15 research outputs found

    Fragmento de cartílago, detectado en un ganglio linfático, tras punción aspirativa transbronquial guiada con ultrasonografía endobronquial

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    n the last years, the endoscopic units introduce the ultrasonic bronchofibrescope with a convex probe that allows for real-time needle aspiration of mediastinal and hilar lymph nodes guided by ultrasound images. This technique, known as real-time EBUS–TBNA, is minimally invasive and has the potential to replace mediastinoscopy, since it enables the same part of the mediastinum to be accessed

    A foreign body reaction to Surgicel® in a lymph node diagnosed by endobronchial ultrasound-guided transbronchial needle aspiration

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    Surgicel® (Ethicon, North Ryde, NSW, Australia) is an absorbable sheet of oxidized cellulose polyanhydroglucuronic acid polymer used as an hemostatic in cardiovascular and thoracic surgery. In some cases, the retained material may cause foreign body granulomatous reactions and simulate tumor recurrence, an abscess, an hematoma, or an infection. We report the case of a 55-year-old patient who was operated of a lung adenocarcinoma. In the thoracic computed tomography scan 1 year after the surgery, a right paratracheal lymph node was detected, so endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) was performed suspecting recurrence of the tumor. The cytology results of the lymph node showed a nonnecrotizing granulomatous reaction secondary to Surgicel®, used as an hemostatic during the surgery. The objective of presenting this case is to consider foreign body reaction to Surgicel® in the differential diagnosis of postoperative suspicion of neoplastic recurrence, and on the other hand, to note that EBUS-TBNA enables diagnosis

    FDG PET- CT SUVmax and IASLC/ATS/ERS histologic classification: a new profile of lung adenocarcinoma with prognostic value

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    Quantitative analysis of glucose consumption measured by maximum standardized uptake value (SUVmax) in lung adenocarcinoma (LA) remains in discussion and metabolic information provided by FDG-PET is not included in cancer staging. The first aim of this work was to evaluate the correlation between SUVmax and different histologic subtypes of LA. The second aim was to establish the correlation between SUVmax and TNM, genetic mutations and prognostic. Glucose consumption of primary tumor was quantified using SUVmax in 112 patients with histologically-confirmed LA. Specimens were classified according to the IASLC/ATS/ERS into in situ -AIS-, minimally invasive -MIA-, invasive (lepidic, papillary, acinar, solid and micropapillary) and invasive mucinous adenocarcinoma. Tumors were grouped according to three histological grades; low-grade: AIS, MIA, intermediate-grade: lepidic, acinar, papillary and high-grade: micropapillary, solid and mucinous. Comparisons between SUVmax and histologic subtypes were performed with Kruskal-Wallis followed by a Dunn's test. Overall (OS) and disease-free survival (DFS) were calculated. SUVmax was histologically-dependent (P<0.001): AIS 0.5±0.1, MIA 1.1±0.9 lepidic 3.3±3.1, acinar 8.6±6.7, papillary 3.9±5.1, micropapillary 4.9±3.4, solid 10.4±5.4 and invasive mucinous 2.7±1.2. SUVmax was associated with TNM stage in stage IA and IB. SUVmax was significantly lower in patients with K-RAS and EGFR mutation. Low SUVmax was associated with low-grade histology and with a higher OS and DSF compared to high SUVmax (intermediate and high-grade histology). SUVmax on FDG-PET is a powerful information in the presurgical evaluation of LA patients. It provides prognostic data and should be considered in the staging algorithm of patients with LA

    FDG PET- CT SUVmax and IASLC/ATS/ERS histologic classification: a new profile of lung adenocarcinoma with prognostic value

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    Quantitative analysis of glucose consumption measured by maximum standardized uptake value (SUVmax) in lung adenocarcinoma (LA) remains in discussion and metabolic information provided by FDG-PET is not included in cancer staging. The first aim of this work was to evaluate the correlation between SUVmax and different histologic subtypes of LA. The second aim was to establish the correlation between SUVmax and TNM, genetic mutations and prognostic. Glucose consumption of primary tumor was quantified using SUVmax in 112 patients with histologically-confirmed LA. Specimens were classified according to the IASLC/ATS/ERS into in situ -AIS-, minimally invasive -MIA-, invasive (lepidic, papillary, acinar, solid and micropapillary) and invasive mucinous adenocarcinoma. Tumors were grouped according to three histological grades; low-grade: AIS, MIA, intermediate-grade: lepidic, acinar, papillary and high-grade: micropapillary, solid and mucinous. Comparisons between SUVmax and histologic subtypes were performed with Kruskal-Wallis followed by a Dunn's test. Overall (OS) and disease-free survival (DFS) were calculated. SUVmax was histologically-dependent (P<0.001): AIS 0.5±0.1, MIA 1.1±0.9 lepidic 3.3±3.1, acinar 8.6±6.7, papillary 3.9±5.1, micropapillary 4.9±3.4, solid 10.4±5.4 and invasive mucinous 2.7±1.2. SUVmax was associated with TNM stage in stage IA and IB. SUVmax was significantly lower in patients with K-RAS and EGFR mutation. Low SUVmax was associated with low-grade histology and with a higher OS and DSF compared to high SUVmax (intermediate and high-grade histology). SUVmax on FDG-PET is a powerful information in the presurgical evaluation of LA patients. It provides prognostic data and should be considered in the staging algorithm of patients with LA

    Updated guidelines for predictive biomarker testing in advanced non-small-cell lung cancer: a national consensus of the Spanish Society of Pathology and the Spanish Society of Medical Oncology

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    Data de publicació electrònica: 09-10-2019In 2011 the Spanish Society of Medical Oncology (SEOM) and the Spanish Society of Pathology (SEAP) started a joint project to establish guidelines on biomarker testing in patients with advanced non-small-cell lung cancer (NSCLC) based on current evidence. As this field is constantly evolving, these guidelines have been updated, previously in 2012 and 2015 and now in 2019. Current evidence suggests that the mandatory tests to conduct in all patients with advanced NSCLC are for EGFR and BRAF mutations, ALK and ROS1 rearrangements and PD-L1 expression. The growing need to study other emerging biomarkers has promoted the routine use of massive sequencing (next-generation sequencing, NGS). The coordination of every professional involved and the prioritisation of the most suitable tests and technologies for each case remains a challenge

    Systemic and Tumor Th1 and Th2 Inflammatory Profile and Macrophages in Lung Cancer: Influence of Underlying Chronic Respiratory Disease.

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    INTRODUCTION: Chronic respiratory conditions, especially chronic obstructive pulmonary disease (COPD), and inflammatory events underlie lung cancer (LC). We hypothesized that profiles of T helper 1 and T helper 2 cytokines and type 1 and type 2 macrophages (M1 and M2) are differentially expressed in lung tumors and blood of patients with NSCLC with and without COPD and that the ratio M1/M2 specifically may influence their survival. METHODS: In blood, inflammatory cytokines (determined by enzyme-linked immunosorbent assay) were quantified in 80 patients with LC (60 with LC and COPD [the LC-COPD group] and 20 with LC only [the LC-only group]) and lung specimens (tumor and nontumor) from those undergoing thoracotomy (20 in the LC-COPD group and 20 in the LC-only group). RESULTS: In the LC-COPD group compared with in the LC-only group, systemic levels of tumor necrosis factor-α, interleukin-2 (IL-2), transforming growth factor-β, and IL-10 were increased, whereas vascular endothelial growth factor and IL-4 levels were decreased. In lung tumors, levels of tumor necrosis factor-α, transforming growth factor-β, and IL-10 were higher than in nontumor parenchyma in the LC-COPD group, whereas IL-2 and vascular endothelial growth factor levels were higher in tumors of both the LC-only and LC-COPD groups. Compared with in nontumor lung, M1 macrophage counts were reduced whereas M2 counts were increased in tumors of both patient groups, and the M1/M2 ratio was higher in the LC-COPD group than the LC-only group. M1 and M2 counts did not influence patients' survival. CONCLUSIONS: The relative predominance of T helper 1 cytokines and M1 macrophages in the blood and tumors of patients with underlying COPD imply that a stronger proinflammatory pattern exists in these patients. Inflammation should not be targeted systematically in all patients with LC. Screening for the presence of underlying respiratory diseases and identification of the specific inflammatory pattern should be carried out in patients with LC, at least in early stages of their disease.This study has been supported by SEPAR 2008, FUCAP 2009, 391 FUCAP 2011, FUCAP 2012, and FIS 11/02029 (FEDER), FIS 14/00713 (FEDER), 392 PT13/0010/0005 (FEDER), CIBERES (Instituto de Salud Carlos III, Spain), and the 393 "Xarxa de Bancs de tumors sponsored by Pla Director d'Oncologia de Catalunya 394 (XBTC)”, Catalan Government

    Markers of stroma in lung cancer: influence of COPD

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    Background: Stroma, mainly composed by fibroblasts, extracellular matrix (ECM) and vessels, may play a role in tumorigenesis and cancer progression. Chronic Obstructive Pulmonary Disease (COPD) is an independent risk factor for LC. We hypothesized that markers of fibroblasts, ECM and endothelial cells may differ in tumors of LC patients with/without COPD. Methods: Markers of cultured cancer-associated fibroblasts and normal fibroblasts [CAFs and NFs, respectively, vimentin and alpha-smooth muscle actin (SMA) markers, immunofluorescence in cultured lung fibroblasts], ECM, and endothelial cells (type I collagen and CD31 markers, respectively, immunohistochemistry) were identified in lung tumor and non-tumor specimens (thoracotomy for lung tumor resection) from 15 LC-COPD patients and 15 LC-only patients. Results: Numbers of CAFs significantly increased, while those of NFs significantly decreased in tumor samples compared to non-tumor specimens of both LC and LC-COPD patients. Endothelial cells (CD31) significantly decreased in tumor samples compared to non-tumor specimens only in LC patients. No significant differences were seen in levels of type I collagen in any samples or study groups. Conclusions: Vascular endothelial marker CD31 expression was reduced in tumors of non-COPD patients, while type I collagen levels did not differ between groups. A rise in CAFs levels was detected in lung tumors of patients irrespective of airway obstruction. Low levels of CD31 may have implications in the overall survival of LC patients, especially in those without underlying airway obstruction. Identification of CD31 role as a prognostic and therapeutic biomarker in lung tumors of patients with underlying respiratory diseases warrants attention

    Comprehensive NGS profiling to enable detection of ALK gene rearrangements and MET amplifications in non-small cell lung cancer

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    Introduction: Next-generation sequencing (NGS) is currently widely used for biomarker studies and molecular profiling to identify concurrent alterations that can lead to the better characterization of a tumor's molecular landscape. However, further evaluation of technical aspects related to the detection of gene rearrangements and copy number alterations is warranted. Methods: There were 12 ALK rearrangement-positive tumor specimens from patients with non-small cell lung cancer (NSCLC) previously detected via fluorescence in situ hybridization (FISH), immunohistochemistry (IHC), and an RNA-based NGS assay, and 26 MET high gene copy number (GCN) cases detected by FISH, selected for this retrospective study. All 38 pre-characterized cases were reassessed utilizing the PGDx™ elio™ tissue complete assay, a 505 gene targeted NGS panel, to evaluate concordance with these conventional diagnostic techniques. Results: The detection of ALK rearrangements using the DNA-based NGS assay demonstrated excellent sensitivity with the added benefit of characterizing gene fusion partners and genomic breakpoints. MET copy number alterations were also detected; however, some discordances were observed likely attributed to differences in algorithm, reporting thresholds and gene copy number state. TMB was also assessed by the assay and correlated to the presence of NSCLC driver alterations and was found to be significantly lower in cases with NGS-confirmed canonical driver mutations compared with those without (p=0.0019). Discussion: Overall, this study validates NGS as an accurate approach for detecting structural variants while also highlighting the need for further optimization to enable harmonization across methodologies for amplifications

    EGFR and KRAS mutations in the non-tumoral lung. Prognosis in patients with adenocarcinoma

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    Tumor recurrence is frequent and survival rates remain extremely low in lung adenocarcinoma (ADC). We hypothesize that carcinogenic factors will promote loco-regional modifications not only in the future tumor, but throughout the exposed lung. Objective: To analyze whether the most prevalent mutations observed in ADC can also be observed in the non-neoplastic lung tissue, as well as the short-term prognosis implications of this finding. Methods: Non-tumoral lung parenchyma specimens obtained during surgery from 47 patients with EGFR and/or KRAS abnormalities in their ADC tumors underwent similar genomic testing. Short-term outcomes were also recorded. Results: The same mutations were present in the tumor and the histologically normal tissue in 21.3% of patients (SM group). Although local recurrences were similar in both groups, distant metastases were more frequent in the former (60 vs. 5.4%, p < 0.001). Moreover, SM patients showed lower time-to-progression (8.5 vs. 11.7 months, p < 0.001) and disease-free survival (8.5 vs. 11.2 months, p < 0.001). COX regression showed a higher risk of progression or death (DFS) in the SM group (HR 5.94, p < 0.01]. Similar results were observed when adjusting for potential confounding variables. Conclusions: These results confirm that genetic changes are present in the apparently normal lung in many ADC patients, and this finding has prognostic implications
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