Upper gastrointestinal (GI) neoplasia account for 35% of GI cancers and 1.5 million cancer-related deaths every year. Despite its efficacy in preventing cancer mortality, diagnostic upper GI endoscopy is affected by a substantial miss rate of neoplastic lesions due to failure to recognize a visible lesion or imperfect navigation. This may be offset by the real-time application of artificial intelligence (AI) for detection (computer-aided detection [CADe]) and characterization (computer-aided diagnosis [CADx]) of upper GI neoplasia. Stand-alone performance of CADe for esophageal squamous cell neoplasia, Barrett's esophagus-related neoplasia, and gastric cancer showed promising accuracy, sensitivity ranging between 83% and 93%. However, incorporation of CADe/CADx in clinical practice depends on several factors, such as possible bias in the training or validation phases of these algorithms, its interaction with human endoscopists, and clinical implications of false-positive results. The aim of this review is to guide the clinician across the multiple steps of AI development in clinical practice.

Cancer-associated fibroblasts (CAFs) play an important role in colorectal cancer (CRC) progression and predict poor prognosis in CRC patients. However, the cellular origins of CAFs remain unknown, making it challenging to therapeutically target these cells. Here, we aimed to identify the origins and contribution of colorectal CAFs associated with poor prognosis.

Owing to the high load of immunogenic frameshift neoantigens, tumors arising in individuals with Lynch syndrome (LS), the most common inherited colorectal cancer (CRC) syndrome, are characterized by a pronounced immune infiltration. However, the immune status of normal colorectal mucosa in LS is not well characterized. We assessed the immune infiltrate in tumor-distant normal colorectal mucosa from LS CRC patients, sporadic microsatellite-unstable (MSI) and microsatellite-stable (MSS) CRC patients, and cancer-free LS carriers.