SRY-box transcription factor 9 (SOX9) has been reported to be overexpressed in a wide variety of gastrointestinal malignancies. While its role has been studied in gastric cancer (GC), the results remain conflicting. This study aimed to evaluate the relationship between SOX9 immunohistochemistry results and the pathological and clinical characteristics of gastric adenocarcinoma, assessing its potential as a prognostic marker. Gastric tissue samples from 150 patients with gastric cancer were included in the study. Tissue sections were stained using an anti-SOX9 antibody, and relevant data were retrospectively collected from digital records. Immunostaining results were scored based on the proportion and intensity of stained nuclei throughout the tumor. A final immunostaining score was calculated by multiplying the SOX9 intensity score by the proportion score. Strong SOX9 nuclear staining was observed in 68 patients (45.3%), while moderate staining was seen in 60 patients (40%). SOX9 nuclear staining was absent in three patients (2%). A final SOX9 immunostaining score of ≥10, classified as high expression, was identified in 60 patients (40%). Patients with higher SOX9 expression or strong intensity scores exhibited significantly larger tumor sizes, higher rates of perineural and vascular invasion, more advanced T or lymph node staging, and greater likelihoods of lymphatic or distant metastases compared to those with lower SOX9 expression or intensity scores (all P < 0.05). These findings suggest that SOX9 staining intensity and expression are associated with increased tumor malignancy and disease progression. Therefore, SOX9 may serve as a prognostic pathological indicator in GC patients.

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Abstract Introduction Thyroid carcinomas constitute less than 3% of all cancers (1). Papillary thyroid carcinoma (PTC) accounts for 80% of thyroid carcinomas and generally has a good prognosis(2). Lymph node metastases are frequently observed in thyroid cancers(30-40%). However, distant metastases are quite rare(1-4%)(2). Clinical Case A 52-year-old female patient presented to the neurosurgery department due to back pain of approximately 2 months. A mass lesion was observed in the T9 vertebral body on a thoracic CT scan, which was destroying the bone structure, causing a compression fracture in the vertebra, and extending into the spinal canal. A total laminectomy of T9 vertebra and partial laminectomies of T8 and T10 vertebrae were performed. Pathology revealed strongly positive for Vimentin, TTF-1, Thyroglobulin, and Pax 8, consistent with carcinoma metastasis. It was recommended to perform a whole-body scan, primarily focusing on the thyroid gland. PET-CT, thoracic and abdominal CT scans revealed a 62x48 mm metastatic lesion in the right iliac bone and metastatic involvement of the T9 vertebra, with no other pathological findings. The patient's history revealed that she had undergone a total thyroidectomy six years ago, and the result was reported as benign. She was on levothyroxine sodium replacement therapy. Blood tests revealed TSH: 0.288 (0.27-4.2 µIU/ml), T4: 18.7 (12-22 pmol/L), T3: 4.78 (3.1-6.8 pmol/L), Anti-Thyroglobulin Antibody: 60.8 (0-115 IU/ml), and Thyroglobulin: &gt;500 (3.5-77 ng/ml). Neck ultrasonography did not reveal any residual thyroid tissue or pathological lymph nodes. Given the suspicion of thyroid carcinoma metastasis and high thyroglobulin levels, the pathology preparations of the total thyroidectomy were re-consulted by our hospital's pathology department. The pathology result was consistent with papillary thyroid carcinoma composed of 55% follicular subtype and 45% solid/trabecular subtype. As surgery for the iliac bone metastasis was not considered appropriate, the patient was referred to the nuclear medicine department for radioactive iodine therapy and to the radiation oncology department for radiotherapy. The nuclear medicine, radiation oncology, and our department continue to follow up and treat the patient. Conclusion PTC is generally a slowly progressing cancer with a good prognosis. The most common site of metastasis in all PTC cases is the cervical lymph node, and only 3.5-3.8% have distant metastases(3). Distant metastases are most commonly seen in the lungs (53.4%), followed by bones (28.1%), liver (8.3%), and brain (4.7%) (1,4). Distant metastases significantly increase mortality from PTC. Therefore, the importance of adjuvant therapy (endocrine therapy, radiotherapy, etc.) and regular follow-up after thyroid cancer surgery should be emphasized. It should be kept in mind that, as in our case, papillary thyroid carcinomas can also present with isolated bone metastases without cervical lymph node metastases.

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Abstract Antibody (Ab) crosslinking of HLA class II (HLA II) molecules on the surface of endothelial cells (ECs) triggers proliferative and prosurvival intracellular signaling, which are implicated in promoting chronic Ab-mediated rejection (cAMR). Despite the importance of cAMR in transplant medicine, the mechanisms involved remain incompletely understood. Here, we examined the regulation of yes-associated protein (YAP) nuclear cytoplasmic localization and phosphorylation in human ECs challenged with Abs that bind HLA II, which are strongly associated with cAMR. To examine changes in YAP localization in response to Ab-mediated engagement of HLA II, we used an adenoviral vector to express the class II transactivator or treatment with interferon γ. In unstimulated ECs expressing HLA II, YAP localized mainly in the cytoplasm. Stimulation with HLA II Ab (0.1–1 µg/mL) induced marked translocation of YAP to the nucleus. HLA II signaling triggered by high concentrations of HLA II Ab (1 µg/mL) also induced prominent YAP localization in cytoplasmic punctate structures that were disassembled by exposure to 1,6-hexanediol, suggesting that these structures are biomolecular condensates. Using multiple treatments, including stimulation with serum, thrombin or HLA I Ab and conditions (eg ECs plated at different densities) indicate that formation of YAP cytoplasmic puncta can be dissociated from YAP nuclear localization and phosphorylation at Ser127, a site in YAP targeted by the Hippo kinases LATS1/2. The results revealed that HLA II signaling regulates YAP subcellular distributions in ECs and demonstrate, for the first time, that HLA II Ab selectively stimulates YAP concentration in punctate structures.

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