23.6 months in the GU arm (p = 0.381). CONCLUSION: Gefitinib plus UFT treatment had better PFS than gefitinib alone treatment. Gefitinib is effective in patients with EGFR mutations, and the addition of UFT treatment produced better PFS in these patients with mutations.

Different efficacies of erlotinib and gefitinib in taiwanese patients with advanced non-small cell lung cancer: a retrospective multicenter study.

INTRODUCTION: Epidermal growth factor receptor-tyrosine kinase inhibitors are used as effective first-line and salvage therapy in the treatment of advanced non-small cell lung cancer (NSCLC) patients in East Asia. The objective of this study was to compare the efficacy of gefitinib and erlotinib in Taiwanese patients with advanced NSCLC. METHODS: Clinical data of NSCLC patients treated with gefitinib or erlotinib from January 2004 to December 2008 were collected retrospectively. Five tertiary referral centers in Taiwan participated in the study. RESULTS: Of the 1122 patients enrolled, 506 (45%) were female, 594 (53%) were never smokers or former light smokers, and 867 (77%) were diagnosed with adenocarcinoma. Epidermal growth factor receptor-tyrosine kinase inhibitors were prescribed as first-line treatment in 465 (41%) patients and as second-line or salvage therapy in 657 patients (59%). The objective response rate was similar between the gefitinib and erlotinib treatment groups, while disease control rate was 58.9 and 65.8% (p = 0.025), respectively. Median progression-free survival of gefitinib and erlotinib groups was 3.6 and 4.6 months, respectively (p = 0.027). Median overall survival of gefitinib and erlotinib groups was 9.6 and 10.7 months, respectively (p = 0.013). CONCLUSION: Taiwanese patients with advanced NSCLC treated with erlotinib reported higher disease control rate, longer progression-free survival, and overall survival compared with patients treated with gefitinib.

Second-line therapy for elderly patients with non-small cell lung cancer who failed previous chemotherapy is as effective as for younger patients.

INTRODUCTION: It was found that second-line or thereafter therapies for patients with non-small cell lung cancer (NSCLC) who failed previous chemotherapy yielded a modest survival benefit. However, whether elderly patients (> or =70 years) benefit and are as suitable for salvage therapy as nonelderly patients (<70 years) are unknown. Whether epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is more favorable than chemotherapeutic agents as a salvage therapy agent in elderly patients with NSCLC is also undetermined. METHODS: We retrospectively reviewed and updated the data of our patients with NSCLC who received second-line salvage therapies, classified them into elderly and nonelderly groups, and compared the efficacy, toxicities, and survival of the patients. RESULTS: Four hundred sixty-one cases were reviewed. The nonelderly group had a similar response rate, control rate, and median survival time than the elderly group (p = 0.2, p = 0.9, and p = 0.5, respectively). The median progression-free time was numerically longer in the elderly than the nonelderly patients (p = 0.08). The nonelderly group had statistically insignificantly less hematologic toxicities than the elderly group, but more nausea and vomiting. In addition, the use of EGFR-TKI salvage therapy, compared with salvage chemotherapies in the elderly group, resulted in a similar disease control rate and median survival time and more favorable toxicity profiles. CONCLUSIONS: There were no differences in the efficacy of salvage chemotherapies and EGFR-TKI therapy, in terms of response rate, control rate, and overall survival, in elderly and nonelderly patients, and the therapies had acceptable toxicities. Age itself should not preclude patients with NSCLC from second-line salvage therapy.