Colorectal cancer is one of the most commonly diagnosed cancers worldwide. Traditionally, mechanisms of colorectal cancer formation have focused on genetic alterations including chromosomal damage and microsatellite instability. In recent years, there has been a growing body of evidence supporting the role of inflammation in colorectal cancer formation. Multiple cytokines, immune cells such T cells and macrophages, and other immune mediators have been identified in pathways leading to the initiation, growth, and metastasis of colorectal cancer. Outside the previously explored mechanisms and pathways leading to colorectal cancer, initiatives have been shifted to further study the role of inflammation in pathogenesis. Inflammatory pathways have also been linked to some traditional risk factors of colorectal cancer such as obesity, smoking and diabetes, as well as more novel associations such as the gut microbiome, the gut mycobiome and exosomes. In this review, we will explore the roles of obesity and diet, smoking, diabetes, the microbiome, the mycobiome and exosomes in colorectal cancer, with a specific focus on the underlying inflammatory and metabolic pathways involved. We will also investigate how the study of colon cancer from an inflammatory background not only creates a more holistic and inclusive understanding of this disease, but also creates unique opportunities for prevention, early diagnosis and therapy.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. It is well known that repeated inflammatory insults in the liver can cause hepatic cellular injury that lead to cirrhosis and, ultimately, hepatocellular carcinoma. Furthermore, the microbiome has been implicated in multiple inflammatory conditions which predispose patients to malignancy. With this in mind, we explore the inflammatory implications of the microbiome on pathways that lead to HCC. We also focus on how an understanding of these underlying inflammatory principles lead to a more wholistic understanding of this deadly disease, as well as potential therapeutic implications.

No abstract available. Manuscript truncated after 150 words. In consideration of dysphagia, most cases predominate in the oropharyngeal region with the remainder caused primary by esophageal causes. Lesser known and studied is the development of dysphagia and globus sensation from epiglottic pathology, namely epiglottic calcification. With less than a dozen published cases in literature, very little data exists on identification, diagnosis, and treatment of this known cause of morbidity. Here we present a case of oropharyngeal dysphagia arising from a rare cause, epiglottic calcification. An 81-year-old man with a history of aortic stenosis and carotid artery stenosis presented with worsening dysphagia over the course of one month. The patient reported significant dysphagia, initially to solids and subsequently to liquids causing a weight loss of over 50 pounds. Physical exam of the oropharynx and neck were unremarkable. A bedside swallow evaluation suggested mildly decreased hyolaryngeal movement, but no other significant abnormalities. A barium swallow study revealed incomplete epiglottic excursion …

Introduction: Pancreatic heterotopia is defined as pancreatic tissue found outside the normal anatomical location. It is often an incidental finding but becomes clinically evident when complicated by pathologic changes such as inflammation, bleeding, obstruction, and malignant transformation. We present a case of a 57 years old female who presented with dyspepsia and was found to have ectopic pancreatic tissue at the gastroesophageal junction on esophagogastroduodenoscopy (EGD). Case Description/Methods: A 57-year-old female with a past medical history of Cecal polyp presents to the gastroenterology clinic for epigastric pain under the rib cage ongoing for several months; pain worsens if she bends over. She denies nausea, vomiting, fever, chills, dysphagia, or weight loss. She used to take pantoprazole but stopped taking it 2 months ago. CT chest was significant for small hiatal hernia. EGD significant normal esophagus but irregular Z-line (Figure 1A), small hiatal hernia, and gastric erythema. Z-line was mildly irregular and was biopsied, which shows junctional mucosa showing focal pancreatic metaplasia/heterotopia with no malignant changes. Negative for intestinal metaplasia or dysplasia (Figure 1B) Discussion: Heterotopic pancreas in the stomach is usually located within 5 cm of the pylorus and is more common along the greater curve, but the involvement of the GE junction is very rare [1]. Symptoms vary depending on the affected location and size of the mass. Patients with ectopic pancreatic tissue at the GE junction can be asymptomatic or present with epigastric pain, reflux or heartburn. These patients can be managed conservatively with medical treatment [2]. The risk of malignancy arising in the heterotopic pancreas is exceedingly rare, but several documented cases have appeared in the literature. Pancreatic heterotopia should be considered as a source of a potentially malignant lesion, and early treatment or close monitoring for aberrant pancreas is recommended.[2363] Figure 1. Circumferential induration with irregular, reticulated erosions found in the mid esophagus during upper endoscopy.