Background Unruptured intracerebral aneurysm wall enhancement (AWE) on vessel wall magnetic resonance imaging scans may be a promising predictor for rupture‐prone intracerebral aneurysms. However, the pathophysiology of AWE remains unclear. To this end, the association between AWE and histopathological changes was assessed in this study. Methods and Results A total of 35 patients with 41 unruptured intracerebral aneurysms who underwent surgical clipping were prospectively enrolled. A total of 27 aneurysms were available for histological evaluation. The macroscopic and microscopic features of unruptured intracerebral aneurysms with and without enhancement were assessed. The microscopic features studied included inflammatory cell invasion and vasa vasorum, which were assessed using immunohistochemical staining with CD68, CD3, CD20, and myeloperoxidase for the former and CD34 for the latter. A total of 21 (51.2%) aneurysms showed AWE (partial AWE, n=7; circumferential AWE, n=14). Atherosclerotic and translucent aneurysms were identified in 17 and 14 aneurysms, respectively. Aneurysm size, irregularity, and atherosclerotic and translucent aneurysms were associated with AWE on univariate analysis ( P <0.05). Multivariate logistic regression analysis showed that atherosclerosis was the only factor significantly and independently associated with AWE ( P =0.027). Histological assessment revealed that inflammatory cell infiltration, intraluminal thrombus, and vasa vasorum were significantly associated with AWE ( P <0.05). Conclusions Though AWE on vessel wall magnetic resonance imaging scans may be associated with the presence of atherosclerotic lesions in unruptured intracerebral aneurysms, inflammatory cell infiltration within atherosclerosis, intraluminal thrombus, and vasa vasorum may be the main pathological features associated with AWE. However, the underlying pathological mechanism for AWE still needs to be further studied.

Background Succinate dehydrogenase deficient gastrointestinal stromal tumors (SDH-deficient GISTs), which lack KIT or PDGFRA mutations demonstrate unique clinical and pathological features, and they respond poorly to standard targeted therapy. We herein present a novel case of SDH-deficient GIST in a three-month-old infant’s colon mesentery, and he is the youngest patientto date. Case presentation The infantpresented with complaints of blood in the stool. CT showed a 6.3 × 4.6 cm mass in the left lower retroperitoneal. Complete resection of tumor and segmental bowel resection was performed without regional lymphadenectomy. Histologically, tumor cells were distinctive in their multinodular colon wall involvement with interspersed tracts of colon wall smooth muscle. The tumor was composed mainly of epithelioid cells. Immunohistochemically, the tumor cells were positive for Vim, CD117, PDGFR, while negative for SDHB. Mutational analysis showed a synonymous mutation for SDHB and wild-type for KIT and PDGFRA. Two months after surgery, metastases were found and Imatinib was administered. Unfortunately, the disease continued to progress, and the infant died 5 months after surgery. Conclusions SDH-deficient GISTs comprise a subgroup of a relatively rare tumor type and show a number of clinically and biologically unique features, especially for infants. It is of great importance to developing new therapeutic targets and novel specific drugs.

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Background: Succinate dehydrogenase deficient gastrointestinal stromal tumors (SDH-deficient GISTs), which lack KIT or PDGFRA mutations demonstrate unique clinical and pathological features, and they respond poorly to standard targeted therapy. We herein present a novel case of SDH-deficient GIST in a three-month-old infant’s colon mesentery, and he is the youngest patient to date .Case presentation: The infant presented with complaints of blood in the stool. CT showed a 6.3×4.6 cm mass in the left lower retroperitoneal. Complete resection of tumor and segmental bowel resection was performed without regional lymphadenectomy. Histologically, tumor cells were distinctive in their multinodular colon wall involvement with interspersed tracts of colon wall smooth muscle. The tumor was composed mainly of epithelioid cells. Immunohistochemically, the tumor cells were positive for Vim, CD117, PDGFR, while negative for SDHB. Mutational analysis showed a synonymous mutation for SDHB and wild-type for KIT and PDGFRA. Two months after surgery, metastases were found and Imatinib was administered. Unfortunately, the disease continued to progress, and the infant died 5 months after surgery.Conclusions: SDH-deficient GISTs comprise a subgroup of a relatively rare tumor type and show a number of clinically and biologically unique features, especially for infants. It is of great importance to developing new therapeutic targets and novel specific drugs.

Background: Succinate dehydrogenase deficient gastrointestinal stromal tumors (SDH-deficient GISTs) which lack KIT or PDGFRA mutations demonstrate unique clinical and pathological features, and respond poorly to standard targeted therapy. We herein present a novel case of SDH-deficient GIST in a three-month-old boy in colon mesentery which is the youngest patient until now. Case presentation: The baby presented with complaints of blood in the stool. CT showed a 6.3×4.6 cm mass in the left lower retroperitoneal. Complete resection of tumor and segmental bowel resection was performed without regional lymphadenectomy. Histologically, tumors are distinctive in their multinodular colon wall involvement with interspersed tracts of colon wall smooth muscle. The tumor was composed mainly of epithelioid cells. Immunohistochemically, the tumor cells were positive for Vim, CD117, PDGFR, while negative for SDHB. Mutational analysis showed a synonymous mutation for SDHB and wild-type for KIT and PDGFRA. Two months after surgery, metastases were found and Imatinib was administered. Unfortunately, the disease continued to progress, the baby died 5 months after surgery. Conclusions: SDH-deficient GISTs comprise a subgroup of a relatively rare tumor type and show a number of clinically and biologically unique features, especially for infants. It is of great importance to developing new therapeutic targets and novel specific drugs.

Background Phyllodes tumors belong to a spectrum of biphasic fibroepithelial lesions and are most commonly found in the breast. They are extremely rare in the urinary tract and only one case of bladder phyllodes tumor has been reported. Case presentation We present a 69-year-old man with gross hematuria without an apparent cause. Computed tomography-urography and cystoscopic examination revealed a 5 × 4 cm lesion in the right ureteral orifice. He underwent a laparoscopic nephroureterectomy and partial cystectomy. Postoperative pathology confirmed a leaf-like structure consisting of myxoid stroma and peripheral urothelium. Stromal cells were spindle-shaped and stellate in appearance with no conspicuous cytological atypia or mitosis. The outlining urothelium had varying degrees of dysplasia, while in areas with moderate-to-severe dysplasia, active mitotic activity, abnormal giant cells, and focal early infiltration were observed. Overall, this case had the morphological features of benign phyllodes tumors and concomitant invasive urothelial carcinoma inside. The patient remained disease-free at 7 months after surgery. Conclusion We report the first ureteral tumor with the morphological characteristics of a phyllodes tumor and concomitant invasive urothelial carcinoma inside. Considering the potential for local recurrence of phyllodes tumors and invasive urothelial carcinoma, long-term clinical and radiological follow-up of such lesions are advisable.