Jennifer S. Davids

Surgeon Volume and Elective Resection for Colon Cancer: An Analysis of Outcomes and Use of Laparoscopy

BACKGROUND Surgeon volume may be an important predictor of quality and cost outcomes. We evaluated the association between surgeon volume and quality and cost of surgical care in patients with colon cancer. STUDY DESIGN We performed a retrospective study of patients who underwent resection for colon cancer, using data from the University HealthSystem Consortium from 2008 to 2011. Outcomes evaluated included use of laparoscopy, ICU admission, postoperative complications, length of stay, and total direct hospital costs by surgeon volume. Surgeon volume was categorized according to high (HVS), medium (MVS), and low (LVS) average annual volumes. RESULTS A total of 17,749 patients were included in this study. The average age of the cohort was 65 years and 51% of patients were female. After adjustment for potential confounders, compared with LVS, HVS and MVS were more likely to use laparoscopy (HVS, odds ratio [OR] 1.27, 95% CI 1.15, 1.39; MVS, OR 1.16 95% CI 1.65, 1.26). Postoperative complications were significantly lower in patients operated on by HVS than LVS (OR 0.77 95% CI 0.76, 0.91). The HVS patients were less likely to require reoperation than those in the LVS group (OR 0.70, 95% CI 0.53, 0.92) Total direct costs were

Mesenchymal Stromal Cell Mutations and Wound Healing Contribute to the Etiology of Desmoid Tumors

927 (95% CI -

Clinical and financial impact of hospital readmissions after colorectal resection: predictors, outcomes, and costs.

1,567 to -

Persistent cyclooxygenase-2 inhibition downregulates NF-{kappa}B, resulting in chronic intestinal inflammation in the min/+ mouse model of colon tumorigenesis.

287) lower in the HVS group compared with the LVS group. CONCLUSIONS Higher quality, lower cost care was achieved by HVS in patients undergoing surgery for colon cancer. An assessment of differences in processes of care by surgeon volume may help further define the mechanism for this observed association.

Chronic cyclooxygenase-2 inhibition promotes myofibroblast-associated intestinal fibrosis

Desmoid tumors are nonmalignant neoplasms of mesenchymal origin that mainly contain fibroblast lineage cells. These tumors often occur in patients with familial adenomatous polyposis (FAP) coli who have germ line mutations in the APC gene. Given emerging data that has implicated multipotent mesencyhmal stromal cells (MSC) in the origin of mesenchymal tumors, we hypothesized that desmoid tumors may arise in patients with FAP after MSCs acquire somatic mutations during the proliferative phase of wound healing. To test this idea, we examined 16 desmoid tumors from FAP-associated and sporadic cases, finding that all 16 of 16 tumors expressed stem cell markers, whereas matching normal stromal tissues were uniformly negative. Desmoid tumors also contained a subclass of fibrocytes linked to wound healing, angiogenesis, and fibrosis. Using an MSC cell line derived from an FAP-associated desmoid tumor, we confirmed an expected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional repressor BMI-1 while documenting the coexpression of markers for chondrocytes, adipocytes, and osteocytes. Together, our findings argue that desmoid tumors result from the growth of MSCs in a wound healing setting that is associated with deregulated Wnt signaling due to APC loss. The differentiation potential of these MSCs combined with expression of BMI-1, a transcriptional repressor downstream of Hedgehog and Notch signaling, suggests that desmoid tumors may respond to therapies targeting these pathways.

Examination of Racial Disparities in the Receipt of Minimally Invasive Surgery Among a National Cohort of Adult Patients Undergoing Colorectal Surgery.

BACKGROUND:After passage of the Affordable Care Act, 30 -day hospital readmissions have come under greater scrutiny. Excess readmissions for certain medical conditions and procedures now result in penalizations on all Medicare reimbursements. OBJECTIVE:The purpose of this work was to define the risk factors, outcomes, and costs of 30-day readmissions after colorectal surgery. DESIGN:Adults undergoing colorectal surgery were studied using data from the University HealthSystem Consortium. Univariate and multivariable analyses were used to identify patient-related risk factors for, and 30-day outcomes of, readmission after colorectal surgery. SETTINGS:This study was conducted at an academic hospital and its affiliates. PATIENTS:Adults ≥18 years of age who underwent colorectal surgery for cancer, diverticular disease, IBD, or benign tumors between 2008 and 2011 were included in this study. MAIN OUTCOME MEASURES:Readmission within 30 days of index discharge was the main outcome measured. RESULTS:A total of 70,484 patients survived the index hospitalization after colorectal surgery; 9632 (13.7%) were readmitted within 30 days of discharge. The strongest independent predictors of readmission were length of stay ≥4 days (OR 1.44; 95% CI 1.32–1.57), stoma (OR 1.54; 95% CI 1.46–1.51), and discharge to skilled nursing (OR 1.62; 95% CI 1.49–1.76) or rehabilitation facility (OR 2.93; 95% CI 2.53–3.40). Of those readmitted, half of the readmissions occurred within 7 days, 13% required the intensive care unit, 6% had a reoperation, and 2% died during the readmission stay. The median combined total direct hospital cost was more than 2 times higher (

Impact of Procedural Specialty on Maternity Leave and Career Satisfaction Among Female Physicians

26,917 vs

Routine preoperative restaging CTs after neoadjuvant chemoradiation for locally advanced rectal cancer are low yield: A retrospective case study

13,817; p < 0.001) for readmitted than for nonreadmitted patients. LIMITATIONS:Follow-up was limited to 30 days after initial discharge. CONCLUSIONS:Readmissions after colorectal resection occur frequently and incur a significant financial burden on the health-care system. Future studies aimed at targeted interventions for high-risk patients may reduce readmissions and curb escalating health-care costs.

Characterizing Short-Term Outcomes Following Surgery for Rectal Cancer: the Role of Race and Insurance Status

Cyclooxygenase-2 (COX-2) inhibition prevents adenoma formation in humans and mouse models of colon cancer. The selective COX-2 inhibitor celecoxib reduces COX-2 and prostaglandin E(2) (PGE(2)) expression and adenomas in the intestine of Min/+ mice after treatment for several weeks, but prolonged treatment increases PGE(2) production, resulting in drug-resistant tumor formation and transforming growth factor beta (TGFbeta)-dependent intestinal fibrosis. In this study, we examined pathways that regulate COX-2 expression and suppress chronic intestinal inflammation. We show that NF-kappaB signaling was inhibited in the ileum of Min/+ mice receiving long-term treatment with celecoxib. This effect was associated with inhibition of TGFbeta-associated kinase-1 and IkappaB kinase alpha/beta activities and reduced expression of the Toll-like receptor (TLR) 2 and TLR4 that enhance colonic barrier function. Additionally, we observed reduced activities of protein kinases c-Jun NH(2)-terminal kinase 1 and protein kinase A and transcription factor cyclic AMP-responsive element binding protein, regulators of COX-2 expression, which cross-talk with NF-kappaB. In ileum subjected to long-term celecoxib treatment, we noted relatively higher expression of COX-2, vascular endothelial growth factor, and interleukin-1beta in Paneth cells, whereas NF-kappaB and COX-2 were more strongly expressed by an expanded population of stromal myofibroblasts. Our findings argue that celecoxib resistance is an acquired adaptation to changes in the crypt microenvironment that is associated with chronic intestinal inflammation and impaired acute wound-healing responsiveness.

Colorectal Cancer in Ukraine: Regional Disparities and National Trends in Incidence, Management, and Mortality

Anti-inflammatory drugs prevent intestinal tumor formation, an activity related to their ability to inhibit inflammatory pathway signaling in the target tissue. We previously showed that treatment of Min/+ mice with the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib induced rapid tumor regression; however, drug-resistant tumors appeared with long-term treatment. In this study, we investigated whole-tissue changes in inflammatory signaling by studying constituents of the tissue stroma and extracellular matrix. We found that celecoxib resistance was associated with changes in factors regulating autocrine transforming growth factor-β (TGFβ) signaling. Chronic drug treatment expanded the population of bone marrow–derived CD34+ vimentin+ αSMA− myofibroblast precursors and αSMA+ vimentin+ F4/80− myofibroblasts in the lamina propria and submucosa, providing a source of increased TGFβ and COX-2 expression. Membrane constituents regulating TGFβ availability, including syndecan-1 and heparanase-1, were also modified by chronic treatment in a manner promoting increased TGFβ signaling. Finally, long-term celecoxib treatment induced tissue fibrosis, as indicated by increased expression of collagen, fibronectin, and laminin in the basement membrane. We conclude that chronic COX-2 inhibition alters TGFβ signaling in the intestinal mucosa, producing conditions consistent with chronic inflammation. Cancer Prev Res; 3(3); 348–58