Pulmonary Tumors Research Articles

Randomized Evaluation of the PET-Adjusted IMRT for NSCLC Trial (REPAINT).

Standard radiotherapy (RT) for locally advanced NSCLC (LA-NSCLC) employs a uniform dose of approximately 60 Gy. Recent trials demonstrated that radiotherapy dose escalation may not improve outcomes and may cause added toxicity. XXX previously performed a single-arm trial testing a personalized, risk-adapted, and de-intensified RT strategy. We now report findings from a randomized trial testing this novel approach. LA-NSCLC patients with ECOG performance status 0-2 were eligible for this trial. Metabolic tumor volume (MTV) for each pulmonary tumor and involved lymph node was calculated using FDG-PET. Participants were randomized 1:1 to receive standard RT (60 Gy in 30 fractions delivered to pulmonary tumors and involved lymph nodes) versus dose-painted RT (55 Gy delivered to tumors and lymph nodes with metabolic volume exceeding 20 cm3 and 44-48 Gy to other lesions, all in 20 fractions). Concurrent chemotherapy and standard adjuvant therapy were given in both arms. The primary objective was to characterize patient-reported outcomes utilizing PRO-CTCAE. Secondary objectives included comparing outcomes between study arms. Fifty patients were enrolled. The most common grade 3 patient-reported adverse events within 90 days of RT completion were dysphagia (38%), fatigue (38%), cough (32%), and wheezing (28%). The median progression-free survival (PFS) duration is 18 months, and the median overall survival (OS) duration is 42 months. PFS and OS rates are similar across study arms (logrank p=0.562 and 0.765, respectively). There have been three cases of in-field disease progression, with one in the control arm and two in the dose-painted arm. Grade 3-4 lymphopenia was reduced with dose-painted RT (48% v. 81%, chi-square p=0.012). High-grade patient-reported toxicity in LA-NSCLC patients who are treated with concurrent chemoradiotherapy is common. We found no evidence that risk-adapted radiotherapy de-escalation compromises clinical outcomes. Follow-up studies testing the ability of this approach to improve the safety profile of chemoradiotherapy are warranted.

Early Effects of Bronchoscopic Cryotherapy in Metastatic Non-Small Cell Lung Cancer Patients Receiving Immunotherapy: A Single-Center Prospective Study.

Background/Objectives: Cryotherapy is used for local tissue destruction through rapid freeze-thaw cycles. It induces cancer cell necrosis followed by inflammation in the treated tumor microenvironment, and it stimulates systemic adaptive immunity. Combining cryotherapy with immunotherapy may provide a sustained immune response by preventing T cell exhaustion. Methods: Fifty-five patients with metastatic non-small cell lung cancer who had received no prior treatment were randomized into two groups in a 1:1 ratio: the bronchoscopic cryotherapy group or the control group. Patients received up to four cycles of pembrolizumab as monotherapy or in combination with platinum-based chemotherapy. Immune-related adverse events (irAEs), complications, tumor size changes, overall response rate (ORR), and disease control rate (DCR) were evaluated. Results: Lung tumors, treated with cryotherapy, demonstrated continuous reduction from the baseline (22.4 cm2 vs. 14.4 cm2 vs. 10.2 cm2, p < 0.001). Similar changes were observed in pulmonary tumors in the control group (19.0 cm2 vs. 10.0 cm2, p < 0.001). The median change in pulmonary tumors between two groups was not significant (-42.9% vs. -27.7%, p = 0.175). No significant differences were observed in the ORR (28.6% vs. 23.1%, p = 0.461) or target lesion decrease (-24.0% vs. -23.4%, p = 0.296) between the groups. However, the DCR was significantly higher in the cryotherapy group (95.2% vs. 73.1%, p = 0.049). No cases of serious bleeding during cryotherapy or pneumothorax were observed. Six patients (25.0%) in the cryotherapy group and eight (26.7%) in the control group experienced irAEs. Conclusions: Our study demonstrated that combined bronchoscopic cryotherapy and immunotherapy with or without chemotherapy may reduce the rate of progressive disease in metastatic non-small cell lung cancer patients while maintaining a satisfactory safety profile.

A case of an ectopic adrenocorticotropic hormone-releasing pulmonary carcinoid tumor presenting with acute Cushing's syndrome

A case of an ectopic adrenocorticotropic hormone-releasing pulmonary carcinoid tumor presenting with acute Cushing's syndrome

Recent Advances in the Clinical Translation of Small-Cell Lung Cancer Therapeutics.

Small-cell lung cancer (SCLC) is a recalcitrant form of cancer, representing 15% of lung cancer cases globally. SCLC is classified within the range of neuroendocrine pulmonary neoplasms, exhibiting shared morphologic, ultrastructural, immunohistochemical, and molecular genomic features. It is marked by rapid proliferation, a propensity for early metastasis, and an overall poor prognosis. The current conventional therapies involve platinum-etoposide-based chemotherapy in combination with immunotherapy. Nonetheless, the rapid emergence of therapeutic resistance continues to pose substantial difficulties. The genomic profiling of SCLC uncovers significant chromosomal rearrangements along with a considerable mutation burden, typically involving the functional inactivation of the tumor suppressor genes TP53 and RB1. Identifying biomarkers and evaluating new treatments is crucial for enhancing outcomes in patients with SCLC. Targeted therapies such as topoisomerase inhibitors, DLL3 inhibitors, HDAC inhibitors, PARP inhibitors, Chk1 inhibitors, etc., have introduced new therapeutic options for future applications. In this current review, we will attempt to outline the key molecular pathways that play a role in the development and progression of SCLC, together with a comprehensive overview of the most recent advancements in the development of novel targeted treatment strategies, as well as some ongoing clinical trials against SCLC, with the goal of improving patient outcomes.

Atypical Small Cell Lung Cancer: A New Malignancy Characterized by Chromothripsis, Carcinoid Tumors, and Wild-type RB1 and TP53.

Small cell lung cancer (SCLC) and pulmonary carcinoid tumors are traditionally seen as unrelated, with SCLC linked to smoking and characterized by biallelic loss of RB1 and TP53 and rapid progression. Rekhtman and colleagues upend these assumptions by discovering an "atypical" SCLC that arises in nonsmokers with intact RB1 and TP53 loci, chromothripsis-induced oncogene amplifications on extrachromosomal DNA, and frequent synchronous carcinoid tumors. See related article by Rekhtman et al., p. 83.

The analysis of molecular classification of pulmonary neuroendocrine tumors and relationship between YAP1 and efficacy.

A novel molecular classification for small cell lung cancer (SCLC) has been established utilizing the transcription factors achaete-scute homologue 1 (ASCL1), neurogenic differentiation factor 1 (NeuroD1), POU class 2 homeobox 3 (POU2F3), and yes-associated protein 1 (YAP1). This classification was predicated on the transcription factors. Conversely, there is a paucity of information regarding the distribution of these markers in other subtypes of pulmonary neuroendocrine tumors (PNET). Clinical and survival data for PNET patients were gathered from January 2008 to December 2020. Immunohistochemical analysis was employed to evaluate the expression. The relationship between YAP1 expression and outcomes in patients with pulmonary large cell neuroendocrine carcinoma (LCNEC) was examined. Data from low-grade PNET patients who had previously undergone immunotherapy were retrospectively gathered and analyzed. The ASCL1 positive rate was markedly elevated in SCLC (7.1% vs. 60%; P < 0.001) and LCNEC patients (7.1% vs. 38.5%; P = 0.034) compared to PC patients. The YAP1-positive rate was elevated in LCNEC compared to SCLC (43.6% vs. 20%, P = 0.028) and pulmonary carcinoid (PC) patients (43.6% vs. 21.4%; P = 0.021). The DLL3-positive rate in SCLC patients was greater than in SCLC and PC patients (37.1% vs. 23.1% vs. 0%; P = 0.028, P = 0.021). A significant level of tumor heterogeneity was noted, with SCLC and LCNEC patients exhibiting markedly higher heterogeneity than PC patients (65.7% vs. 56.3% vs. 21.4%; P = 0.005, P = 0.025). In patients with LCNEC, YAP1 positivity exhibited no correlation with PD-L1 expression (17.1% vs. 45.7%, P = 0.518). Tumor heterogeneity was also noted in transformed SCLC, with no significant differences in the expression levels of transcription factors between transformed and traditional SCLC. In 13 LCNEC patients with a history of ICI application, YAP1 exhibited no significant effect on PFS (P = 0.331) or OS (P = 0.17) in the subgroup analysis of LCNEC patients. Among the 14 patients with low-grade PNET who underwent immunotherapy, the disease control rate was 85.7%. Patients with high-grade PNET have high levels of expression of ASCL1 and DLL3, whereas patients with LCNEC have high levels of expression of YAP1. With regard to the transcription factor level, it was found that patients with SCLC and LCNEC had a much higher degree of tumor heterogeneity than those with PC. In patients with LCNEC who were receiving monotherapy of ICIs or chemotherapy in combination with ICIs, the expression of YAP1 did not appear to have any clear impact on the prognosis. This is due to the limited sample size of the study, which requires additional investigation. When compared to the expression of TFs in regular SCLC, the expression of TFs in converted SCLC is comparable.

Associations of short-term exposure to air pollution with risk of pulmonary space-occupying lesions morbidity based on a time-series study

BackgroundPulmonary space-occupying lesions are typical chronic pulmonary diseases that contribute significantly to healthcare resource use and impose a large disease burden in China. A time-series ecological trend study was conducted to investigate the associations between environmental factors and hospitalizations for pulmonary space-occupying lesions in North of China from 2014 to 2022.MethodsThe DLNM was used to quantify the association of environmental factors with lung cancer admissions. The heating-, age-, gender-, malignancy-specific effects were further estimated to identify the susceptible groups.ResultsDuring the study period, fluctuations in air pollutants and climate conditions closely mirrored changes in hospitalizations for pulmonary space-occupying lesions. Totally, the distributed lag surface showed clear positive associations between pulmonary tumor hospitalization and PM2.5 (RRlag30: 1.000912; 95%CI: 1.000076, 1.00175), PM10 (RRlag30: 1.002246; 95%CI: 1.000474, 1.004021), SO2 (RRlag30: 1.002714; 95%CI: 1.001071, 1.004414), CO (RRlag30: 1.002231; 95%CI: 1.000592, 1.003873). Additionally, the associations between air pollutants and hospitalizations for pulmonary space-occupying lesions were significantly stronger during the heating season. Population aged 65 or older, females and those diagnosed with malignancies were more vulnerable for the risk of pulmonary space-occupying lesions diseases due to air pollution exposure.ConclusionsThe present study illustrated risk and burden for pulmonary space-occupying lesions hospitalization associated with air pollution, especially among population aged ≥ 65, or female.

Point-of-Care Lung Ultrasound in Small Animal Emergency and Critical Care Medicine: A Clinical Review

Thoracic point-of-care ultrasound (T-POCUS) has grown in popularity and usage in small animal emergencies and critical care settings due to its non-invasive nature, mobility, and ability to acquire images in real time. This review summarizes current understanding about T-POCUS in dogs and cats with respiratory illnesses, including normal thoracic ultrasonography appearance and numerous pathological situations. The basics of T-POCUS are covered, including equipment, scanning procedures, and picture settings. Practical applications in patients with respiratory distress are discussed, with an emphasis on pleural space abnormalities and lung diseases. Ultrasound results define pulmonary disorders such as pneumonia, atelectasis, cardiogenic and non-cardiogenic pulmonary edema, lung lobe torsion, pulmonary fibrosis, pulmonary thromboembolism, pulmonary neoplasms, and pulmonary bleeding. The evaluation focuses on T-POCUS diagnostic skills in a variety of clinical settings. Limitations and the need for more study to standardize techniques, establish agreed terminology, and create specialized educational routes are highlighted.

The diagnostic accuracy of HE4 in the differential diagnosis of pleural effusions

BackgroundPleural effusions are challenging to diagnose, with approximately 20–50% of malignant effusions not diagnosed by cytology. Human epididymal protein 4 (HE4) may be useful in the differential diagnosis of pleural effusions. In serum, this biomarker shows false-positive results in some benign diseases. The aim of this study was to evaluate the diagnostic utility of HE4 in this setting and to identify false positives. MethodsConcentrations of HE4, adenosine deaminase, % polynuclear cells, and C-reactive protein, were determined in 238 pleural fluid samples and the estimated glomerular filtration rate (eGFr) in serum. ResultsHE4 values ​​differed significantly (p < 0.01) between malignant [median (IQR)] [1065 (2085)] pmol/L and benign effusions [699 (589)] pmol/L. HE4 concentrations in gynecological and pulmonary tumors were significantly higher than in other tumors.For a cut-off point of 3050 pmol/L, 22 % sensitivity and 100 % specificity were obtained.In patients with benign disease, significant increases in HE4 were identified only in those with eGFr < 30 mL/min/1.73 m2 [1050(596)] pmol/L, and not in those with eGFr > 30 mL/min/1.73 m2 [597(532)] pmol/L).Two cut-offs were established for maximum specificity, depending on the eGFr: 3050 pmol/L for eGFr < 30 mL/min/1.73 m2 and 1992 pmol/L for eGFr > 30 mL/min/1.73 m2. A sensitivity of 28.5 % was obtained for patients with eGFr > 30 mL/min/1.73 m2 and 36.3 % for patients with eGFr < 30 mL/min/1.73 m2. The sensitivity using a specific cut-off point was 29.7 %. ConclusionsThe determination of HE4 in pleural fluids demonstrates high specificity and low sensitivity. The use of specific cutoff points that are clinically adjusted improves sensitivity while maintaining maximum specificity.

Pulmonary Tumor Thrombotic Microangiopathy Associated With Gastric Cancer: Clinical Characteristics and Outcomes

Pulmonary Tumor Thrombotic Microangiopathy Associated With Gastric Cancer: Clinical Characteristics and Outcomes

Bioorthogonal strategy-triggered In situ co-activation of aggregation-induced emission photosensitizers and chemotherapeutic prodrugs for boosting synergistic chemo-photodynamic-immunotherapy.

In situ activation of prodrugs or photosensitizers is a promising strategy for specifically killing tumor cells while avoiding toxic side effects. Herein, we originally develop a bioorthogonally activatable prodrug and pro-photosensitizer system to synchronously yield an aggregation-induced emission (AIE) photosensitizer and a chemotherapeutic drug for synergistic chemo-photodynamic-immunotherapy of tumors. By employing molecular engineering strategy, we rationally design a family of tetrazine-functionalized tetraphenylene-based photosensitizers, one of which (named TzPS5) exhibits a high turn-on ratio, a NIR emission, a typical AIE character, and an excellent ROS generation efficiency upon bioorthogonal-activation. With the aid of integrin- or mitochondria-pretargeting, TzPS5 is successfully applied for highly effective PDT ablation of cancer cells both in vitro and in vivo. On this basis, tumor-targeting TzPS5 (TzPS5-cRGD) is constructed and used jointly with a bioorthogonal prodrug, DOX-TCO, and the two are mutually activated to induce cooperative and tumor-specific PDT and chemotherapy, resulting in amplified therapeutic outcomes and improved biosafeties. Moreover, this combination modality elicits robust immunogenic cell death, stimulates systemic antitumor immunity, thereby suppressing both primary and distant tumors, and blocking the pulmonary tumor metastasis. This work is expected to provide a useful guidance for the rational design of activatable phototheranostic agents, and offer a new strategy for co-activation of prodrugs/pro-photosensitizers to boost synergistic antitumor chemo-photodynamic-immunotherapy.

Comparative performance of marking of small-diameter peripheral lung neoplasms by preoperative transthoracic use of methylene blue preparations and placement of an anchor marker system

The study compared marking of small-diameter peripheral lung neoplasms by preoperative transthoracic use of 1% aqueous methylene blue solution and placement of an anchor marker system. The study evaluated the results of treatment of 36 patients with pulmonary nodules, including 27 men and 9 women aged 52 to 76 years, who were examined and treated at the Surgical Clinic of the S.M. Kirov Military Medical Academy in 2020-2023. Marking of small-diameter peripheral lung neoplasms by transthoracic use of 1% aqueous methylene blue solution made possible to detect abnormalities and lesions and perform a biopsy in 73.3% of cases. The duration of the diagnostic procedures was 30 [20-40] minutes. No postoperative complications were reported. The mean length of stay in this group of patients was 8 [6; 12] patient days. Placement of an anchor marker system allowed detection and verification of lung lesions in 95% of cases. In addition, the duration of videothoracoscopic biopsies was also 30 [20-40] minutes. No complications or deaths were reported. The mean length of stay was 7 [5; 11] patient days. The use of anchor markers to label small peripheral pulmonary nodules in the preoperative phase has some significant advantages compared with dye injection techniques, such as shorter duration of lesion mapping (p = 0.046) and less manipulation complications (p = 0.04), as well as a higher frequency of lesion detection during minimally invasive procedures. When comparing various techniques for marking pulmonary lesions, it was found that mapping of small-diameter peripheral pulmonary infiltrates using anchor markers is characterized by high performance, greater safety, facilitates intraoperative navigation for biopsy of small-diameter peripheral pulmonary neoplasms, and is superior than transthoracic use of 1% aqueous methylene blue in terms of rates of detection of pulmonary nodules during minimally invasive procedures, duration of manipulation, and complication rates.

Revisión de los métodos diagnósticos de la Trombosis Venosa Profunda y Embolismo Pulmonar. Rol del Fragmento D de fibrina

Introduction. Venous thromboembolic disease, represented by deep venous thrombosis and pulmonary embolism, constitutes a highly prevalent pathology in both in- and out-of-hospital patients, with an increasing number of associated risk factors, some of them not represented in the risk and prognosis scales currently implemented, such as solid organ neoplastic and hematological pathologies, which have been associated with false positives in the results of tests such as D-dimer and recurrent thrombotic events, which makes it difficult to establish a diagnostic algorithm and anticoagulation time after resolution of the initial thrombotic event. Objective. To document the use of compression Doppler ultrasound of the lower limbs, Pulmonary Resonance Angiography (PRA), and Chest Computed Tomography with Iodine Mapping (CTIM) in patients with cancer and suspected thrombotic events have a negative predictive value comparable to D-dimer in the absence of cancer. Therefore, more significant implementation of these diagnostic strategies in the algorithms for these patients is required. Materials and methods. A search of published literature in the Medline (PubMed), OncoWeb, and CancerLit (HealthGate) databases, with the following MeSH terms: pulmonary embolism, venous thrombosis, neoplasms, diagnosis, D-dimer or fibrin fragment D, and epidemiology (epidemiology).

Contralateral metachronous pulmonary carcinoid tumor 7 years after lobectomy

Contralateral metachronous pulmonary carcinoid tumor 7 years after lobectomy

Differentiating Separate Primary Lung Adenocarcinomas From Intrapulmonary Metastases With Emphasis on Pathological and Molecular Considerations: Recommendations From the International Association for the Study of Lung Cancer Pathology Committee

IntroductionWith the implementation of low-dose computed tomography screening, multiple pulmonary tumor nodules are diagnosed with increasing frequency and the selection of surgical treatments versus systemic therapies has become challenging on a daily basis in clinical practice. In the presence of multiple carcinomas, especially adenocarcinomas, pathologically determined to be of pulmonary origin, the distinction between separate primary lung carcinomas (SPLCs) and intrapulmonary metastases (IPMs) is important for staging, management, and prognostication. MethodsWe systemically reviewed various means that aid in the differentiation between SPLCs and IPMs explored by histopathologic evaluation and molecular profiling, the latter includes DNA microsatellite analysis, array comparative genomic hybridization, TP53 and oncogenic driver mutation testing and, more recently, with promising effectiveness, next-generation sequencing comprising small- or large-scale multi-gene panels. ResultsComprehensive histologic evaluation may suffice to differentiate between SPLCs and IPMs. Nevertheless, molecular profiling using larger-scale next-generation sequencing typically provides superior discriminatory power, allowing for more accurate classification. On the basis of the literature review and expert opinions, we proposed a combined four-step histologic and molecular classification algorithm for addressing multiple pulmonary tumor nodules of adenocarcinoma histology that encourages a multidisciplinary approach. It is also noteworthy that new technologies combining machine learning and digital pathology may develop into valuable diagnostic tools for distinguishing SPLCs from IPMs in the future. ConclusionsAlthough histopathologic evaluation is often adequate to differentiate SPLCs from IPMs, molecular profiling should be performed when possible, especially in cases with tumors exhibiting similar morphology. This manuscript summarized the previous efforts in resolving the current challenges and highlighted the recent progress in the differentiation methods and algorithms used in categorizing multiple lung adenocarcinomas into SPLCs or IPMs, which are becoming more and more critical in precision lung cancer management.

Delta-like ligand 3 (DLL3) landscape in pulmonary and extra-pulmonary neuroendocrine neoplasms.

Delta-like Ligand 3 (DLL3) targeting therapies are promising in small cell lung cancer (SCLC) treatment. However, DLL3 expression in SCLC and other neuroendocrine neoplasms (NEN) is heterogeneous and not well characterized. We describe the landscape of DLL3 at the mRNA and protein levels across SCLC, large cell neuroendocrine carcinoma (LCNEC), and non-small cell lung cancer. Additionally, we explore its expression in extra-pulmonary NEN (EP-NEN) using a standardized DLL3 IHC assay. DLL3 expression is enriched in SCLC, LCNEC along with combined histology lung cancers. Moreover, we find a wide range of DLL3 expression in high-grade EP-NEN. We describe heterogenous DLL3 expression not only in SCLC but also in different NEN types. This comprehensive characterization of DLL3 can help guide future clinical trial design targeting DLL3 in NEN including LCNEC and EP-NEN that are lacking standard of care treatment options.

Enhanced Gαq Signaling in TSC2-deficient Cells Is Required for Their Neoplastic Behavior.

Inherited or sporadic loss of the TSC2 gene can lead to pulmonary lymphangioleiomyomatosis (LAM), a rare cystic lung disease caused by protease-secreting interstitial tumor nodules. The nodules arise by metastasis of cells that exhibit features of neural crest and smooth muscle lineage ('LAM cells'). Their aberrant growth is attributed to increased activity of 'mechanistic target of rapamycin complex 1' (mTORC1), an anabolic protein kinase that is normally suppressed by the TSC1-TSC2 protein complex. The mTORC1 inhibitor rapamycin slows the progression of LAM, but fails to eradicate disease, indicating a role for mTORC1-independent mechanisms in LAM pathogenesis. Our previous studies revealed G-protein coupled urotensin-II receptor (UT) signaling as a candidate mechanism, but how it promotes oncogenic signaling in TSC2-deficient cells remained unknown. Using a human pluripotent stem cell-derived in vitro model of LAM, we now show hyperactivation of UT, which was required for their enhanced migration and pro-neoplastic signaling in a rapamycin-insensitive mechanism that required heterotrimeric Gαq/11 (Gαq). Bioluminescence resonance energy transfer assays in HEK 293T cells lacking TSC2 demonstrated selective and enhanced activation of Gαq and its RhoA-associated effectors compared to wild-type control cells. By immunoprecipitation, recombinant UT was physically associated with Gαq and TSC2. The augmented Gαq signaling in TSC2-deleted cells was independent of mTOR activity, and associated with increased endosomal targeting of p63RhoGEF, a known RhoA-activating effector of Gαq. These studies identify potential mTORC1-independent pro-neoplastic mechanisms that can be targeted for prevention or eradication of pulmonary and extrapulmonary LAM tumors.

Congenital Peribronchial Myofibroblastic Tumors Harbor a Recurrent EGFR Kinase Domain Duplication

Congenital peribronchial myofibroblastic tumor (CPMT) is a rare benign infantile pulmonary neoplasm that presents prenatally, or early in infancy, and exhibits distinctive histologic features characterized by the presence of cartilaginous islands intermixed with bland spindle cells, not uncommonly displaying prominent mitoses. Despite its benign nature, CPMT can lead to fetal demise, postnatal respiratory distress, or complications from perinatal surgical resection. Although the morphologic and clinical features of CPMT are well described, its molecular features and oncogenesis remain elusive. Following the detection of EGFR kinase domain duplication (KDD) of exons 18 to 25 in an index case, we identified 3 additional cases of morphologically classic and clinically well-characterized CPMTs from the archives and performed targeted RNA- and DNA-based profiling via next-generation sequencing for detection of rearrangements, sequence variants, and copy number variants on all cases. Two cases were detected prenatally, 1 patient presented at birth, and 1 at 8 weeks of life. All tumors were resected, with a follow-up period ranging from 0 days to 10 years. One patient died shortly after surgical resection, and the other 3 had no recurrences. In all cases, EGFR KDD was detected. In 2 out of 4 cases, gains of select whole chromosomes were noted. Our findings establish EGFR KDD as a recurrent oncogenic driver of CPMT. Notably, this alteration is also found in classical congenital mesoblastic nephromas, infantile kidney tumors with which CPMTs share striking morphologic and clinical similarities. This strongly suggests that CPMTs and classical congenital mesoblastic nephromas share common oncogenesis, and represent the same tumor in different locations. EGFR KDDs have also been reported in neonatal soft tissue tumors with infantile fibrosarcoma-like histology and cartilaginous differentiation, raising questions about their relationship. EGFR KDD emerges as a diagnostic marker, a potential therapeutic target, and a window into the oncogenesis of a distinct subset of infantile mesenchymal tumors.

Synchronous bilateral typical pulmonary carcinoid tumours diagnosed by robotic navigation bronchoscopy: A unique case.

Pulmonary carcinoids are uncommon malignant neoplasms, believed to derive from specialized neuroendocrine cells known as Kulchitsky cells. We evaluated a 69-year-old female presenting symptoms consistent with carcinoid syndrome, such as intermittent flushing and diarrhoea, along with complaints of shortness of breath and cough. Imaging revealed bilateral lung nodules, confirmed by biopsy to be carcinoid tumours. The treatment of choice for carcinoid tumours is complete surgical resection. Nonetheless, individualized management plans are crafted based on the tumour's location and the patient's respiratory function as these present challenges to anatomical resection of tumours.

Clinical and cytological characteristics of malignant pericardial effusion and estimation of the rate of progression until its evacuation by pericardiocentesis

Abstract Introduction Pericardial effusion (PE) is a complication of neoplastic processes that worsens the prognosis and can lead to symptomatic presentations requiring pericardiocentesis (PC). There is limited literature regarding the evolution of PE from its onset to the need for PC, characteristics of these patients, progression rate of PE, and potential accelerating factors. Purpose This study aims to: i) Analyze the baseline characteristics of patients undergoing PC; ii) Evaluate the correlation between PE appearance and cytology; iii) Analyze the progression rate until PC performance. Methods This retrospective observational study includes patients with active neoplasia and significant symptomatic PE treated with PC at our hospital from 01/01/2010 to 06/30/23, with subsequent follow-up until 10/31/23. Clinical characteristics related to neoplastic processes and PE diagnosis were analyzed, including PE appearance, cytology, and computed tomography scans performed as neoplasia follow-up prior to PC. Results A total of 75 patients were included, with 6 excluded because of non-malignant conditions (2 acute pericarditis-related PE, 3 purulent PE, and 1 chylous PE). The remaining 69 patients had a median age of 59 years, with 55.1% being male. Lung neoplasm was most frequent (63.8%, with 84% adenocarcinoma), followed by lymphomas/lymphoid leukemia (7.3%), upper digestive tract (7.3%), and breast cancer (7.3%). 52.2% of PEs undergoing PC were diagnosed simultaneously with neoplasm (70.45% associated with pulmonary neoplasms); 43.5% had ECOG 1, and 89.9% had metastases (excluding PE) at PC. Cardiac tamponade was present in 27.5%, with percutaneous pericardiostomy added in 21.7%. PE appearance was sero-haematic in 49.3%, haematic in 36.2%, and serous in 14.5%. Cytology showed mostly positive results (69.2%: 50% in serous PE and 71.93% in haematic/sero-haematic PE). The median time from the last CT scan prior to PE to PC was 5 months (160 days, range: 24-943 days). PC recurrence was observed in 30.4% of cases. Follow-up mortality was 82.6%, higher in breast, renal, digestive, thymoma, and genital neoplasms (100%), with hematological neoplasms having the lowest mortality (40%), followed by pulmonary neoplasms (79.5%). Mortality was higher in patients with more lines of treatment at PC and with a higher number of metastases. The median time from PC to death was 2 months (68.5 days, range: 1 day-2007 days). Conclusions The most common neoplastic PE was associated with lung adenocarcinoma, though a variety of neoplasms were observed. Half of PEs were diagnosed concurrently with neoplasm diagnosis. Cytology sensitivity was not high, and PE appearance did not adequately predict outcomes. The median time from the last CT scan prior to PE to PC was 5 months, potentially guiding echocardiographic follow-up once PE is observed on CT. Overall mortality was high (82.6%), except for onco-hematological PE.Iconographic summary of malignant PE