Endoscopic mucosal resection of a large inflammatory fibroid polyp (Vanek's tumor): a case report.

Vanek's Tumor (inflammatory fibroid polyp) is a rare benign mesenchymal lesion occurring throughout the digestive tract. Classical Vanek's tumor ("gastric") contains concentric formations of proliferating spindle cells, which are CD34 positive. Atypical-inflammatory pseudotumor-like Vanek's tumor ("intestinal") lacks concentric formations and is CD34 negative. A 70-years-old man patient presented during hematochemical routine tests, sideropenic anemia and leukopiastrinosis. The patient performed osteomyelitis biopsy and esophagogastroduodenoscopy (EGD) showing a gastric wall with nodular appearance and, in antrum pre-pyloric, a polypoid pedunculated lesion, measuring approximately 3 cm in diameter, surrounded by hyperemic mucosa. The lesion then was removed by en bloc endoscopic mucosal resection (EMR) and histo-morphological, immune-cytochemical and biomolecular evaluations were performed. The data were compatible with a benign polyp fibroid inflammatory (Vanek's Tumor). The results of this study suggest that endoscopic mucosal resection is a safe and efficacy solution for the resection of these gastrointestinal polyps and the two morphological patterns of Vanek's tumor more probably represent only variants of one type of tumor than two different lesions. BRAF mutations were not shown growth PDGFRA wild-type Vanek's tumor.

A narrative review of MET inhibitors in non-small cell lung cancer with MET exon 14 skipping mutations.

Treatment of advanced non-small cell lung cancer (NSCLC) has radically improved in the last years due to development and clinical approval of highly effective agents including immune checkpoint inhibitors (ICIs) and oncogene-directed therapies. Molecular profiling of lung cancer samples for activated oncogenes, including epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), c-ros oncogene 1 (ROS1) and BRAF, is routinely performed to select the most appropriate up-front treatment. However, the identification of new therapeutic targets remains a high priority. Recently, MET exon 14 skipping mutations have emerged as novel actionable oncogenic alterations in NSCLC, sensitive to MET inhibition. In this review we discuss: (I) MET gene and MET receptor structure and signaling pathway; (II) MET exon 14 alterations; (III) current data on MET inhibitors, mainly focusing on selective MET tyrosine kinase inhibitors (TKIs), in the treatment of NSCLC with MET exon 14 skipping mutations. We identified the references for this review through a literature search of papers about MET, MET exon 14 skipping mutations, and MET inhibitors, published up to September 2020, by using PubMed, Scopus and Web of Science databases. We also searched on websites of main international cancer congresses (ASCO, ESMO, IASLC) for ongoing studies presented as abstracts. MET exon 14 skipping mutations have been associated with clinical activity of selective MET inhibitors, including capmatinib, that has recently received approval by FDA for clinical use in this subgroup of NSCLC patients. A large number of trials are testing MET inhibitors, also in combinatorial therapeutic strategies, in MET exon 14-altered NSCLC. Results from these trials are eagerly awaited to definitively establish the role and setting for use of these agents in NSCLC patients.