Background: Current guidelines recommend resection with primary anastomosis with diverting loop ileostomy over Hartmann's procedure if deemed safe for acute diverticulitis. The primary objective of the current study was to compare the utilization of these strategies and describe nationwide ostomy closure patterns and readmission outcomes within 1 year of discharge.
Methods: This was a retrospective, population-based, cohort study of United States Hospitals reporting to the Nationwide Readmissions Database from January 2011 to December 2019.
Strategies to augment immunity to self/neoantigens expressed by cancers are urgently needed to expand the proportion of patients benefiting from immunotherapy, particularly for GI cancers where only a fraction of patients respond to immunotherapies. However, current vaccine strategies are limited by poor immunogenicity, pre-existing vector-specific immunity, and vaccine-induced vector-specific immunity. Here, we examined a prime-boost strategy using a chimeric adenoviral vector (Ad5.
View Article and Find Full Text PDFColorectal cancer continues to represent a significant burden on public health as the second highest cause of cancer mortality, when men and women are combined, in the US. About 50% of patients either present with late-stage metastatic disease, or develop metastatic recurrences, and ultimately die. In turn, this mortality largely reflects cancer stem cells, tumor-initiating cells that are responsible for cancer progression, drug resistance, recurrence and metastasis.
View Article and Find Full Text PDFMost sporadic colorectal cancer reflects acquired mutations in the adenomatous polyposis coli () tumor suppressor gene, while germline heterozygosity for mutant produces the autosomal dominant disorder Familial Adenomatous Polyposis (FAP) with a predisposition to colorectal cancer. In these syndromes, loss of heterozygosity (LOH) silences the remaining normal allele of , through an unknown mechanism, as the initiating step in transformation. Guanylyl cyclase C receptor (GUCY2C) and its hormones, uroguanylin and guanylin, have emerged as a key signaling axis opposing mutations driving intestinal tumorigenesis.
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