BACKGROUND: Recent studies show small-bore chest tubes, commonly 14 French pigtail catheters (PCs), are noninferior to large-bore chest tubes for treating various conditions, and they are associated with better patient comfort. The Medical College of Wisconsin implemented a bedside procedure service (BPS) that has been trained in the placement of PCs as an adjunct to its interventional radiology department. METHODS: The data regarding consults for PC placement was collected by the BPS over a 2-year period. Primary outcomes reviewed were insertion-related complications (IRCs), unsuccessful attempts (UAs), and adverse outcomes (AOs) because the authors believe these represent the safety and effectiveness of the group. It was determined which services consulted the BPS for PC placement, the indications for consults, and a brief review of declined PC consults. RESULTS: Of the 124 accepted consults, the service had 3 IRCs (2.4%), 2 UAs (1.6%), and 3 AOs (2.4%). A total of 18 consults were declined. The BPS was consulted by 12 services with 8 primary reasons for PC placement. CONCLUSIONS: At high-volume, tertiary care centers, and with the support of cardiothoracic surgical and interventional radiology services, procedure-focused hospitalists can safely serve as an adjunct service for PC placement in selected hospitalized patients.

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<div>Abstract<p>The dual pathway inhibitor rigosertib inhibits phosphoinositide 3-kinase (PI3K) pathway activation as well as polo-like kinase 1 (PLK1) activity across a broad spectrum of cancer cell lines. The importance of <i>PIK3CA</i> alterations in squamous cell carcinoma of the head and neck (HNSCC) has raised interest in exploring agents targeting PI3K, the product of <i>PIK3CA</i>. The genetic and molecular basis of rigosertib treatment response was investigated in a panel of 16 HNSCC cell lines, and direct patient tumor xenografts from eight patients with HNSCC [four HPV-serotype16 (HPV16)–positive]. HNSCC cell lines and xenografts were characterized by pathway enrichment gene expression analysis, exon sequencing, gene copy number, Western blotting, and immunohistochemistry (IHC). Rigosertib had potent antiproliferative effects on 11 of 16 HPV⁻ HNSCC cell lines. Treatment sensitivity was confirmed in two cell lines using an orthotopic <i>in vivo</i> xenograft model. Growth reduction after rigosertib treatment was observed in three of eight HNSCC direct patient tumor lines. The responsive tumor lines carried a combination of a <i>PI3KCA</i>-activating event (amplification or mutation) and a p53-inactivating event (either HPV16- or mutation-mediated <i>TP53</i> inactivation). In this study, we evaluated the <i>in vitro</i> and <i>in vivo</i> efficacy of rigosertib in both HPV⁺ and HPV⁻ HNSCCs, focusing on inhibition of the PI3K pathway. Although consistent inhibition of the PI3K pathway was not evident in HNSCC, we identified a combination of <i>PI3K</i>/<i>TP53</i> events necessary, but not sufficient, for rigosertib sensitivity. <i>Mol Cancer Ther; 12(10); 1994–2005. ©2013 AACR</i>.</p></div>

<p>PDF file - 956K, Supplementary Figure 1. A, Cellular viability of 6 sensitive and 5 resistant cell lines at 1.0μM rigosertib treatment as measured by SRB assay; Supplementary Figure 2. Proliferation of 2 rigosertib-sensitive (584 and HN11) and 2 rigosertib-resistant (MSK921 and UMSCC19) cell lines; Supplementary Figure 3. Western blot analysis of EGFR pathway activation in vitro in vehicle control (C), 1.0 μM rigosertib (R), and 1.0 μM ZSTK474 (Z) treated cultures; Supplementary Figure 4. A, Representative IHC of orthotopically xenografted HNSCC cell lines. B, Western blot analysis of EGFR pathway activation and representative IHC; Supplemental Figure 5. Graphical representation of tumor growth for the control (♦) and rigosertib (■) treatment groups from the sensitive CUHN026 (A) and resistant CUHN013 (B) tumor lines. Supplemental Figure 6. Western blot analysis of EGFR pathway activation in the control (C) and rigosertib (R) treated direct patient xenografted tissue; Supplemental Figure 7. Representative IHC from treated direct patient xenografted tissue.</p>

<div>Abstract<p>The dual pathway inhibitor rigosertib inhibits phosphoinositide 3-kinase (PI3K) pathway activation as well as polo-like kinase 1 (PLK1) activity across a broad spectrum of cancer cell lines. The importance of <i>PIK3CA</i> alterations in squamous cell carcinoma of the head and neck (HNSCC) has raised interest in exploring agents targeting PI3K, the product of <i>PIK3CA</i>. The genetic and molecular basis of rigosertib treatment response was investigated in a panel of 16 HNSCC cell lines, and direct patient tumor xenografts from eight patients with HNSCC [four HPV-serotype16 (HPV16)–positive]. HNSCC cell lines and xenografts were characterized by pathway enrichment gene expression analysis, exon sequencing, gene copy number, Western blotting, and immunohistochemistry (IHC). Rigosertib had potent antiproliferative effects on 11 of 16 HPV⁻ HNSCC cell lines. Treatment sensitivity was confirmed in two cell lines using an orthotopic <i>in vivo</i> xenograft model. Growth reduction after rigosertib treatment was observed in three of eight HNSCC direct patient tumor lines. The responsive tumor lines carried a combination of a <i>PI3KCA</i>-activating event (amplification or mutation) and a p53-inactivating event (either HPV16- or mutation-mediated <i>TP53</i> inactivation). In this study, we evaluated the <i>in vitro</i> and <i>in vivo</i> efficacy of rigosertib in both HPV⁺ and HPV⁻ HNSCCs, focusing on inhibition of the PI3K pathway. Although consistent inhibition of the PI3K pathway was not evident in HNSCC, we identified a combination of <i>PI3K</i>/<i>TP53</i> events necessary, but not sufficient, for rigosertib sensitivity. <i>Mol Cancer Ther; 12(10); 1994–2005. ©2013 AACR</i>.</p></div>