Herein we describe the clinicopathologic and immunohistochemical features of 13 primary mucinous (colloid) carcinomas (MCs) of the lung, an uncommon and controversial tumor. The patients, 7 males and 6 females, ranged in age from 50 to 79 years (mean, 64.5 years). All the tumors presented as a peripheral solitary nodule with gelatinous cut-surface and well circumscribed but lacking a complete fibrous wall. The size ranged from 1 to 5.5 cm. Microscopically, they consisted of neoplastic elements floating in large mucin pools and focally lining the alveolar spaces. Eleven cases were predominantly composed of tall, columnar goblet cells (goblet cell-type MC), while 2 consisted of signet-ring tumor cells (signet-ring cell-type MC). Five tumors were incidentally discovered by chest radiographs, while the others were symptomatic. All patients underwent complete surgical resection (six lobectomies and seven wedge resections). Postoperative chemotherapy was performed in 3 cases. Overall, the median follow-up was 26 months (mean 33 months; range 9-95 months). All patients with goblet cell-type MC were alive and well, while the 2 patients with signet-ring cell-type MC died of disease. Immunohistochemically, all the 11 goblet cell-type MCs were strongly stained with CDX-2 and MUC2, 8 reacted with TTF-1, 6 with cytokeratin 20 (CK20), 9 with cytokeratin 7 (CK7), and 2 with MUC-5AC. Conversely, the two signet-ring cell-type MCs were stained with TTF-1, CK7, and MUC5AC but were negative for CDX-2, MUC2, and CK20. Surfactant apoprotein-A (SP-A) was positive in four goblet cell-type and one signet-ring cell-type MC. When compared with 10 mucinous bronchioloalveolar carcinomas (m-BAC), the latter reacted with CK7, CK20, MUC5AC, TTF-1, SP-A, CDX-2, and MUC2 in 100%, 90%, 100%, 30%, 10%, 0%, and 0% of the cases, respectively. In summary, MC of the lung represents an entity with two distinct clinicopathologic and immunophenotypic variants: 1) the goblet cell-type, presenting a more indolent clinical behavior and frequently co-expressing markers of intestinal and pulmonary differentiation; and 2) the more aggressive signet-ring cell-type, which retains only markers of pulmonary origin. On morphologic and immunohistochemical grounds, MCs are easily distinguishable from m-BAC. Since goblet cell-type MC strongly stains with CDX2, MUC2, and CK20, differential diagnosis with metastatic colorectal carcinoma is very challenging and requires appropriate clinical correlation.

Laryngeal cancer is a very common tumor in the upper aero-digestive tract. Understanding its biological mechanisms has garnered significant interest in recent years. The development of laryngeal squamous cell carcinoma (LSCC) follows a multistep process starting from precursor lesions in the epithelium. Various risk factors have been associated with laryngeal tumors, including smoking, alcohol consumption, opium use, as well as infections with HPV and EBV viruses, among others. Cancer development involves multiple steps, and genetic alterations play a crucial role. Tumor suppressor genes can be inactivated, and proto-oncogenes may become activated through mechanisms like deletions, point mutations, promoter methylation, and gene amplification. Epigenetic modifications, driven by miRNAs, have been proven to contribute to LSCC development. Despite advances in molecular medicine, there are still aspects of laryngeal cancer that remain poorly understood, and the underlying biological mechanisms have not been fully elucidated. In this narrative review, we examined the literature to analyze and summarize the main steps of carcinogenesis and the risk factors associated with laryngeal cancer.

Endobronchial metastases from extrapulmonary solid tumors are a rare event and currently available epidemiological and clinico-pathological data mainly derive from anecdotal case reports. A series of 174 consecutive cases of endobronchial metastases from extrathoracic solid tumors were collected over a period of 18 years. Immunohistochemistry was performed in 115 cases. Complete imaging features were available in 81 patients, and analysis of the latency period between primitive tumor diagnosis and occurrence of endobronchial metastasis was obtained. Among all bronchoscopic examinations performed in the same period for malignancy, a mean of 5.6 cases per year consisted of endobronchial metastases (range 2-17 cases), with a statistically significant increase when comparing the periods 1992-2000 (65 cases, 37%) and 2001-2009 (109 cases, 63%) (p = 0.05). Overall, 4% of endobronchial biopsies for suspected malignancy disclosed an endobronchial metastasis from extrapulmonary tumor. Breast (52 cases, 30%), colorectal (42 cases, 24%), renal (14%), gastric (6%) and prostate (4.5%) cancers and melanoma (4.5%) were the most common metastatic neoplasms presenting as endobronchial mass. One-hundred fifty-four cases were identified after the primitive tumor diagnosis (metachronous cases, 89%), 11 cases were simultaneously evidenced in extrapulmonary and endobronchial sites (synchronous cases, 6%), while 9 occult metastatic cases (5%) first presented as endobronchial mass (anachronous cases). Overall, mean latency from extrapulmonary tumor diagnosis and endobronchial metastasis was 136 months (range, 1-300 months). The most frequent symptoms were dyspnea (23%), cough (15%) and haemoptysis (12%), while 26% of patients were totally asymptomatic. At radiology, 53% presented as multiple pulmonary nodules, while other cases presented as hilar and mediastinal mass, single peripheral nodule, atelectasis or pleural effusion. Endobronchial metastases from extrapulmonary tumors account for about 4% of all bronchoscopic biopsies performed for suspected malignancy and in 5% of the cases the metastasis is the first manifestation of the neoplasm.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrosing interstitial lung disease (ILD) of unknown aetiology, with a median survival of 2–4 years from the time of diagnosis. Although IPF has unknown aetiology by definition, there have been identified several risks factors increasing the probability of the onset and progression of the disease in IPF patients such as cigarette smoking and environmental risk factors associated with domestic and occupational exposure. Among them, cigarette smoking together with concomitant emphysema might predispose IPF patients to lung cancer (LC), mostly to non-small cell lung cancer (NSCLC), increasing the risk of lung cancer development. To this purpose, IPF and LC share several cellular and molecular processes driving the progression of both pathologies such as fibroblast transition proliferation and activation, endoplasmic reticulum stress, oxidative stress, and many genetic and epigenetic markers that predispose IPF patients to LC development. Nintedanib, a tyrosine–kinase inhibitor, was firstly developed as an anticancer drug and then recognized as an anti-fibrotic agent based on the common target molecular pathway. In this review our aim is to describe the updated studies on common cellular and molecular mechanisms between IPF and lung cancer, knowledge of which might help to find novel therapeutic targets for this disease combination.

Ultrasound (US) evaluation of diaphragmatic dysfunction (DD) has proved to be a reliable technique in critical care. In this single-center prospective study, we investigated the impact of US-assessed DD on noninvasive ventilation (NIV) failure in patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) and its correlation with the transdiaphragmatic pressure assessed using the invasive sniff maneuver (Pdi sniff). A population of 75 consecutive patients with AECOPD with hypercapnic acidosis admitted to our respiratory intensive care unit (RICU) were enrolled. Change in diaphragm thickness (ΔTdi) < 20% during tidal volume was the predefined cutoff for identifying DD+/− status. Correlations between ΔTdi < 20% NIV failure and other clinical outcomes were investigated. Correlation between ΔTdi and Pdi sniff values was analyzed in a subset of ten patients. DD+ patients had a higher risk for NIV failure than DD− patients (risk ratio, 4.4; p < 0.001), and this finding was significantly associated with higher RICU, in-hospital, and 90-day mortality rates; longer mechanical ventilation duration; higher tracheostomy rate; and longer RICU stay. Huge increases in NIV failure (HR, 6.2; p < 0.0001) and 90-day mortality (HR, 4.7; p = 0.008) in DD+ patients were found by Kaplan-Meier analysis. ΔTdi highly correlated with Pdi sniff (Pearson’s r = 0.81; p = 0.004). ΔTdi < 20% showed better accuracy in predicting NIV failure than baseline pH value and early change in both arterial blood pH and partial pressure of carbon dioxide following NIV start (AUCs 0.84 to DTdi < 20%, 0.51 to pH value at baseline, 0.56 to early change in arterial blood pH following NIV start, and 0.54 to early change in partical pressure of carbon dioxide following NIV start, respectively; p < 0.0001). Early and noninvasive US assessment of DD during severe AECOPD is reliable and accurate in identifying patients at major risk for NIV failure and worse prognosis.