In the last two decades, the vision of a unique carcinogenesis model for colorectal carcinoma (CRC) has completely changed. In addition to the adenoma to carcinoma transition, colorectal carcinogenesis can also occur via the serrated pathway. Small non-coding RNA, known as microRNAs (miRNAs), were also shown to be involved in progression towards malignancy. Furthermore, increased expression of certain miRNAs in premalignant sessile serrated lesions (SSLs) was found, emphasizing their role in the serrated pathway progression towards colon cancer. Since miRNAs function as post-transcriptional gene regulators, they have enormous potential to be used as useful biomarkers for CRC and screening in patients with SSLs particularly. In this review, we have summarized the most relevant information about the specific role of miRNAs and their relevant signaling pathways among different serrated lesions and polyps as well as in serrated adenocarcinoma. Additional focus is put on the correlation between gut immunity and miRNA expression in the serrated pathway, which remains unstudied.

BACKGROUND Russell body gastritis (RBG) is very rare type of chronic inflammation of gastric mucosa. The pathologic hallmark of the disease is Russell bodies (RB) which represent accumulation of eosinophilic cytoplasmic inclusions in endoplasmic reticulum of mature plasma cells (Mott cells). Most published cases are associated with Helicobacter pylori ( H. pylori ) infection because of correlation between plasma cell activation and antigenic stimulation. There are insufficient data about H. pylori -negative RBG and very little is known about the natural course of the disease. CASE SUMMARY A 51-year-old male patient underwent endoscopic screening for mild iron deficiency anemia. Gastroscopy revealed diffuse hyperemia, edema and nodularity of the fundic and corpus mucosa. Due to non-specific endoscopic findings and iron-deficiency anemia our preliminary diagnosis was diffuse type of gastric carcinoma or gastric lymphoma. Biopsy specimens of gastric mucosa showed inflammatory infiltrate rich in Mott cells, consisting entirely of cytoplasmic RB. Absence of nuclear atypia and mitosis of the plasma cells, polyclonal pattern of the Mott cells and negative staining for cytokeratins favored diagnosis of RBG. The patient was treated with proton-pump inhibitor for 8 wk. Long-term clinical and endoscopic surveillance was scheduled. Albeit, there was no improvement in endoscopic features of the gastric mucosa in three consecutive gastroscopies, histopathological findings demonstrated that the chronic inflammatory infiltrate in the fundic mucosa is less pronounced, rich in plasma cells, with almost absent RB and Mott cells. CONCLUSION The prognosis of this entity is uncertain, that is why these patients are subjects of continuous follow up.

In liver transplant patients, solid tumors and post-transplant lymphoproliferative disorders (PTLD) have emerged as significant long-term mortality causes. Additionally, it is assumed that de novo malignancy (DNM) after liver transplantation (LT) is the second-leading cause of death after cardiovascular complications. Well-established risk factors for PTLD and solid tumors are calcineurin inhibitors (CNIs), tacrolimus (TAC), and cyclosporine, the cornerstones of all immunosuppressive (IS) therapies used after LT. The loss of immunocompetence facilitated by the host immune system due to prolonged IS therapy leads to cancer development, including in LT patients. Hindering DNA repair mechanisms, promoting tumor cell invasiveness, and hampering apoptosis are critical events in tumorigenesis and tumor growth in LT patients resulting from IS administration. This paper aims to overview the refined mechanisms of IS-induced tumorigenesis after LT and the loss of immunocompetence facilitated by the host immune system due to prolonged IS therapy. In addition, we also discuss in detail the mechanisms of action in different types of IS regimen used after LT, and their putative effect on DNM.

BACKGROUND Although ABO-nonidentical and ABO-incompatible liver transplantation (LT) are other options for end-stage liver disease treatment, the development of antibodies against blood group antigens (anti-A/B antibodies) is still a challenge in managing and follow-up of the recipients. CASE SUMMARY A 56-year-old male with end-stage liver disease with rapid deterioration and poor prognosis was considered to receive a deceased ABO-nonidentical liver graft. All required tests were performed according to our pre-LT diagnostic protocol. The orthotopic LT procedure involving O+ donor and A1B+ recipient was performed. Our treatment strategy to overcome the antibody‐mediated rejection included a systemic triple immunosuppressive regimen: methylprednisolone, mycophenolate mofetil, and tacrolimus. The immunological desensitization consisted of the chimeric anti-CD20 monoclonal antibody rituximab and intravenous immunoglobulins. The patient was also on antibiotic treatment with amoxicillin/clavulanate, cefotaxime, and metronidazole. On the 10 th postoperative day, high titers of IgG anti-A and anti-B antibodies were found in the patient’s plasma. We performed a liver biopsy, which revealed histological evidence of antibody-mediated rejection, but the rejection was excluded according to the Banff classification. The therapy was continued until the titer decreased significantly on the 18 th postoperative day. Despite the antibiotic, antifungal, and antiviral treatment, the patient deteriorated and developed septic shock with anuria and pancytopenia. The conservative treatment was unsuccessful, which lead to the patient’s fatal outcome on the 42 nd postoperative day. CONCLUSION We present a patient who underwent ABO-nonidentical LT from a deceased donor. Even though we implemented the latest technological advancements and therapeutic approaches in the management of the patient and the initial results were promising, due to severe infectious complications, the outcome was fatal.