Background: Mucinous adenocarcinoma (MAC) is a distinct type of colorectal cancer (CRC) associated with poor response to treatment and poorer prognosis. MAC is diagnosed by WHO definition when the extracellular mucin is more than 50% of the lesion. We aimed at assessing the gene expression profiles of the CRCs with any mucinous features (>5%) in a retrospective study. Methods: The data of a 50-gene next generation sequencing (NGS) panel of 166 CRCs was analyzed and the gene mutational profile with morphologic features was correlated. Results: We identified the different genetic mutation profiles between CRCs with and without mucinous component, but noticed a similar genetic profile between MACs and CRCs with mucinous component, irrespective of the percentage (if mucinous component more than 5%). The different genetic mutation profile related to MSI status was also identified between two groups of tumors. The most frequent mutations in CRCs with mucinous component are KRAS (28/49, 57.1%) and BRAF (19/49, 38.7%), PIK3CA (16/49, 32.6%), followed by APC (12/49, 24.5%) and TP53 (11/49, 22.5%). The combined mutation frequency of the two key factors in the EGFR signaling pathway, KRAS and BRAF, in the CRCs with and without mucinous component is 95.9% and 52.1%, respectively. Conclusions: The dysregulation of EGFR pathway plays a critical role in the development of CRCs with mucinous component, irrespective of the percentage. The result suggested that the current cut off of 50% mucin component to define mucinous adenocarcinoma might be challengeable.

Collagenous gastritis has been reported as a rare cause of nausea, diarrhea, weight changes, and early satiety in female patients. Here, we describe two women aged 43 and 71 years who presented with similar symptoms. Gastric biopsies from both individuals showed thickened, irregular subepithelial collagen bands (>10 μm). The pathogenesis of collagenous gastritis is poorly understood, but it may be the presenting symptom for many underlying autoimmune conditions. In particular, there is a well-established connection between collagenous disorders of the gastrointestinal tract and celiac sprue, Sjögren syndrome, and lymphocytic colitis; however, none of these conditions had been diagnosed in our patients. The older woman had incidentally discovered hypogammaglobinemia and IgA deficiency, whereas the younger woman suffered from fibromyalgia. Although a gluten-free diet and budesonide have been effective in some cases, there is no standardized therapy for collagenous gastritis. Our patients trialed diet modification and have required no additional medical interventions.

Background: Mucinous adenocarcinoma (MAC) is a distinct type of colorectal cancer (CRC) associated with poor response to treatment and poorer prognosis. MAC is diagnosed by WHO definition when the extracellular mucin is more than 50% of the lesion. We aimed at assessing the gene expression profiles of the CRCs with any mucinous features (>5%) in a retrospective study. Methods: The data of a 50-gene next generation sequencing (NGS) panel of 166 CRCs was analyzed and the gene mutational profile with morphologic features was correlated. Results: We identified the different genetic mutation profiles between CRCs with and without mucinous component, but noticed a similar genetic profile between MACs and CRCs with mucinous component, irrespective of the percentage (if mucin component more than 5%). The different genetic mutation profile related to MSI status was also identified between two groups of tumor. The most frequent mutations in CRCs with mucinous component are KRAS (28/49, 57.1%) and BRAF (19/49, 38.7%), PIK3CA (16/49, 32.6%), followed by APC (12/49, 24.5%) and TP53 (11/49, 22.5%). The combined mutation frequency of the two key factors in the EGFR signaling pathway, KRAS and BRAF , in the CRCs with and without mucin component is 95.9% and 52.1%, respectively. Conclusions: The dysregulation of EGFR pathway plays a critical role in the development of CRCs with mucinous component, irrespective of the percentage. The mucinous differentiation in CRCs may predict the poor response to anti-EGFR therapy.

Native kidney biopsies are high-risk for bleeding complications due to the vascularity of the kidney and the inability to compress the biopsy site within a deep retroperitoneal location. Recommended parameters to minimize bleeding risk include a platelet count above 100 x 109 /L, hemoglobin above 10 g/dL, systolic blood pressure <140 mm Hg, and minimizing the number of biopsy cores. In this paper we present patient cases to discuss management of other factors pertinent to kidney biopsy planning including interruption of anticoagulation, treatment of anxiety which can elevate blood pressure, and use of Doppler. Undiagnosed chronic kidney disease can affect triaging of tissue to light, immunofluorescence and electron microscopy, as sclerosed glomeruli are difficult to visualize in fresh cores. It is recommended to have a back-up retrieval protocol in place to obtain immunofluorescence and electron microscopy results, in the event that only limited kidney tissue was acquired for light histology. A collaborative effort between nephrology, interventional radiology and pathology is essential to optimize the diagnostic yield while minimizing bleeding risk with kidney biopsies. Of paramount importance is physician judgment of whether there is an acceptable balance of benefits/risks to proceed with a kidney biopsy.