Intraosseous hemangioma with aneurysmal bone cyst-like changes of the hyoid bone: Case report and literature review.

RATIONALE: Intraosseous hemangioma is a rare benign vascular tumor of the bone that can affect any body part; however, the most common site is the vertebra, followed by calvarial bones. PATIENT CONCERNS: We present a case of intraosseous hemangioma in a 23-year-old male who presented a feeling of fullness in the throat for 3 months. The hyoid bone level had a hard mass of about 5 cm. Fine needle aspiration showed 5 mL dark bloody aspirates. Magnetic resonance image showed a 5.3 cm mixed signal intensity lesion in the hyoid body. DIAGNOSIS: Histopathologic examination showed intraosseous hemangioma with aneurysmal bone cyst (ABC)-like changes in the hyoid bone. INTERVENTIONS: The mass was completely removed without significant problems. OUTCOMES: Complete mass excision and symptomatic improvements were achieved, and no subsequent relapses were observed. LESSONS: The authors experienced a case of intraosseous hemangioma with ABC-like changes. There has been no case report of intraosseous hemangioma in the hyoid bone. This case showed a spectral pattern of the ABC-like changes developing from the underlying bone tumor as a secondary change. ABC-like changes in bone tumors can mislead the diagnosis. Careful examination of the tumor is essential for the correct diagnosis of ABC or ABC-like changes.

Anaplastic Transformation in Papillary Thyroid Carcinoma: A Case Report.

Anaplastic thyroid cancer (ATC), a rare thyroid malignancy, accounts for only 5% of all thyroid cancers. However, it is the most aggressive form and has a very poor prognosis. Increasing evidence suggests that ATC arises from papillary thyroid carcinoma (PTC). However, the exact mechanism underlying this transformation remains unclear. In almost all cases, ATC originates within, but rarely outside, the thyroid gland. Transformation of metastatic PTC into ATC within the cervical lymph nodes is extremely rare. In this report, we present a rare case in a 63-year-old male patient who was initially diagnosed with PTC at his first hospital visit, which underwent anaplastic transformation in lymph node metastasis, and was subsequently diagnosed during the follow-up visit.

An Ectopic Parathyroid Adenoma of the Retropharynx in a Patient with Primary Hyperparathyroidism and Papillary Thyroid Cancer-A Rare Case.

The frequency of concurrent thyroid cancer in patients with primary hyperparathyroidism (pHPT) varies. While the pathological association between thyroid and parathyroid disorders is frequently noted, the co-occurrence of parathyroid adenoma and papillary thyroid cancer is exceptionally rare. Furthermore, an ectopic parathyroid adenoma in the retropharyngeal space is exceedingly rare. Therefore, anatomical variations through the utilization of relevant diagnostic tools play a crucial role in guiding decisions pertaining to clinical manifestations, diagnostic methods, surgical interventions, and operative strategies for parathyroid tumors. We present a case of a 51-year-old female patient with papillary thyroid carcinoma in the right thyroid lobe and an ectopic parathyroid adenoma in the retropharyngeal space confirmed through surgical intervention. The elevated preoperative levels of serum calcium and parathyroid hormone, along with low serum phosphate, returned to normal ranges after surgery. This case sheds light on the unusual occurrence of an ectopic parathyroid adenoma in the retropharyngeal region within a thyroid cancer patient, providing valuable insights into the realm of thyroid malignancies.

Traumatic Anterior Cervical Disc Herniation Presenting as Severe Dysphagia.

Due to the anatomical characteristics of the cervical spine, few cases of traumatic anterior cervical disc herniation have been reported in the literature. Here, we present a rare case of a traumatic anterior cervical disc herniation presenting as severe dysphagia. A 75-year-old male patient presented with severe dysphagia following an accident three days prior when he fell from a height of stairs. Cervical magnetic resonance (MR) imaging revealed a 1.3 × 1.0 cm extruded disc in the anterior aspect of the C4 level with the base at the C3-4 disc, which displaced the esophagus anteriorly. Esophagography revealed an extrinsic esophageal lesion that was considered to be responsible for the obstruction of the airway at the same level. He underwent a ruptured disc removal via the anterior approach. Preoperative dysphagia was resolved gradually after surgery, and he remained asymptomatic six months after surgery.

Novel electrochemical PMI marker biosensor based on quantum dot dissolution using a double-label strategy.

A novel and facile post-mortem interval (PMI) biosensor was fabricated using a double-label strategy to detect the glyceraldehyde 3-phosphate dehydrogenase (GAPDH) biomarker. A monoclonal anti-GAPDH antibody was immobilized on a surface label containing cadmium selenide quantum dots (CdSe QDs) on a cysteamine graphene oxide (Cys-GO) self-assembled monolayer. Glucose oxidase (GOx) was used as a signal label to conjugate with GAPDH. GAPDH recognition was achieved through the dissolution of the surface-attached CdSe QDs by hydrogen peroxide generated through GAPDH-conjugated GOx-catalyzed ß-glucose oxidation. To enhance sensitivity, a competitive interaction was introduced between free and conjugated GAPDH to the active site of the anti-GAPDH antibody. The electrochemical response due to CdSe dissolution decreased proportionally with the concentration of free GAPDH. Differential pulsed voltammetry was conducted to determine the analytical characteristics of the immunosensor, including the limit of detection, linear dynamic range, target selectivity, system stability, and applicability toward the analysis of real samples.

Oleanolic acid 3-acetate, a minor element of ginsenosides, induces apoptotic cell death in ovarian carcinoma and endometrial carcinoma cells via the involvement of a reactive oxygen species-independent mitochondrial pathway.

OBJECTIVES: Oleanolic acid, a minor element of ginsenosides, and its derivatives have been shown to have cytotoxicity against some tumor cells. The impact of cytotoxic effect of oleanolic acid 3-acetate on ovarian cancer SKOV3 cells and endometrial cancer HEC-1A cells were examined both in vivo and in vitro to explore the underlying mechanisms. METHODS: Cytotoxic effects of oleanolic acid 3-acetate were assessed by cell viability, phosphatidylserine exposure on the cell surface, mitochondrial release of cytochrome C, nuclear translocation of apoptosis-inducing factor, depolarization of mitochondrial transmembrane potential (ΔΨm), and generation of reactive oxygen species (ROS). In vivo inhibition of tumor growth was also assessed with xenografts in immunocompromised mice. RESULTS: Oleanolic acid 3-acetate exhibited potent cytotoxicity toward SKOV3 and HEC-1A cells by decreasing cell viability in a concentration-dependent manner. Importantly, oleanolic acid 3-acetate effectively suppressed the growth of SKOV3 cell tumor xenografts in immunocompromised mice. Furthermore, oleanolic acid 3-acetate induced apoptotic cell death as revealed by loss of ΔΨm, release of cytochrome c, and nuclear translocation of apoptosis-inducing factor with a concomitant activation of many proapoptotic cellular components including poly(ADP-ribose) polymerase, Bcl-2, and caspases-8, caspase-3, and caspase-7. Oleanolic acid 3-acetate, however, caused a decrease in ROS production, suggesting the involvement of an ROS-independent pathway in oleanolic acid 3-acetate-induced apoptosis in SKOV3 and HEC-1A cells. CONCLUSION: These findings support the notion that oleanolic acid 3-acetate could be used as a potent anticancer supplementary agent against ovarian and endometrial cancer. Oleanolic acid 3-acetate exerts its proapoptotic effects through a rather unique molecular mechanism that involves an unconventional ROS-independent but mitochondria-mediated pathway.

Protective Effect of Tempol against Cisplatin-Induced Ototoxicity.

One of the major adverse effects of cisplatin chemotherapy is hearing loss. Cisplatin-induced ototoxicity hampers treatment because it often necessitates dose reduction, which decreases cisplatin efficacy. This study was performed to investigate the effect of Tempol on cisplatin-induced ototoxicity in an auditory cell line, House Ear Institute-Organ of Corti 1 (HEI-OC1). Cultured HEI-OC1 cells were exposed to 30 µM cisplatin for 24 h with or without a 2 h pre-treatment with Tempol. Cell viability was determined using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay and apoptotic cells were identified using terminal deoxynucleotidyl transferase dUTP nick end labeling of nuclei (TUNEL) assay and flow cytometry. The effects of Tempol on cisplatin-induced cleaved poly(ADP-ribose) polymerase, cleaved caspase, and mitochondrial inducible nitric oxide synthase expression were evaluated using western blot analysis. Levels of intracellular reactive oxygen species (ROS) were measured to assess the effects of Tempol on cisplatin-induced ROS accumulation. Mitochondria were evaluated by confocal microscopy, and the mitochondrial membrane potential was measured to investigate whether Tempol protected against cisplatin-induced mitochondrial dysfunction. Cisplatin treatment decreased cell viability, and increased apoptotic features and markers, ROS accumulation, and mitochondrial dysfunction. Tempol pre-treatment before cisplatin exposure significantly inhibited all these cisplatin-induced effects. These results demonstrate that Tempol inhibits cisplatin-induced cytotoxicity in HEI-OC1, and could play a preventive role against cisplatin-induced ototoxicity.

Syndecan-1 overexpression promotes tumor growth and angiogenesis in an endometrial cancer xenograft model.

OBJECTIVES: Upregulation of syndecan-1, a member of the transmembranous proteoglycans that serves as a coreceptor for a wide pool of extracellular ligands, has been well documented in enabling the promotion of growth and invasion of endometrial cancer. As a step toward understanding a potential role for syndecan-1 in this process, we questioned whether syndecan-1 upregulates tumor-promoting characteristics, particularly, angiogenesis in an in vivo human xenograft tumor model. METHODS: Human syndecan-1 was stably transfected into human endometrial adenocarcinoma 1A cells, and resulting transfectants were subcutaneously grafted into athymic mice; their outcomes were examined with respect to the enhancement of tumor growth and angiogenesis by immunohistochemistry, immunoblotting, and zymography. RESULTS: Overexpression of syndecan-1 promoted tumor growth concomitant with increased angiogenesis in tumor xenografts as evidenced by an increase in immunoreactivity for vascular endothelial growth factor and vascular endothelial cell marker CD34. Furthermore, zymographic studies revealed that syndecan-1 overexpression markedly enhanced activities of matrix metalloproteinases 2 and 9. CONCLUSIONS: This is the first in vivo xenograft analysis providing evidence that supports that syndecan-1 has a critical role in carcinogenic progression, particularly, contributing to the development of angiogenesis and invasive phenotype in association with matrix metalloproteinases 2 and 9 activations in endometrial cancer.

Syndecan-1 enhances the endometrial cancer invasion by modulating matrix metalloproteinase-9 expression through nuclear factor kappaB.

OBJECTIVES: Up-regulated expression of syndecan-1, a member of the transmembranous proteoglycans that serves as a co-receptor for a wide pool of extracellular ligands, has been ascribed to the promotion of growth of various cancers including breast, ovarian, and endometrial cancers. Here, we have extended these observations to gain insight into correlation between the expression level of syndecan-1 and its tumor-promoting characteristics, particularly, cancer invasion, in endometrial cancer. METHODS: Human syndecan-1 was stably transfected into three human endometrial cancer cell lines, and its effects were examined with respect to cell survival/proliferation and invasion. In addition, the activation of underlying signaling components, including integrins, focal adhesion kinase (FAK), and nuclear factor kappaB (NF-kappaB) was examined. The activity of NF-kappaB as a transcription factor for matrix metalloproteinase (MMP)-9 was assessed. RESULTS: The innate expression level of syndecan-1 was moderate to high in all endometrial cancer cell lines. Overexpression of syndecan-1 promoted tumor cell proliferation concomitant with the activation of NF-kappaB. Furthermore, overexpression of syndecan-1 markedly enhanced the cancer invasion accompanied by enhanced expression of integrin alphav/beta5 and enhanced phosphorylation of FAK. The transcriptional activation of MMP-9 by NF-kappaB was up-regulated in syndecan-1 overexpression. CONCLUSION: These findings provide evidence that supports that syndecan-1 may have a critical role in carcinogenic progression, particularly, contributing to the development of proliferative and invasive phenotype through NF-kappaB-mediated MMP-9 gene expression in endometrial cancer.