Impact of the Mental Health Care Continuity-Chain among Individuals Expressing Suicidal Behaviour in a Spanish Sample.

Poor coordination between different healthcare services means that the proper follow-up of patients cannot be guaranteed, thus increasing the risk of relapse in cases of attempted suicide. This study describes the sociodemographic variables related to suicidal behaviour in a Spanish sample and analyses how the use of a continued nursing care protocol influences the follow-up of patients who have shown suicidal behaviour. A cohort of 213 patient was identified from the emergency department medical records because of suicide attempters during 2011; 51.6% were included in the intervention group (n = 110) and 48.4% (n = 103) in the control group. We used a specific continuity of care chain protocol with the patients in the intervention group. More than half of all the initial suicide attempts were made by women; 80.3% had a previous history of a mental disorder and 65.7% of the attempts were made by ingesting medications. Significantly more patients in the intervention group attended their first follow-up visit. This study highlights the need to implement protocols that favour the continuity of mental health care processes-especially those designed to treat individuals expressing suicidal behaviour-with the aim of reducing the risk of suicide in them by intensifying their monitoring.

Value contribution of blood-based neurofilament light chain as a biomarker in multiple sclerosis using multi-criteria decision analysis.

Introduction: Multiple sclerosis (MS) is a chronic autoimmune demyelinating disease that represents a leading cause of non-traumatic disability among young and middle-aged adults. MS is characterized by neurodegeneration caused by axonal injury. Current clinical and radiological markers often lack the sensitivity and specificity required to detect inflammatory activity and neurodegeneration, highlighting the need for better approaches. After neuronal injury, neurofilament light chains (NfL) are released into the cerebrospinal fluid, and eventually into blood. Thus, blood-based NfL could be used as a potential biomarker for inflammatory activity, neurodegeneration, and treatment response in MS. The objective of this study was to determine the value contribution of blood-based NfL as a biomarker in MS in Spain using the Multi-Criteria Decision Analysis (MCDA) methodology. Materials and methods: A literature review was performed, and the results were synthesized in the evidence matrix following the criteria included in the MCDA framework. The study was conducted by a multidisciplinary group of six experts. Participants were trained in MCDA and scored the evidence matrix. Results were analyzed and discussed in a group meeting through reflective MCDA discussion methodology. Results: MS was considered a severe condition as it is associated with significant disability. There are unmet needs in MS as a disease, but also in terms of biomarkers since no blood biomarker is available in clinical practice to determine disease activity, prognostic assessment, and response to treatment. The results of the present study suggest that quantification of blood-based NfL may represent a safe option to determine inflammation, neurodegeneration, and response to treatments in clinical practice, as well as to complement data to improve the sensitivity of the diagnosis. Participants considered that blood-based NfL could result in a lower use of expensive tests such as magnetic resonance imaging scans and could provide cost-savings by avoiding ineffective treatments. Lower indirect costs could also be expected due to a lower impact of disability consequences. Overall, blood-based NfL measurement is supported by high-quality evidence. Conclusion: Based on MCDA methodology and the experience of a multidisciplinary group of six stakeholders, blood-based NfL measurement might represent a high-value-option for the management of MS in Spain.

Evaluation of 2- and 3-dimensional anatomic parameters of C-shaped root canals with cone beam computed tomography, microcomputed tomography, and nanocomputed tomography.

OBJECTIVE: The objective of this study was to evaluate 2-dimensional (2D) and 3D morphometric parameters of C-shaped root canals on cone beam computed tomography (CBCT) and microcomputed tomography (microCT) images using nanocomputed tomography (nanoCT) as the reference standard. STUDY DESIGN: Sixty mandibular molars with C-shaped canals were individually scanned using nanoCT and microCT. Cone beam computed tomography acquisitions were then performed with 4 CBCT systems, using high and standard resolutions. The 2D parameters of roundness and major and minor diameters were obtained in the cross sections of the root canals at 1, 2, and 3 mm from the root apex. The 3D parameters of surface area, volume, and structure model index were measured considering the entire extension of the root canals. Absolute error (AE) in measurement was calculated against the nanoCT values. Data were statistically analyzed with the Shapiro-Wilk test and analysis of variance (α = 0.05). RESULTS: No significant differences in AE were discovered for the 2D parameters among microCT and the CBCT scans. The AE values for the 3D parameters of volume and surface area were significantly smaller in microCT compared to all CBCT units (P < .05). Significantly lower AE values for surface area were observed in high resolution compared to standard resolution for all CBCT units (P < .05). Structure model index did not differ significantly among microCT and all CBCT protocols. CONCLUSIONS: Cone beam computed tomography images showed accuracy for evaluating 2D parameters and over- and underestimation for 3D parameters.

Baseline Profiles of Drug Prescriptions Prior to Diagnosis of Mild Cognitive Impairment (MCI) Obtained by Latent Class Analysis (LCA), and Assessment of Their Association with Conversion to Dementia.

Polypharmacy has been linked to cognitive decline. However, interventions targeting modifiable risk factors, some of which are targets of the most commonly used drugs, could reduce the prevalence of dementia. Our aim was to determine the drug prescription regimen at baseline, prior to the diagnosis of mild cognitive impairment (MCI), and its possible association with progression to dementia. Data were collected from the electronic medical records of 342 MCI outpatients diagnosed during 2006-2017 at their first neurology consultation. We followed the classical three-step method of statistical analysis, starting with a Latent Class Analysis (LCA) to discover subgroups of drug prescription probability. Half of the patients were under polypharmacy (≥5 drugs), 17.5% had no recorded medication, 33.3% progressed to dementia (94.7% in ≤5 years), and 84.1% of them to Alzheimer's disease (AD). According to the LCA and based on 20 therapeutic indicators obtained from 240 substances and regrouped according the Anatomical Therapeutic Chemical Classification, we identified a four-profile model: (1) low (35.7% of patients); (2) mixed (28.7%); (3) cardio-metabolic (19.3%); and (4) psychotropic (16.4%). The binomial regression logistic model showed that profiles 2 and 3 (and 4 for AD), with a higher drug prescription conditioned probability against classic risk factors, were protective than profile 1 (OR = 0.421, p = 0.004; OR = 0.278, p = 0.000; OR = 0.457, p = 0.040, respectively), despite polypharmacy being significant in profiles 2 and 3 (mean > 7 drugs) vs. profile 1 (1.4 ± 1.6) (p = 0.000). Patients in the latter group were not significantly older, although being aged 65-79 years old quadrupled (OR = 4.217, p = 000) and being >79 tripled (OR = 2.945, p = 0.010) the conversion risk compared to patients <65 years old. According to the proposed analytical model, profiling the heterogeneous association of risk factors, which were taken prior to diagnosis, could be explored as an indicator of prior care and a predictor of conversion to dementia.

Screening for epidermal growth factor receptor mutations in lung cancer.

BACKGROUND: Activating mutations in the epidermal growth factor receptor gene (EGFR) confer hypersensitivity to the tyrosine kinase inhibitors gefitinib and erlotinib in patients with advanced non-small-cell lung cancer. We evaluated the feasibility of large-scale screening for EGFR mutations in such patients and analyzed the association between the mutations and the outcome of erlotinib treatment. METHODS: From April 2005 through November 2008, lung cancers from 2105 patients in 129 institutions in Spain were screened for EGFR mutations. The analysis was performed in a central laboratory. Patients with tumors carrying EGFR mutations were eligible for erlotinib treatment. RESULTS: EGFR mutations were found in 350 of 2105 patients (16.6%). Mutations were more frequent in women (69.7%), in patients who had never smoked (66.6%), and in those with adenocarcinomas (80.9%) (P<0.001 for all comparisons). The mutations were deletions in exon 19 (62.2%) and L858R (37.8%). Median progression-free survival and overall survival for 217 patients who received erlotinib were 14 months and 27 months, respectively. The adjusted hazard ratios for the duration of progression-free survival were 2.94 for men (P<0.001); 1.92 for the presence of the L858R mutation, as compared with a deletion in exon 19 (P=0.02); and 1.68 for the presence of the L858R mutation in paired serum DNA, as compared with the absence of the mutation (P=0.02). The most common adverse events were mild rashes and diarrhea; grade 3 cutaneous toxic effects were recorded in 16 patients (7.4%) and grade 3 diarrhea in 8 patients (3.7%). CONCLUSIONS: Large-scale screening of patients with lung cancer for EGFR mutations is feasible and can have a role in decisions about treatment.

Combined FGFR and Akt pathway inhibition abrogates growth of FGFR1 overexpressing EGFR-TKI-resistant NSCLC cells.

EGFR tyrosine kinase inhibitor (TKI) resistance in non-small cell lung cancer (NSCLC) patients is inevitable. Identification of resistance mechanisms and corresponding targeting strategies can lead to more successful later-line treatment in many patients. Using spectrometry-based proteomics, we identified increased fibroblast growth factor receptor 1 (FGFR1) expression and Akt activation across erlotinib, gefitinib, and osimertinib EGFR-TKI-resistant cell line models. We show that while combined EGFR-TKI and FGFR inhibition showed some efficacy, simultaneous inhibition of FGFR and Akt or PI3K induced superior synergistic growth inhibition of FGFR1-overexpressing EGFR-TKI-resistant NSCLC cells. This effect was confirmed in vivo. Only dual FGFR and Akt inhibition completely blocked the resistance-mediating signaling pathways downstream of Akt. Further, increased FGFR1 expression was associated with significantly lower PFS in EGFR-TKI-treated NSCLC patients, and increased FGFR1 were demonstrated in a few post- vs. pre-EGFR-TKI treatment clinical biopsies. The superior therapeutic benefit of combining FGFR and Akt inhibitors provide the rationale for clinical trials of this strategy.

Clinicopathologic Features and Response to Therapy of NRG1 Fusion-Driven Lung Cancers: The eNRGy1 Global Multicenter Registry.

PURPOSE: Although NRG1 fusions are oncogenic drivers across multiple tumor types including lung cancers, these are difficult to study because of their rarity. The global eNRGy1 registry was thus established to characterize NRG1 fusion-positive lung cancers in the largest and most diverse series to date. METHODS: From June 2018 to February 2020, a consortium of 22 centers from nine countries in Europe, Asia, and the United States contributed data from patients with pathologically confirmed NRG1 fusion-positive lung cancers. Profiling included DNA-based and/or RNA-based next-generation sequencing and fluorescence in situ hybridization. Anonymized clinical, pathologic, molecular, and response (RECIST v1.1) data were centrally curated and analyzed. RESULTS: Although the typified never smoking (57%), mucinous adenocarcinoma (57%), and nonmetastatic (71%) phenotype predominated in 110 patients with NRG1 fusion-positive lung cancer, further diversity, including in smoking history (43%) and histology (43% nonmucinous and 6% nonadenocarcinoma), was elucidated. RNA-based testing identified most fusions (74%). Molecularly, six (of 18) novel 5' partners, 20 unique epidermal growth factor domain-inclusive chimeric events, and heterogeneous 5'/3' breakpoints were found. Platinum-doublet and taxane-based (post-platinum-doublet) chemotherapy achieved low objective response rates (ORRs 13% and 14%, respectively) and modest progression-free survival medians (PFS 5.8 and 4.0 months, respectively). Consistent with a low programmed death ligand-1 expressing (28%) and low tumor mutational burden (median: 0.9 mutations/megabase) immunophenotype, the activity of chemoimmunotherapy and single-agent immunotherapy was poor (ORR 0%/PFS 3.3 months and ORR 20%/PFS 3.6 months, respectively). Afatinib achieved an ORR of 25%, not contingent on fusion type, and a 2.8-month median PFS. CONCLUSION: NRG1 fusion-positive lung cancers were molecularly, pathologically, and clinically more heterogeneous than previously recognized. The activity of cytotoxic, immune, and targeted therapies was disappointing. Further research examining NRG1-rearranged tumor biology is needed to develop new therapeutic strategies.

Epidermal growth factor receptor tyrosine kinase inhibitors as first-line treatment in advanced nonsmall-cell lung cancer.

PURPOSE OF REVIEW: Classic activating mutations in the form of deletions in exon 19 or a missense mutation L858R in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) predict dramatic responses to EGFR tyrosine kinase inhibitors such as gefitinib and erlotinib. We review here the clinical benefits of targeted therapy with erlotinib and gefitinib in white and Asian nonsmall-cell lung cancer patients. RECENT FINDINGS: Two separate analyses of pooled data from small phase II prospective studies show that therapy with gefitinib and erlotinib induces responses in over 70% of nonsmall-cell lung cancer patients harboring classic EGFR mutations, with progression-free survival ranging from 9 to 13 months and median survival of around 23 months. Two separate studies in white and Asian patients have recently confirmed that these subgroups of patients attain response rates of 70% with erlotinib and gefitinib, including complete responses, progression-free survival of up to 14 months, and median survival of up to 27 months. The serial monitoring of EGFR mutations in the blood will permit the assessment of molecular responses and be an important tool for the surveillance of clinical progression. SUMMARY: Nonsmall-cell lung cancer with EGFR mutations constitute a new entity with a unique opportunity for further refinement of different genetic subgroups among patients with EGFR mutations, requiring different personalized treatment strategies. Despite the impressive outcomes attained with EGFR tyrosine kinase inhibitors, patients with EGFR mutations at present require continuous treatment, and only a fraction of these patients will reach sustainable long-term survival.

Detection of EGFR mutations with mutation-specific antibodies in stage IV non-small-cell lung cancer.

BACKGROUND: Immunohistochemistry (IHC) with mutation-specific antibodies may be an ancillary method of detecting EGFR mutations in lung cancer patients. METHODS: EGFR mutation status was analyzed by DNA assays, and compared with IHC results in five non-small-cell lung cancer (NSCLC) cell lines and tumor samples from 78 stage IV NSCLC patients. RESULTS: IHC correctly identified del 19 in the H1650 and PC9 cell lines, L858R in H1975, and wild-type EGFR in H460 and A549, as well as wild-type EGFR in tumor samples from 22 patients. IHC with the mAb against EGFR with del 19 was highly positive for the protein in all 17 patients with a 15-bp (ELREA) deletion in exon 19, whereas in patients with other deletions, IHC was weakly positive in 3 cases and negative in 9 cases. IHC with the mAb against the L858R mutation showed high positivity for the protein in 25/27 (93%) patients with exon 21 EGFR mutations (all with L858R) but did not identify the L861Q mutation in the remaining two patients. CONCLUSIONS: IHC with mutation-specific mAbs against EGFR is a promising method for detecting EGFR mutations in NSCLC patients. However these mAbs should be validated with additional studies to clarify their possible role in routine clinical practice for screening EGFR mutations in NSCLC patients.

Biomarkers in lung oncology.

The survival of advanced non-small-cell lung cancer patients is short in spite of advances in new combination chemotherapy regimens. The benefit of adding antiangiogenic drugs and/or EGFR inhibitors is unclear. For the vast majority of patients without EGFR mutations, treatment approaches based on customization should be pursued. BRCA1 is central to the repair of DNA damage and is an important modulator of the differential effect of chemotherapy. Retrospective and prospective data indicate that low BRCA1 mRNA levels predict better response and survival when patients are treated with cisplatin, non-taxane combinations. For an important subgroup of patients with EGFR mutations, selective treatment with EGFR tyrosine kinase inhibitors is a major advance, with a dramatic impact on clinical outcomes. In a prospective study of customized erlotinib [1], overall response rate was 70% (including 12% complete responses), median progression free survival was 14 months (even longer in women and in patients with del 19), 20% of patients were disease-free at three years, and median survival was 27 months. Nonetheless, these clinical outcomes fall short of curability and continuous treatment with erlotinib or gefitinib is required. It is plausible that several genetically defined subclasses of EGFR mutations could help to improve current clinical outcomes by combining erlotinib or gefitinib with other targeted drugs.

[Poland's syndrome. Case report]. / Síndrome de Poland. Informe de un caso.

OBJECTIVE: To report a case of Poland syndrome in a 67-year-old woman. CLINICAL CASE: The patient was questioned and examined for a history of malformations characteristic of this syndrome on a routine medical visit. Thorax, bone thorax, and comparative hand X-ray were taken. Mammary ultrasound, mastography, and computed axial tomography were taken also. The right hemithorax showed a thin subcutaneous cell tissue. Axillary alopecia, mammary hypoplasia and areola-nipple complex retraction, hypoplasia of major pectoral muscles was observed. In the right upper limb, there was forearm shortening, hypoplasia of the second phalanx in all five fingers, and absence of distal phalanx in the index finger. CONCLUSIONS: The patient showed 4 out of the 5 characteristics considered as typical by Hester and Bostwick. In terms of hand anomalies, she was classified as type 1 according to Gausewitz and according with Al-Qaifan, the patient belongs to type 2.

IL-6/gp130/STAT3 signaling axis in cancer and the presence of in-frame gp130 somatic deletions in inflammatory hepatocellular tumors.

Evaluation of: Rebouissou S, Amessou M, Couchy G et al.: Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumours. Nature 457, 200-204 (2009). Recently, in-frame somatic deletions activating gp130, the receptor of IL-6, have been identified in inflammatory hepatocellular adenomas. This is a novel class of mutation in a receptor that is central to the IL-6/gp130/STAT3 pathway, which is relevant in a variety of cancers. STAT3 is a cancer transcriptional node activating several prosurvival and proliferation genes. The activation of IL-6/gp130 also promotes the activation of the RAS and PI3K pathways. Intriguingly, the overexpression of IL-6 and STAT3 has been observed in lung adenocarcinomas, including those with EGF-receptor mutations. Further clinical research should be performed on the IL-6/gp130/STAT3 signaling axis, since it constitutes an autocrine and paracrine amplification loop in several tumors, including those with RAS mutations.

Impact of single nucleotide polymorphisms on the efficacy and toxicity of EGFR tyrosine kinase inhibitors in advanced non-small cell lung cancer patients.

EGFR tyrosine kinase inhibitors (EGFR-TKIs) are the treatment of choice for advanced-stage (IIIB-IV) NSCLC patients with mutations in EGFR. However, EGFR-TKIs clinical outcomes vary from person to person and these inter-individual differences may be due to genetic factors such as single nucleotide polymorphisms (SNPs). SNPs in genes involved in EGFR-TKIs pharmacodynamics, metabolism and mechanism of action have been demonstrated to be associated with response, survival and toxicity in advanced NSCLC patients treated with EGFR-TKIs. Here we review the influence of gene polymorphisms in the EGFR pathway on clinical outcome and toxicity to EGFR-TKIs in advanced NSCLC patients. The EGFR-216 polymorphism has reported a strong association between response and/or survival to EGFR-TKIs in Caucasian population. Similarly, the effect of EGFR-CA repeats polymorphisms on survival of advanced NSCLC patients treated with EGFR-TKIs have been confirmed both in Caucasian and Asian population. The influence on toxicity of the -216, -191, CA repeats, Arg497Lys and Asp994Asp polymorphisms in EGFR have also been confirmed. Polymorphisms in AKT (rs1130214 and rs1130233) and SMAD3 (rs6494633, rs11071938 and rs11632964) have been associated with survival in advanced NSCLC patients treated with EGFR-TKIs. However, data come from a limited number of studies and need to be confirmed. Finally, polymorphisms in genes coding proteins of the membrane transporters and cytochrome P450 enzymes have been less extensively investigated. There are few studies with small samples, which complicated the generalization of their role in EGFR-TKIs treatment.

Characterising acquired resistance to erlotinib in non-small cell lung cancer patients.

Introduction: The therapy of patients with lung adenocarcinoma has significantly changed after the discovery of epidermal growth factor receptor (EGFR) mutations. EGFR mutations occur in 10-15% of Caucasian lung cancer patients and are associated with favorable outcome to orally administered EGFR tyrosine kinase inhibitors (TKIs), like erlotinib. However, as soon as the tumor cells are under the pressure of the specific inhibitor, compensatory signaling pathways are activated and resistance emerges. Areas covered: In this review we will focus on the mechanisms of resistance to the first-generation EGFR TKI, erlotinib, and will mainly summarize the findings throughout the last 10 years in the field of EGFR-mutant lung cancer. Expert opinion: Widespread research has been performed and several mechanisms of resistance to EGFR TKIs, especially first- and second-generation, have been identified. Still, no adequate combinatory therapies have received regulatory approval for the treatment of EGFR-mutant patients at the time of resistance. The third-generation EGFR TKI, osimertinib has been approved for patients whose tumor has become resistant through the secondary T790M resistant EGFR mutation. The identification of the mechanisms of resistance and the application of the adequate therapy to each patient is still an unmet need.

Association between the novel classification of lung adenocarcinoma subtypes and EGFR/KRAS mutation status: A systematic literature review and pooled-data analysis.

OBJECTIVES: This study aims to determine the association of EGFR/KRAS mutation status with histological subtypes of lung adenocarcinoma (LAC) based on the IASLC/ATS/ERS classification. METHODS: Pubmed and Cochrane databases were searched from January 2011 to June 2018 for studies that included patients with LAC who underwent surgical resection were classified according to the new IASLC/ATS/ERS classification. EGFR/KRAS status assessment was requireded. The primary outcome was determined by the odds ratio (OR) of the incidence of mutation status of certain of each histological subtype. The reference group consisted of EGFR/KRAS mutation negative patients. RESULTS: Twenty-seven eligible studies involving 9022 patients with mutation gene detection were included for analysis. Among them, 6717 (74.5%) patients were from the Asian region and, 2305 (25.5%) patients were from Non-Asian regions. The most prevalent subtype was acinar (34.7%), followed by papillary (22.9%), lepidic (18.9%), solid (13.6%), micropapillary (6.3%), and invasive mucinous adenocarcinoma (3.5%). EGFR mutations were more common in patients with resected lepidic predominant adenocarcinoma (OR,1.76; 95%CI, 1.38-2.24;p < 0.01) and were rarely found in solid predominant adenocarcinoma (OR,0.28; 95%CI, 0.23-0.34;p < 0.01) or IMA (OR,0.10; 95%CI, 0.06-0.14;p < 0.01). Conversely, KRAS mutations were characterized by IMA (OR,7.01; 95%CI, 5.11-9.62;p < 0.01), and were less frequently identified in lepidic (OR,0.58; 95%CI, 0.45-0.75;p < 0.01) and acinar (OR,0.65; 95%CI, 0.55-0.78;p < 0.01) predominant subtypes. Further analyses were performed in Asian and Non-Asian groups and the results were consistent. CONCLUSIONS: The current study confirms that the IASLC/ATS/ERS classification is associated with driver gene alterations in resected LAC.

A Single-Center Retrospective Study of Patients with Double Primary Cancers: Breast Cancer and EGFR-Mutant Non-Small Cell Lung Cancer.

BACKGROUND: Second primary malignancies (SPM) in the lung are not common in breast cancer (BC) patients. EGFR-mutant lung cancer (LC) is a separate molecular subset, and the co-existence of EGFR-mutant LC and BC has not been explored. We hypothesized that EGFR-mutant LC patients could have higher rates of primary BC than those with EGFR-wild type (WT). METHODS: We collected data on clinical and molecular characteristics and outcomes of female patients with LC and a previous or simultaneous history of primary BC treated in our hospital from 2008 to 2014. RESULTS: Data on treatment, follow-up, and EGFR mutation status were available for 356 patients. 17.7% (11/62) of patients with EGFR mutations had BC, compared to 1.02% (3/294) of EGFR-WT patients (p < 0.001). Both tumors were metachronous in 81.8%, with LC diagnosed 9 years after the diagnosis of BC. 5 of the 6 (83.3%) BC patients treated with radiotherapy developed LC in an area within the radiation field. No EGFR mutations were detected in BC tissue and no HER2 expression was detected in LC samples. CONCLUSION: SPM in the lung and breast occur more frequently among EGFR-mutant compared to EGFR-WT LC patients. Radiotherapy for BC may increase the risk of developing primary LC.

Translational research in glioblastoma multiforme: molecular criteria for patient selection.

In spite of the dismal outcome of glioblastoma multiforme (GBM), we are in a position to provide a ray of hope to patients and families. Methylation of MGMT in tumor occurs in approximately a third of patients and predicts meaningful response and survival to adjuvant radiotherapy plus temozolomide. Limited access to tumor tissue in some patients could be circumvented by examining MGMT methylation in circulating serum DNA, although this approach needs to be validated. Molecular signatures are also promising prognostic and predictive markers, and clinical trials should be carried out to validate their use in the selection of patients for specific targeted therapies. Gene expression by quantitative PCR of key components of these molecular signatures could pave the way for easy identification of different subgroups of patients. Translational clinical trials are warranted in order to detect the subgroups of patients resistant to radiotherapy who may derive benefit from novel therapies, including antiangiogenic drugs.

Possible application of circulating free tumor DNA in non-small cell lung cancer patients.

Liquid biopsies have been heralded as a game changer in cancer management. Blood tests offer a minimally invasive, safe and sensitive complementary (or even alternative) approach for tissue biopsies. With lung cancer being the second most commonly diagnosed cancer and the leading cause of cancer deaths worldwide, due to the limitations of tissue sampling, liquid biopsies must urgently materialize in the clinic. In this short review, we will present the current applications of cell-free DNA (cfDNA) in lung cancer management, emphasizing on our own experience and previous work. We will also shortly comment on the challenges and need for a coordinated collaboration combining disciplines and sectors (from academia to health economies) in order to accelerate liquid biopsy development in lung cancer and other cancers.