Development and Validation of a Prognostic Nomogram for Extremity Soft Tissue Leiomyosarcoma

Conclusions: The proposed nomogram is a reliable and robust tool for accurate prognostic prediction in patients with extremity soft tissue LMS. Introduction Soft tissue leiomyosarcoma (LMS) is an aggressive sarcoma, which originates from smooth muscle cells (1). Soft tissue LMS accounts for about 5–10% of all soft tissue sarcomas (2). It occurs in different sites, including the retroperitoneum, intraabdominal sites, and extremities (3). Extremity LMS comprised about 10–15% of extremity sarcomas, with a preference for the lower limb (4–6). Extremity LMS tends to have a better prognosis than uterine, retroperitoneal, or major vessel LMS (1, 7), but worse overall survival (OS) than other soft tissue sarcoma subtypes (8). Moreover, patients with metastasis usually have a poorer prognosis (2, 9, 10). Current treatment for extremity LMS includes systemic chemotherapy along with surgery and/or radiation therapy for local control. Surgical resection is the most widely accepted treatment modality (11). Significant independent predictors for survival in LMS patients are primary site, age, tumor location, tumor size, margin status, and histological grade (2, 12–14), whereas abdominal site, tumor size>15 cm, positive resection margin and higher histological grade predict poor survival. Further, tumor size and margin status were independent predictors of local recurrence, while tumor size and grade were independent predictors for metastasis in LMS patien...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research

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NF-κB transcription factors, driven by the IRAK/IKK cascade, confer treatment resistance in pancreatic ductal adenocarcinoma (PDAC), a cancer characterized by near-universal KRAS mutation. Through reverse-phase protein array and RNA sequencing we discovered that IRAK4 also contributes substantially to MAPK activation in KRAS-mutant PDAC. IRAK4 ablation completely blocked RAS-induced transformation of human and murine cells. Mechanistically, expression of mutant KRAS stimulated an inflammatory, autocrine IL-1β signaling loop that activated IRAK4 and the MAPK pathway. Downstream of IRAK4, we uncovered TPL2 (also k...
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