INVESTIGATION KRAS MUTATION IN CIRCULATION TUMOR DNA IN DIFFERENT STAGES OF COLORECTAL CANCER

2019 ◽  
Vol 65 (5) ◽  
pp. 701-707
Author(s):  
Vitaliy Shubin ◽  
Yuriy Shelygin ◽  
Sergey Achkasov ◽  
Yevgeniy Rybakov ◽  
Aleksey Ponomarenko ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Plasma Volume ◽  
Kras Mutation ◽  
Stage Iv ◽  
Circulating Tumor Dna ◽  
Stage Ii ◽  
Kras Gene ◽  
Kras Mutations ◽  
Droplet Pcr ◽  
Tumor Dna

To determine mutations in the plasma KRAS gene in patients with colorectal cancer was the aim of this study. The material was obtained from 44 patients with colorectal cancer of different stages (T1-4N0-2bM0-1c). Plasma for the presence of KRAS gene mutation in circulating tumor DNA was investigated using digital droplet polymerase chain reaction (PCR). KRAS mutations in circulating tumor DNA isolated from 1 ml of plasma were detected in 13 (30%) patients with cancer of different stages. Of these, with stage II, there were 3 patients, with III - 5 and with IV - 5. Patients who did not have mutations in 1 ml of plasma were analyzed for mutations of KRAS in circulating tumor DNA isolated from 3 ml of plasma. Five more patients with KRAS mutations were found with II and III stages. The highest concentrations of circulating tumor DNA with KRAS mutation were found in patients with stage IV. The increase in plasma volume to 3 ml did not lead to the identification of mutations in I stage. This study showed that digital droplet PCR allows identification of circulating tumor DNA with the KRAS mutations in patients with stage II-IV of colon cancer. The results can be used to determine the degree of aggressiveness of the tumor at different stages of the disease, but not the 1st, and it is recommended to use a plasma volume of at least 3 ml.

An improved method for detection of methylated circulating tumor DNA in colorectal cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15120-e15120 ◽  
Author(s):  
Nicky Boulter ◽  
Gregor Tevz ◽  
Betty Yu ◽  
Michelle Chan ◽  
David Murray ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Stage Iv ◽  
Circulating Tumor Dna ◽  
Qpcr Assay ◽  
Stage I ◽  
Stage Ii ◽  
Detection Methods ◽  
Assay Sensitivity ◽  
Crc Screening ◽  
Tumor Dna

e15120 Background: Assays detecting methylated circulating tumor DNA (ctDNA) hold promise for colorectal cancer (CRC) screening, but there is a need to develop more accurate assays for early stages. In this study, we examined modifications to COLVERA (an IKZF1 and BCAT1 methylation marker qPCR assay) that added a third biomarker (IRF4) as well as introducing double stranded detection. Methods: Bisulfite converted DNA extracted from plasma collected from subjects undergoing diagnosis for CRC was assayed using either a double-stranded (ds) specific multiplexed qPCR for BCAT1 and IKZF1 detection (Assay 1) and/or a single-stranded (ss) specific BCAT1/IRF4, ds-specific IKZF1 multiplexed qPCR (Assay 2). The unmodified COLVERA test (Clinical Genomics) was used for comparison. Detection of any marker was considered positive. Results: Assay 1 performance evaluated against COLVERA on bisulfite converted DNA from 1453 samples showed an improved sensitivity for CRC detection (93/134 (69.4%) vs 79/134 (59.0%) COLVERA, p = 0.02), but specificity was suboptimal (no neoplasia: 861/1023 (84.2%) vs 946/1023 (92.5%) COLVERA, p < 0.0001). The decrease in specificity resulted primarily from modifications in the BCAT1 assay component (1023 no neoplasia: 60 positive with ss- BCAT1 vs 146 positive with ds- BCAT1, p < 0.0001). Thus, a novel configuration, Assay 2 (ss- BCAT1, ss- IRF4 and ds- IKZF1) was compared to Assay 1 using 189 previously untested specimens. Assay 2 showed a notable improvement in specificity (99/104 (95.2%) vs 93/104 (89.4%) Assay 1; p = 0.0351). Both assays exhibited comparable sensitivities for CRC (41/49 (83.7%) vs 39/49 (79.6%), Assay 1, p = 0.3633). Assay 2 was positive in: adenomas, 9/36 (25.0%); Stage I, 3/7 (42.9%); Stage II, 17/19 (89.5%); Stage III, 6/6 (100%); Stage IV, 7/7 (100%) and 8/10 (80%) unstaged CRCs. Prior COLVERA sensitivity estimates were 9% adenoma, 41% Stage I and 76% Stage II. Conclusions: Targeting both of the non-complementary bisulfite converted strands of selective regions of interest markedly improve ctDNA assay sensitivity for cancer including early lesions while achieving good specificity. Prospective evaluation in a true CRC screening population is now underway. Clinical trial information: 12611000318987.

scholarly journals KRAS A146 Mutations Are Associated With Distinct Clinical Behavior in Patients With Colorectal Liver Metastases

2021 ◽  
pp. 1758-1767
Author(s):  
Iris van 't Erve ◽  
Nina J. Wesdorp ◽  
Jamie E. Medina ◽  
Leonardo Ferreira ◽  
Alessandro Leal ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Kras Mutation ◽  
Clinical Care ◽  
Prospective Trial ◽  
Predictive Biomarker ◽  
Circulating Tumor Dna ◽  
Kras Mutations ◽  
Molecular Subgroup ◽  
Computed Tomography Images ◽  
Tumor Dna

PURPOSE Somatic KRAS mutations occur in approximately half of the patients with metastatic colorectal cancer (mCRC). Biologic tumor characteristics differ on the basis of the KRAS mutation variant. KRAS mutations are known to influence patient prognosis and are used as predictive biomarker for treatment decisions. This study examined clinical features of patients with mCRC with a somatic mutation in KRAS G12, G13, Q61, K117, or A146. METHODS A total of 419 patients with colorectal cancer with initially unresectable liver-limited metastases, who participated in a multicenter prospective trial, were evaluated for tumor tissue KRAS mutation status. For the subgroup of patients who carried a KRAS mutation and were treated with bevacizumab and doublet or triplet chemotherapy (N = 156), pretreatment circulating tumor DNA levels were analyzed, and total tumor volume (TTV) was quantified on the pretreatment computed tomography images. RESULTS Most patients carried a KRAS G12 mutation (N = 112), followed by mutations in G13 (N = 15), A146 (N = 12), Q61 (N = 9), and K117 (N = 5). High plasma circulating tumor DNA levels were observed for patients carrying a KRAS A146 mutation versus those with a KRAS G12 mutation, with median mutant allele frequencies of 48% versus 19%, respectively. Radiologic TTV revealed this difference to be associated with a higher tumor load in patients harboring a KRAS A146 mutation (median TTV 672 cm3 [A146] v 74 cm3 [G12], P = .036). Moreover, KRAS A146 mutation carriers showed inferior overall survival compared with patients with mutations in KRAS G12 (median 10.7 v 26.4 months; hazard ratio = 2.5; P = .003). CONCLUSION Patients with mCRC with a KRAS A146 mutation represent a distinct molecular subgroup of patients with higher tumor burden and worse clinical outcomes, who might benefit from more intensive treatments. These results highlight the importance of testing colorectal cancer for all KRAS mutations in routine clinical care.

Plasma cell-free DNA and fraction of circulating KRAS mutations as prognostic in patients with metastatic colorectal cancer.

2014 ◽  
Vol 32 (3_suppl) ◽  
pp. 490-490 ◽  
Author(s):  
David Sefrioui ◽  
Nasrin Vasseur ◽  
Richard Sesboüé ◽  
France Blanchard ◽  
Alice Oden-Gangloff ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Plasma Cell ◽  
Circulating Tumor Dna ◽  
Dna Fragments ◽  
Wild Type ◽  
Kras Mutations ◽  
Cell Free Dna ◽  
Free Dna ◽  
Tumor Dna

490 Background: It has been suggested that detection of circulating tumor DNA may be relevant in patients with metastatic colorectal cancer (mCRC). The main objective of the present study was to evaluate a method based on the TaqMan Mutation Detection Assay (TMDA) for the detection of circulating KRAS mutations in mCRC patients. Moreover, we also investigated the prognostic impact of the plasma cell-free DNA and the fraction of circulating KRAS mutations. Methods: The study was conducted from April to July 2013 and plasma samples were prospectively collected in a series of 35 mCRC patients treated with chemotherapy (CT). QIAamp Circulating Nucleic Acid kit was used for DNA extraction and Quant-iT High Sensitivity dsDNA Assay for cf-DNA quantification. Detection of circulating tumor DNA was based on the KRAS mutations detected in tumour and was performed in plasma by the castPCR Technology TMDA. Response to CT was assessed according to RECIST criteria. The results of plasma cf-DNA and level of mutant DNA fragments were correlated with response and 3-months survival. Results: We isolated and quantified plasma cf-DNA in all patients with a mean concentration of 106 ng/mL. Among them, 18 were wild-type and 17 mutated for KRAS in the tumour. Detection of circulating KRAS mutations was performed with TMDA in 23 patients (10 KRAS wild-type and 13 KRAS mutated). The sensitivity was 62% (8/13) and specificity 100% (0/10) with a level of circulating mutant DNA fragments ranging from 0 to 29%. Plasma cf-DNA and level of circulating mutant DNA were both significantly correlated with the 3-months survival (mean 36 versus 524 ng/mL, p=0.0015 and 2% versus 29%, p<0.0001). There was a non significant trend for response to CT (respectively p=0.14 and p=0.12). Conclusions: TMDA method is a simple, accurate and non-invasive tool for the detection of circulating tumor DNA. Our preliminary results also suggest that plasma cf-DNA and fraction of mutant DNA fragments could be prognostic markers in mCRC patients.

Comparative circulating tumor DNA levels for KRAS mutations in patients with nonresectable pancreatic cancer.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 288-288 ◽  
Author(s):  
Julia S. Johansen ◽  
Cecile Rose T. Vibat ◽  
Dan Calatayud ◽  
Benny Vittrup Jensen ◽  
Jane Preuss Hasselby ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Pancreatic Cancer ◽  
Cancer Patients ◽  
Kras Mutation ◽  
Circulating Tumor Dna ◽  
Resectable Pancreatic Cancer ◽  
Kras Mutations ◽  
Study Objective ◽  
Wide Range ◽  
Tumor Dna

288 Background: Non-resectable pancreatic cancer patients have a wide range of median time for overall survival (OS). Currently there is a lack of diagnostic tools to predict patient outcome at diagnosis. KRAS mutations are present in the vast majority of pancreatic tumors. The study objective was to determine if quantitative baseline and longitudinal monitoring of KRAS mutations from plasma circulating tumor DNA (ctDNA) could be used to stratify patients for predicting outcome. Methods: Plasma was prospectively collected from the Danish BIOPAC study for non-resectable pancreatic cancer patients undergoing treatment with gemcitabine or FOLFIRINOX. Feasibility of monitoring ctDNA KRAS mutations was assessed in 10 patients with long OS (median 493 days; range 360-1031) and 10 patients with short OS (median 66 days; range 21-136). KRAS G12A/C/D/R/S/V, and G13D mutations were PCR enriched, sequenced by massively parallel deep sequencing, quantitated and standardized by reporting number of copies detected per 105 genome equivalents (GE). Results: In a pilot study of 20 patients, all 18 patients with evaluable DNA had detectable KRAS mutations. Of 18 patients, 12 had baseline plus longitudinal time points (7 short, 5 long OS). Mutant KRAS copies were higher for short OS (median=994; range 0-34305 copies/105 GE) vs. with long OS (median 196; range, 34-278 copies/105 GE). Longitudinally, KRAS mutation levels remained mostly low with long OS (last time point median 204; range 8-873 copies/105 GE) vs. short OS where levels increased or remained high (median 2363; range 71-47919 copies/105 GE). Identical KRAS mutations were consistently detected for a given patient with short OS. However, long OS patients had variable KRAS mutations in longitudinal analysis. Conclusions: High levels of ctDNA KRAS mutations at diagnosis and post-treatment elevation of KRAS mutations were more associated with short OS. Different levels of KRAS mutation at diagnosis may predict patient outcome and could reflect distinct underlying tumor biology. Expansion of this prospective-retrospective biomarker cohort will be reported.

Dynamics and characteristics of KRAS mutated circulating tumor DNA in patients with metastatic colorectal cancer during various treatments.

2018 ◽  
Vol 36 (4_suppl) ◽  
pp. 665-665
Author(s):  
Yuji Takayama ◽  
Koichi Suzuki ◽  
Kosuke Ichida ◽  
Taro Fukui ◽  
Nao Kakizawa ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Disease Progression ◽  
Kras Mutation ◽  
Circulating Tumor Dna ◽  
Line Treatment ◽  
Tumor Tissues ◽  
Significant Difference ◽  
Before And After ◽  
Tumor Dna

665 Background: KRAS mutated circulating tumor DNA (MctDNA) can be detected in blood of patients with metastatic colorectal cancer (mCRC) but its dynamics and characteristics during anti-EGFR and other treatments are not well known. Methods: Four hundred and fifty-one plasma samples were collected prospectively from 85 patients who underwent chemotherapy due to mCRC in 2014 - 2017. KRAS mutation in codon12/13/61 was explored in tumor tissues and plasma. Results: KRAS assessment in tumor tissues showed 29 patients with KRAS mutation (MT), 56 patients without mutation (WT). Sensitivity and specificity of MctDNA was 86.4% and 100%, respectively. In 29 patients with MT, significant difference in PFS was observed between patients with MctDNA and without during 1st line treatment (3.0 months vs.15.0 months; p = 0.005). In 56 patients with WT, 27 patients showed MctDNA during various treatments. Different characteristics in appearance were recognized during several treatments including anti-VEGF, TAS-102 and regorafenib. KRAS mutation in codon12/13 was appeared before and after disease progression. KRAS mutation in codon 61 was, however, frequently detected before disease progression. A spike like appearance of KRAS mutation in codon12/13 was likely seen in response to induction of the sequential treatment. Significant difference in PFS was observed between patients with MctDNA and without during 1st line treatment (6.0 months vs. 13.0 months; p = 0.0017), as was observed in patients with MT. Conclusions: Dynamics and characteristics of KRAS status in blood may be involved in the treatment response and outcome in mCRC patients.

scholarly journals Effectiveness of circulating tumor DNA for detection of KRAS gene mutations in colorectal cancer patients: a meta-analysis

2017 ◽  
Vol Volume 10 ◽  
pp. 945-953 ◽  
Author(s):  
Yi-xin Hao ◽  
Qiang Fu ◽  
Yan-Yan Guo ◽  
Ming Ye ◽  
Hui-Xia Zhao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Patients ◽  
Meta Analysis ◽  
Gene Mutations ◽  
Circulating Tumor Dna ◽  
Kras Gene ◽  
Colorectal Cancer Patients ◽  
Tumor Dna

Difference in appearance of KRAS mutated circulating tumor DNA in patients with metastatic colorectal cancer during treatments.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23025-e23025
Author(s):  
Yuji Takayama ◽  
Koichi Suzuki ◽  
Kosuke Ichida ◽  
Taro Fukui ◽  
Fumiaki Watanabe ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Kras Mutation ◽  
Treatment Resistance ◽  
Digital Pcr ◽  
Circulating Tumor Dna ◽  
Oil Droplets ◽  
Tumor Tissues ◽  
The Difference ◽  
Tumor Dna

e23025 Background: Emergence of KRAS mutation in blood is observed in colorectal cancer patients who undergo chemotherapy, but its clinical significance is not well known. In this study, we focused on the difference in appearance of KRAS mutated circulating tumor DNA (MctDNA) and elucidated its association with treatments. Methods: Four hundred and fifty-one plasma samples were collected prospectively from 85 patients (pts) who underwent chemotherapy due to metastatic colorectal cancer in 2014 - 2016. Seven types of KRAS mutation in MctDNA were detected by droplet digital PCR creating oil droplets. To exclude false positive detection, mutation was validated. MctDNA amplified in oil droplets was selectively sorted by On-chip sorting system and mutation was determined by Sanger sequencing. Results: KRAS assessment in tumor tissues showed 29 pts with KRAS mutation (MT), 56 pts without KRAS mutation (WT). Among 29 pts with MT, KRAS assessment in plasma displayed 23 pts with MctDNA and 6 pts without MctDNA. The type of mutation in MctDNA was consistent with that detected in tumor tissues, indicating mutual exclusivity in KRAS mutation was confirmed. In 56 pts with WT, 28 pts showed MctDNA during treatments. Difference in appearance of MctDNA was recognized in several treatments. Gradual increase in detection of MctDNA was observed with anti-EGFR antibody, resulted in treatment resistance. Transient spike elevation was frequently seen in TAS-102, which associated with drug response. No specific appearance was recognized during treatments with other drugs including anti-VEGF antibody. MctDNA in oil droplets were successfully sorted even if a few droplets were targeted, and mutation was confirmed. Conclusions: Difference in appearance of MctDNA may associate with treatment response in patients with metastatic colorectal cancer during treatments. [Table: see text]

Circulating tumor DNA as a promising biomarker of relapse risk for stage II-III colorectal cancer.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. 4079-4079
Author(s):  
Gong Chen ◽  
Feng Wang ◽  
Jun-Jie Peng ◽  
San-Jun Cai ◽  
Ke-Feng Ding ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Curative Resection ◽  
Disease Free Survival ◽  
Early Recurrence ◽  
Circulating Tumor Dna ◽  
Stage Ii ◽  
Free Survival ◽  
Colorectal Cancer Patients ◽  
Disease Free ◽  
Tumor Dna

4079 Background: About 30-50% colorectal cancer patients undergoing a curative resection will experience disease recurrence ultimately. Early detection of recurrence is of great significance for improving the prognosis of colorectal cancer patients. Circulating tumor DNA (ctDNA) has been suggested to be a promising biomarker for postoperative surveillance and prognosis prediction in various cancers including colorectal cancer. However, its performance in predicting early recurrence of colorectal cancer as well as appropriate testing procedures still needs large-scale prospective studies to evaluate. Methods: A total of 246 patients with stage II-III colorectal cancer and underwent curative resection from three clinical centers of China were enrolled in this multicenter prospective cohort study. Tissue samples as well as serial plasma samples before surgery, 7 days and 6 months after surgery and 3 months interval afterwards until recurrence were collected, and subjected to deep targeted-panel sequencing containing 425 cancer-related genes. ctDNA baseline genomic alterations and dynamic changes were analyzed. Its performance in predicting early recurrence was evaluated and compared with other clinical routine investigations, including serum biomarkers CEA and CA199, and CT examination. Results: The ctDNA positive rates at baseline (before surgery) and 7 days after surgery were 72.9% and 18.1% respectively. Among 199 patients with complete survival data, 18 patients were recurrent during follow up period with a median disease-free survival of 280.5 days (114-461 days). At baseline, high clinical stage (p = 0.035), and PTEN mutation (p = 0.009) were significantly associated with increased recurrent risk; while APC mutation (p = 0.04) predicted a decreased recurrent risk. Detection of ctDNA 7 days after surgery [HR: 5.9 (1.94-17.97); p = 0.0004] or any time point before clinical recurrence [HR: 6.14 (2.3-16.38); p < 0.0001] was associated with a significantly higher recurrent risk, and the HR increased accordingly with ctDNA mutation level. In multivariate analyses, ctDNA status was independently associated with relapse after adjusting for known clinicopathological risk factors. CEA status was not significantly (p > 0.4) associated with disease-free survival. A risk scoring model comprising of clinical variables and ctDNA detection after surgery was constructed and can predict 18-month recurrence with an AUC of 0.77. Conclusions: ctDNA is a promising marker of risk stratification, and early relapse detection in resected stage II/III CRC patients. Clinical trial information: NCT03312374 .

scholarly journals Circulating Tumor DNA Analysis: Clinical Implications for Colorectal Cancer Patients. A Systematic Review

2019 ◽  
Vol 3 (3) ◽  
Author(s):  
Sander Bach ◽  
Nina R Sluiter ◽  
Jamie J Beagan ◽  
Joost M Mekke ◽  
Johannes C F Ket ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Systematic Review ◽  
Mutation Analysis ◽  
Kras Mutation ◽  
Copy Number ◽  
Circulating Tumor Dna ◽  
Detection Sensitivity ◽  
Methylation Analysis ◽  
Ctdna Analysis ◽  
Tumor Dna

AbstractBackgroundLiquid biopsies could improve diagnosis, prognostication, and monitoring of colorectal cancer (CRC). Mutation, chromosomal copy number alteration, and methylation analysis in circulating tumor DNA (ctDNA) from plasma or serum has gained great interest. However, the literature is inconsistent on preferred candidate markers, hampering a clear direction for further studies and clinical translation. This review assessed the potential of ctDNA analysis for clinical utility.MethodsA systematic review according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines was conducted up to December 3, 2018, followed by methodological quality assessment. Primary endpoints were accuracy for detection, prognostication, and monitoring.ResultsEighty-four studies were included. For CRC detection, sensitivity was 75% using ctDNA mutation analysis and up to 96% using copy number analysis. Septin 9 (SEPT9) hypermethylation analysis showed sensitivities of 100% and specificities of 97%. Regarding prognostication, ctDNA KRAS mutations were associated with oncological outcome and could predict response to anti–epidermal growth factor receptor therapy. For monitoring, sequential ctDNA KRAS mutation analysis showed promise for detection of relapses or therapy resistance.ConclusionsThis comprehensive overview of ctDNA candidate markers demonstrates SEPT9 methylation analysis to be promising for CRC detection, and KRAS mutation analysis could assist in prognostication and monitoring. Prospective evaluation of marker panels in clinical decision making should bring ctDNA analysis into practice.

scholarly journals Circulating Tumor DNA Outperforms Circulating Tumor Cells for KRAS Mutation Detection in Thoracic Malignancies

2015 ◽  
Vol 61 (10) ◽  
pp. 1299-1304 ◽  
Author(s):  
Maxim B Freidin ◽  
Dasha V Freydina ◽  
Maria Leung ◽  
Angeles Montero Fernandez ◽  
Andrew G Nicholson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Cells ◽  
Circulating Tumor Cells ◽  
Kras Mutation ◽  
Mutation Detection ◽  
Mutation Screening ◽  
Circulating Tumor Dna ◽  
Kras Mutations ◽  
Thoracic Malignancies ◽  
Tumor Dna

Abstract BACKGROUND Circulating biomarkers, such as circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA), are both considered for blood-based mutation detection, but limited studies have compared them in a head-to-head manner. Using KRAS (Kirsten rat sarcoma viral oncogene homolog), we performed such a comparison in patients who underwent surgery for suspected lung cancer. METHODS We recruited 93 patients, including 82 with lung cancer and 11 with benign diseases of the lung. Mutations were detected in codons 12 and 13 of KRAS in DNA extracted from CTCs, plasma, and matched tumors or lung tissues with custom-designed coamplification at lower denaturation temperature (COLD)-PCR assays, high-resolution melt analysis (HRM), and commercial assays (Roche Cobas®KRAS mutation test and Qiagen Therascreen® pyrosequencing KRAS kit). RESULTS With the Cobas mutation test, we identified KRAS mutations in 21.3% of tumors. Mutation analysis in matched CTC DNA and ctDNA samples by COLD-PCR/HRM assay revealed mutations in 30.5% (ctDNA) and 23.2% (CTC DNA) of patients with lung cancer. Combined results of different tests revealed KRAS-positive cases for 28% of tumors. The diagnostic sensitivity and specificity of KRAS mutation detection in tumors achieved with ctDNA was 0.96 (95% CI 0.81–1.00) and 0.95 (0.85–0.99), respectively. The diagnostic test performance was lower for CTC DNA, at 0.52 (0.34–0.73) and 0.88 (0.79–0.95). CONCLUSIONS Our results support ctDNA as a preferential specimen type for mutation screening in thoracic malignancies vs CTC DNA, achieving greater mutation detection than either CTCs or limited amounts of tumor tissue alone.

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