Background Heterotopic Ossification (HO) is a common condition referring to ectopic bone formation in soft tissues. It has two major etiologies, acquired (more common) and genetic. The acquired form is closely related to tissue trauma. The exact pathogenesis of this disease remains unclear; however, there is ongoing research in prophylactic and therapeutic treatments that is promising. Conclusions Due to HO potential to cause disability, it is so important to differentiate it from other causes in order to establish the best possible management.

No abstract

No abstract

No abstract

No abstract

No abstract

No abstract

P ancreatic ductal adenocarcinoma (PDAC) is the most common pancreatic malignancy (90%). Although PDAC accounts for 2% of all cancer cases, it constitutes the fourth leading cause of cancer-related deaths in the United States with a 5-year survival of 5%-10% (1). PDAC is also projected to be the second leading cause of cancer-related death by 2030 (2). Ninety percent of PDACs are sporadic in origin; around 10% of cases occur in hereditary and familial predisposition syndromes. To date, certain high-risk factors such as smoking, alcohol use, and chronic pancreatitis have been strongly implicated (3). The risk for PDAC increases with age; more than 80% of cases occur between ages 60 and 80 years (4). The mean size of PDAC is approximately 3.1 cm, and approximately 80% of patients manifest distant metastases or locally advanced disease at presentation, which make them ineligible for surgical cure. Rapid advances in precision medicine and immunotherapy have contributed little to early detection with only modest improvements in patient outcomes (3). Recent advances in high-throughput sequencing technologies have allowed for a better understanding of the PDAC genomic landscape, defined precursor lesions, and delineated genetic alterations that lead to tumorigenesis (5). Moreover, improved knowledge of genetic causes of PDAC may improve prognostication and targeted treatment in select cases (6). In this article, we will review current knowledge about genetic abnormalities of precursor lesions that contribute to PDAC development. Imaging features of PDAC and precursor lesions, the potential role of molecular imaging, and select hereditary syndromes associated with a high risk of PDAC development will also be discussed. Finally, we will review the current guidelines for screening of PDAC and surveillance of precursor lesions.