Robotic Left Upper Lobectomy

<p>Interest and access to robot thoracic surgery has increased over the last decade. This increased interest from surgeons, hospitals, and patients has led many surgeons to transition from their standard practice of open or thoracoscopic lobectomy to robotic lobectomy. High-volume robotic programs have shown a decrease in the length of hospital stay, 30-day mortality, and postoperative transfusion requirements when lung resection is performed with the robotic technique compared to video-assisted thoracoscopic surgery and thoracotomy (1).<br></p> <p>This video demonstrates a robotic left upper lobectomy. The patient was a 73-year-old woman who was found to have a 12 mm left upper lobe nodule on a screening computed tomography scan. Positron emission tomography demonstrated mild hypermetabolic activity. She was asymptomatic, and she was able to walk one mile and climb two flights of stairs. Her medical history included hypertension and chronic obstructive pulmonary disease, and she had a 10 pack-year history of smoking. The results of her pulmonary function tests were adequate.</p><p>She was taken for a left upper lobe wedge resection, and the frozen section confirmed adenocarcinoma. She then had a completion robotic lobectomy with mediastinal lymph node dissection of stations 5, 6, 7, and L9. At the completion of the procedure, an intercostal nerve block was performed and a 28 Fr chest tube was placed. The chest tube was subsequently removed, and the patient was sent home on postoperative day two. The final pathology revealed a 1.2 cm moderately differentiated adenocarcinoma, with zero out of eight lymph nodes positive for malignancy, stage T1aN0M0 IA. The robotic technique provides excellent exposure and visualization, and it allows for a complete oncologic resection. </p> <p> </p> <p><b>Reference</b></p> <p>1. Farivar AS, Cerfolio RJ, Vallieres E, et al. Comparing robotic lung resection with thoracotomy and video-assisted thoracoscopic surgery cases entered into the Society of Thoracic Surgeons Database. <i><a href="https://doi.org/10.1097/IMI.0000000000000043">Innovations. 2014;9(1):10-15</a></i>.</p

¹⁸F-FDG PET intensity correlates with a hypoxic gene signature and other oncogenic abnormalities in operable non-small cell lung cancer

<div><p>Background</p><p>¹⁸F-fluorodeoxyglucose positron emission tomography (FDG-PET) is critical for staging non-small-cell lung cancer (NSCLC). While PET intensity carries prognostic significance, the genetic abnormalities associated with increased intensity remain unspecified.</p><p>Methods</p><p>NSCLC samples (N = 34) from 1999 to 2011 for which PET data were available were identified from a prospectively collected tumor bank. PET intensity was classified as mild, moderate, or intense based on SUVmax measurement or radiology report. Associations between genome-wide expression (RNAseq) and PET intensity were determined. Associations with overall survival were then validated in two external NSCLC cohorts.</p><p>Results</p><p>Overall survival was significantly worse in patients with PET-intense (N = 11) versus mild (N = 10) tumors (p = 0.039). Glycolytic gene expression patterns were markedly similar between intense and mild tumors. Gene ontology analysis demonstrated significant enhancement of cell-cycle and proliferative processes in FDG-intense tumors (p<0.001). Gene set enrichment analysis (GSEA) suggested associations between PET-intensity and canonical oncogenic signaling pathways including <i>MYC</i>, <i>NF-κB</i>, and <i>HIF-1</i>. Using an external cohort of 25 tumors with PET and genomic profiling data, common genes and gene sets were validated for additional study (P<0.05). Of these common gene sets, 20% were associated with hypoxia or HIF-1 signaling. While <i>HIF-1</i> expression did not correlate with poor survival in the NSCLC validation cohort (N = 442), established targets of hypoxia signaling (<i>PLAUR</i>, <i>ADM</i>, <i>CA9</i>) were significantly associated with poor overall survival.</p><p>Conclusions</p><p>PET-intensity is associated with a variety of oncogenic alterations in operable NSCLC. Adjuvant targeting of these pathways may improve survival among patients with PET-intense tumors.</p></div

Patient clinical characteristics.

<p>Patient clinical characteristics.</p

Validated radiogenomic abnormalities in two cohorts of patients with early-stage NSCLC.

<p>(a) The most significantly enriched genes in PET-intense tumors (p<0.05, fold change>2.0) were selected from the study and PET validation cohort. Selected genes that overlapped are displayed in the table. (b) Average rank-based GSEA results for all pathways in the MSigDB database that were enriched in high-intensity tumors in both the study and PET validation cohorts and (c) quantified relative to hypoxia. (d) Kaplan-Meier survivor curves and log-rank test of <i>HIF1A</i> expression in prognostic validation cohort (N = 442) using median gene expression as cutoff to divide low and high expression.</p

Patient demographics.

<p>Patient demographics.</p

Genetic analysis of study group.

<p>(a) Selected genes upregulated in high PET intensity tumors (fold-change high vs. low >2, p<0.05). (b) Kaplan-Meier survivor curve representing overall survival (in months) for patients with high PET-intensity tumors (N = 11), medium intensity tumors (N = 13), and low intensity tumors (N = 10). (c) The most significantly enriched genes in PET-high tumors (p<0.05, fold change>2.0) were interrogated by DAVID gene ontology pathway analysis [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0199970#pone.0199970.ref024" target="_blank">24</a>]. Significant functional groups are shown. P-values are quantified as log units. (d) Average rank-based GSEA results for MSigDB Hallmark pathways. (e) RNA levels of core glycolysis enzymes (red) versus all genes (gray) in PET high (y axis) versus low (x-axis) tumors. “Core” enzymes were labeled such according to the KEGG gene set database.</p

Kaplan-Meier survivor curves and log-rank test of selected targets of HIF signaling in prognostic validation cohort (N = 442) using median gene expression as cutoff to divide low and high expression.

<p>Downstream targets of HIF including (a) <i>GLUT3</i>, (b) <i>ADM</i>, (c) <i>CA9</i>, and (d) <i>PLAUR</i> were associated with worse survival. Genes were selected according to validated MSigDB gene sets related to hypoxia signaling.</p