Biliary tract cancers encompass a group of malignancies that affect the bile ducts and gallbladder and are associated with a poor prognosis, often due to late diagnosis and limited treatment options. The incidence of biliary tract cancer has been increasing gradually, underscoring the need for a better understanding of its pathogenesis and potential risk factors. Research suggests that biliary tract cancer may develop through a combination of genetic and epigenetic alterations, as well as environmental factors. The role of microbial exposure and the human microbiome in the pathogenesis of biliary tract cancer is an emerging area of interest. Traditionally, the biliary tree was considered sterile under normal conditions, but recent studies have identified associations between specific microbiological patterns and inflammatory biliary diseases and cancer. The human microbiome plays a crucial role in maintaining host homeostasis and interacting with the host's immune system. Dysbiosis, or an imbalance in the microbiome composition, has been implicated in the development of various diseases, including cancer. Hence, dysbiosis in the biliary tract might trigger the pathogenesis of biliary tract cancer. Advances in next-generation sequencing technology have provided researchers with a more comprehensive view of the microbiota and their potential roles in health and disease, providing more evidence of the relationship between the microbiota and biliary tract cancer. This review summarizes the latest evidence of the microbiome that would be associated with biliary tract cancer.

Background/Aims: Colorectal cancer is the most common cancer in oncopathology, with an increasing incidence among the elderly during the last decade. Various genetic and environmental factors play important roles in the emergence of colorectal adenocarcinoma. Non-coding RNAs, approximately 20–22 nucleotides, are transcribed irregularly in many cancer cells and play a critical role in many metabolic pathways in clinical cancer cases. DNA methylation is a critical epigenetic alteration that controls gene expression. In the current study, transcriptional silencing and CpG hypermethylation were developed as a therapeutic gene editing strategy for the clinical repression of colorectal adenocarcinoma.
Methods: A human colorectal adenocarcinoma cell line (Caco2) and a normal lung fibroblast cell line (Wi38) were utilized as the paradigms in this research to examine the effect of mir155 molecule transfection and CpGs-island (CGI) methylation. Cell counting was achieved using six-well and 24-well plates before transfection using a hemocytometer. The two cell lines were transfected with the mir155 agomir and antagomir molecules. The transfection efficiency, cell viability, cell IC₅₀, and target gene expression were measured, and CGIs-methylation was achieved by bisulfate conversion.
Results: The outcomes revealed the downregulation of oncogenes (AKT1 and VCAM1 genes as cancer-associated genes) and the upregulation of tumor suppressor genes (TSGs, Tp53 and KEAP1). In addition, CpG-islands methylation showed significant blocking of the oncogene promoter regions, and the switch on of TSG promoter regions was continuous.
Conclusions: miRNA-CGI-methylation led to the regression of Caco2 cell proliferation, suggesting the potential use of RNA silencing and DNA methylation in targeted gene therapy for colorectal cancer.

Background/Aims: Solitary rectal ulcer syndrome (SRUS) can be overlooked, diagnosed late, or misdiagnosed, particularly in childhood. This study reviewed the 13-year experience of the authors’ institution to increase clinicians' awareness of SRUS in the presence of symptoms. This paper reports the endoscopic and histopathological findings in children presenting with hematochezia.
Methods: The clinical and laboratory findings of 22 patients diagnosed with biopsy-proven SRUS in the authors’ clinic between 2007 and 2020 were evaluated retrospectively.
Results: The mean age at diagnosis was 12.5±2.6 years, and 59.1% of the patients were male. The median time of diagnosis was 24 months. A single ulcer lesion was found by colonoscopy in 18 patients (81.8%), two ulcers in two patients (9%), and more than two ulcers in two patients (9%). The pathology reports of all biopsies taken from the lesions were consistent with a solitary rectal ulcer. In the first stage, the treatment was started with toilet training, a high-fiber diet, and laxatives. In 11 patients (50%) who did not respond to the initial treatment, a 5-ASA enema was added. A glucocorticoid enema was added to treatment in five patients (22%) whose complaints did not regress despite this treatment. Clinical remission was achieved in five of the patients (18.1%). The time to diagnosis was significantly shorter in those in remission than those not in remission (p=0.04).
Conclusions: This study is the first large series on Turkish children. An increased awareness of SRUS in children will increase the rate of early diagnosis and treatment, allowing remission in more patients.

Achalasia is an esophageal motility disorder characterized by loss of esophageal peristalsis and impaired relaxation of the lower esophageal sphincter. Patients with achalasia often complain of persistent symptoms for several years before diagnosis. On the other hand, achalasia diagnosed as a sudden esophageal food impaction is uncommon, and no report has been issued on the diagnosis and successful treatment of achalasia in a 95-year-old patient. We report a case of achalasia diagnosed by high-resolution esophageal manometry and timed barium esophagography after food material removal by endoscopy in a 95-year-old woman who visited the hospital due to sudden esophageal food impaction and was successfully treated by endoscopic balloon dilatation.

Undifferentiated carcinoma of the pancreas (UPC) is a rare, aggressive pancreatic cancer subtype. In addition, there is limited data on optimal management and patients tend to present with unresectable disease. This highlights the need to explore non-surgical treatments, such as chemotherapy and radiotherapy. In 2017, a 40-year-old male was diagnosed with UPC, presenting with a 6 cm mass in the pancreas, encasing the major arteries, indicative of a locally advanced stage. Histopathology confirmed UPC with osteoclast-like giant cells. After nine cycles of modified FOLFIRINOX chemotherapy and concurrent chemoradiotherapy, treatment was stopped in 2018 because of his declining health. Remarkably, despite the cessation of treatment, by 2023, the tumor had shrunk to 3.5 cm with no metabolic activity indicated by FDG-PET/CT. This six-year survival and response to non-surgical treatment highlight potential new avenues for managing unresectable pancreatic cancer, underscoring the need for further comprehensive studies to evaluate these therapeutic strategies.

Malignant melanoma is a neoplasm of melanin-producing cells predominantly of cutaneous origin, which uncommonly develops within gut mucosa. We present the case of a 58-year-old woman with complaints of abdominal pain, loss of appetite and weight. Esophagogastroduodenoscopy revealed a gastric mass and systemic imaging demonstrated widespread nodal and bilateral adrenal gland involvement. Histopathology of the gastric mass confirmed primary malignant mucosal melanoma of the stomach. The patient received three cycles of Nivolumab but did not respond, and thus, was then offered best supportive care. Although infrequent, mucosal melanoma can arise from the gastrointestinal tract, and in contrast to the cutaneous form, advanced disease usually has a dismal prognosis and responds poorly to immune checkpoint inhibitors. Primary gastric melanoma is an aggressive disease that is diagnosed by exclusion after the differential diagnosis of metastasis from a cutaneous or unknown primary site has been conducted. If available, patients with treatment-naïve mucosal melanoma should be considered for enrollment in clinical trials.