Soft tissue sarcomas (STS) are rare solid tumors of mesenchymal cell origin that display a heterogenous mix of clinical and pathologic characteristics. STS can develop from fat, muscle, nerves, blood vessels, and other connective tissues. The evaluation and treatment of patients with STS requires a multidisciplinary team with demonstrated expertise in the management of these tumors. The complete NCCN Guidelines for STS provide recommendations for the diagnosis, evaluation, and treatment of extremity/superficial trunk/head and neck STS, as well as intra-abdominal/retroperitoneal STS, gastrointestinal stromal tumors, desmoid tumors, and rhabdomyosarcoma. This portion of the NCCN Guidelines discusses general principles for the diagnosis, staging, and treatment of STS of the extremities, superficial trunk, or head and neck; outlines treatment recommendations by disease stage; and reviews the evidence to support the guidelines recommendations.

Patients selected to receive MIPD for cancer have equivalent short-term and oncologic outcomes, when compared with patients who undergo OPD.

Barrett's esophagus (BE) is defined by the replacement of the normal squamous epithelium of the distal esophagus with metaplastic intestinal-type columnar epithelium. 1-3 BE is an adverse event of chronic GERD and the only identifiable premalignant condition for esophageal adenocarcinoma (EAC), a cancer that continues to increase in incidence. In 2014 there were approximately 18,170 incident cases of esophageal cancer in the United States, nearly 60% of which were EAC. [4][5][6] Although uncommon, EAC is a highly lethal cancer associated with a poor 5year survival rate of 15% to 20% and an overall median survival of <1 year in cases with advanced disease. [5][6][7] It is estimated that BE is present in 1% to 2% of the general adult population. 8,9 The stepwise and hypothesized progression of BE to invasive EAC is believed to occur through the histopathologic stages of intestinal metaplasia to low-grade dysplasia (LGD) to high-grade dysplasia (HGD) to intramucosal EAC and finally to invasive EAC. 3,[10][11][12][13] Endoscopic eradication therapy (EET) has significantly changed the management of patients with BE-related neoplasia and allows a minimally invasive treatment approach that avoids the morbidity and mortality associated with esophagectomy. Contemporary EET, supported by published literature, entails endoscopic mucosal resection (EMR) of visible lesions within the Barrett's segment and ablative techniques that include radiofrequency ablation (RFA) and cryotherapy. Several studies, including randomized controlled trials (RCTs), large observational studies, and population-based studies, have demonstrated the efficacy, effectiveness, and safety of EET to achieve complete eradication of intestinal metaplasia (CE-IM) and neoplasia while maintaining disease remission. [14][15][16][17][18][19][20][21][22] In addition, population-based studies report comparable outcomes between esophagectomy and EET in the management of BE-related HGD and mucosal EAC. 23 Available data suggest that EET is being performed not only at academic and tertiary care centers but also among community practices. 14,18 AIMS/SCOPEThe aim of this document is to offer evidence-based recommendations and clinical guidelines addressing key issues related to EET in the management of BE-related neoplasia. This document addresses the following clinical questions: 1. What is the role of confirmation of diagnosis by an expert GI pathologist or by a panel of pathologists in BE patients with dysplasia or intramucosal EAC referred for EET? 2. Comparing EET with surveillance, what is the optimal management strategy in BE patients with dysplasia (HGD and LGD) and intramucosal EAC? 3. Comparing EET with esophagectomy, what is the optimal management strategy in BE patients with HGD and intramucosal EAC? 4. What is the role of EMR in BE patients with a visible lesion detected during screening or surveillance? 5. What is the role of ablation of the remaining BE segment after EMR of all visible lesions in BE patients referred for EET? 6. Comparing EMR of visibl...

Preoperative chemoradiation with capecitabine and SIB-IMRT is well tolerated and results in an encouraging pCR rate for patients with locally advanced rectal cancer.

Lysophosphatidic acid (LPA) is a bioactive lipid which increases in concentration locally and systemically across different cancer types. Yet, the exact mechanism(s) of how LPA affects CD8 T cell immunosurveillance during tumor progression remain unknown. We show LPA receptor (LPAR) signaling by CD8 T cells promotes tolerogenic states via metabolic reprogramming and potentiating exhaustive differentiation to modulate anti-tumor immunity. We found LPA levels predict response to immunotherapy and Lpar5 signaling drives exhausted phenotypes on CD8 T cells. Importantly, we identify a novel function of Lpar5 to regulate CD8 T cell respiration, proton leak, and reactive oxygen species. Together, our findings reveal that LPA serves as a lipid-regulated immune checkpoint by modulating metabolic efficiency through LPAR5 signaling on CD8 T cells. Our study offers key insights into the mechanisms governing adaptive anti-tumor immunity and demonstrates LPA could be exploited as a novel T cell directed therapy to improve dysfunctional anti-tumor immunity.