OCT4 and Bmi-1 may be good biomarkers to predict the prognosis of patients with completely resected lung adenocarcinoma.
For the detection of epidermal growth factor receptor (EGFR) mutations, tumor tissues may not always be available. Not all the patients harboring EGFR mutation have a clinical response after the treatment of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKI). EGFR mutations were detected in 70 cases of newly diagnosed non-smoking adenocarcinoma, and patients harboring EGFR mutations received EGFR-TKI treatment. The EGFR mutation status of these patients' blood was analyzed by amplification refractory mutation system (ARMS). The patients' carcinoembryonic antigen (CEA) levels were tested on the third, seventh, 15(th), and 30th days after EGFR-TKI treatment. Forty-four cases were found with EGFR mutations. EGFR mutation rate of CEA high-level group was significantly higher than low-level group (70.8% vs. 40.9%, P = 0.017). Multivariate analysis showed that high-level CEA is independently associated with EGFR gene mutation (P = 0.020, OR = 3.508, 95%CI, 1.223-10.059). The sensitivity of high CEA level and ARMS to predict EGFR mutation were 79.1% and 51.2%. We divided the patients who received EGFR-TKI treatment into three groups by the variation types of CEA. Univariate analysis showed that patients in descending type group have longer progression-free survival (P = 0.001, HR 6.981, 95%CI, 2.534-19.237). Multivariate Cox proportional hazards model analyses shows the same result (P = 0.001, HR 9.82, 95%CI, 3.322-26.031). In conditions of the current technique, using high CEA level to predict EGFR mutations seems to be more sensitive than using EGFR mutations in plasma. The variation types of CEA level could help us to predict the efficacy of EGFR-TKI in patients harboring EGFR mutation within only 1 month of tyrosine kinase inhibitor therapy.
Objective: The aim of this study was to assess the value of tumor markers in monitoring chemotherapy response and predicting prognosis in patients with advanced non-small cell lung cancer (NSCLC). Methods: We studied carcinoembryonic antigen (CEA), CYFRA21-1 and neuron-specific enolase (NSE) of 111 untreated patients with advanced NSCLC before and after 2 cycles of chemotherapy, meanwhile evaluating the response according to the image, and analyzed the relationship between tumor markers and response rate, time to progression (TTP) and overall survival (OS). Results: The mean percentages of CEA decrease of the 111 patients with advanced NSCLC whose image response was partial response, no response and progressive disease were 22.8, –5.5 and –59.8% (p = 0.002), 28.1, 1.8 and –70.8% for CYFRA21-1 (p = 0.001), and 17.5, –3.1 and –16.9% for NSE, respectively (p = 0.03). The median TTP for all patients was 6.7 months, while the median TTP for CEA decrease and CEA elevated or stable patients was 9.2 and 4.3 months, respectively (p < 0.001). Radiologic and CYFRA21-1 responses were significant predictive factors for TTP on multivariate analysis (p < 0.001 and p = 0.003, respectively). The median OS was 19.2 months for all patients, with a 1-year survival rate of 69.4%. Baseline CEA, baseline CYFRA21-1 and CEA response were significant predictive factors for OS on multivariate analysis (p = 0.004, p = 0.004 and p < 0.001, respectively). Conclusion: CEA, CYFRA21-1 and NSE can be used in evaluating chemotherapy response, and CYFRA21-1 response was a significant predictive factor for TTP, while baseline CEA, baseline CYFRA21-1 and CEA response were significant predictive factors for OS in Chinese patients with advanced NSCLC.
Circulating tumor cells (CTCs) have important applications in clinical practice on early tumor diagnosis, prognostic prediction, and treatment evaluation. Platinum-based chemotherapy is a fundamental treatment for non-small cell lung cancer (NSCLC) patients who are not suitable for targeted drug therapies. However, most patients progressed after a period of treatment. Therefore, revealing the genetic information contributing to drug resistance and tumor metastasis in CTCs is valuable for treatment adjustment. In this study, we enrolled nine NSCLC patients with platinum-based chemotherapy resistance. For each patient, 10 CTCs were isolated when progression occurred to perform single cell–level whole-exome sequencing (WES). Meanwhile the patients’ paired primary-diagnosed formalin-fixed and paraffin-embedded samples and progressive biopsy specimens were also selected to perform WES. Comparisons of distinct mutation profiles between primary and progressive specimens as well as CTCs reflected different evolutionary mechanisms between CTC and lymph node metastasis, embodied in a higher proportion of mutations in CTCs shared with paired progressive lung tumor and hydrothorax specimens (4.4–33.3%) than with progressive lymphatic node samples (0.6–11.8%). Functional annotation showed that CTCs not only harbored cancer-driver gene mutations, including frequent mutations of EGFR and TP53 shared with primary and/or progressive tumors, but also particularly harbored cell cycle–regulated or stem cell–related gene mutations, including SHKBP1, NUMA1, ZNF143, MUC16, ORC1, PON1, PELP1, etc., most of which derived from primary tumor samples and played crucial roles in chemo-drug resistance and metastasis for NSCLCs. Thus, detection of genetic information in CTCs is a feasible strategy for studying drug resistance and discovering new drug targets when progressive tumor specimens were unavailable.
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