86,865 research outputs found

    Erratum to: Lung Tissue Damage Caused by Heat Accumulation from Adjacent Laser Application: Surgical Implications (Thoracic and Cardiovascular Surgeon (2014) DOI: 10.1055/s-0034-1389086)

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    It has been brought to the Publisher's attention that the author names "Filippo Lococo" and "Alfredo Cesario" were not listed correctly in the above-mentioned article, published on eFirst on September 5, 2014. DOI of the original article is DOI: 10.1055/s-0034-1389086. The names should be read as "Filippo Lococo" and "Alfredo Cesario" in place of "Lococo Filippo" and "Cesario Alfredo."

    Experimental robotic pulmonary lobectomy with the TELELAP/ALFX system in the ovine model

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    A new robotic telesurgical device (TELELAP/ALFX) is used for the first time to execute an anatomical pulmonary resection (lobectomy) plus mediastinal lymph node dissection in the ovine model. This integrated operative system has 2 innovative peculiarities: (a) tactile perception (engineered to give the operator a tactile feedback similar to that experienced when handling thoracoscopy instruments) and (b) eye-tracking (immediate synchronization of the surgeon's eyes movements with that of the robotic camera). Herein, we report a lower right pulmonary lobectomy under complete robotic assistance (TELELAP/ALFX). Standard endoscopic staplers were used in all the major maneuvers (bronchial as well as vascular resections and fissural completion) introduced through a utility 4-cm-sized incision. The specimen was placed in an endoscopic retrieval bag and removed through a service minithoracotomy. With the limitations because of interspecies differences in anatomical landmarks, a mediastinal lymph nodal dissection was also completed. The operative time was acceptable (∼180 minutes) with blood loss of 100 mL. In conclusion, according to this first all experimental experience we may deem the TELELAP/ALFX system completely apt to perform major anatomic pulmonary resections and the regulatory process to run trials in humans are under way

    Solitary choroidal metastasis from atypical carcinoid of the lung detected by 68Ga DOTATATE PET/CT

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    A 71-year-old woman with a history of surgically treated bronchial atypical carcinoid underwent 68Ga DOTATATE PET/CT for restaging. Somatostatin receptor PET/CT revealed a focal area of mild radiopharmaceutical uptake corresponding to a thickening of the right choroid. No other areas of abnormal tracer uptake were detected in the rest of the body. Based on these PET/CT findings, the patient underwent examination of fundus oculi, MRI, and fluoroangiography, which confirmed the presence of a choroidal lesion interpreted as solitary choroidal metastasis of neuroendocrine tumor. Subsequently, the patient was referred for brachytherapy with radical intent

    An epithelial-to-mesenchymal transcriptional switch triggers evolution of pulmonary sarcomatoid carcinoma (PSC) and identifies dasatinib as new therapeutic option

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    Purpose: Pulmonary sarcomatoid carcinoma (PSC) is a rare and aggressive form of NSCLC. Rarity and poor characterization have limited the development of PSC-tailored treatment protocols, leaving patients with inadequate therapeutic options. In this study, we investigated the gene expression profile of PSCs, with the aim to characterize the molecular mechanisms responsible for their evolution and to identify new drugs for their treatment. Experimental Design: A training set of 17 biphasic PSCs was selected and tested for the expression of a large panel of 770 genes related to cancer progression using NanoString technology. Computational analyses were used to characterize a PSCs-gene specific signature from which pathways and drivers of PSC evolution were identified and validated using functional assays in vitro. This signature was validated in a separate set of 15 PSCs and 8 differentiated NSCLC and used to interrogate the cMAP database searching for FDA-approved small molecules able to counteract PSC phenotype. Results: We demonstrated that the transcriptional activation of an epithelial mesenchymal transition (EMT) program drives PSC phylogeny in vivo. We showed that loss of the epithelial-associated transcription factor (TF) OVOL2 characterizes the transition to sarcomatoid phenotype triggering the expression of EMT promoting TFs, including TWIST and ZEB and the expression of the membrane kinase DDR2. Finally, using a drug repurposing approach, we identified dasatinib as potential inhibitor of the PSC-gene expression signature and we confirmed in vitro that this drug efficiently restrains proliferation and reverts the sarcomatoid-associated phenotype. Conclusions: Our data provide new insights into PSC evolution and provide the rationale for further clinical studies with dasatinib
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