11 research outputs found

    Early uptake and continuous accumulation of thallium-201 chloride in a benign mixed tumor of soft tissue: Case Report

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    A case of benign mixed tumor of the soft tissue in a 64-year-old Japanese male is presented. He noticed a painless, elastic hard mass sized 3 cm in the right knee, which gradually grew larger and harder in the last 5 years. Magnetic resonance imaging demonstrated a mass lesion embedded in the subcutaneous tissue with low and high signal intensity at T1- and T2-weighted images, respectively. Tl-201 scintigraphy showed an early uptake of Tl-201 within the lesion at 10 minutes after injection, which was slightly decreased but still continued at 2 hours later. The patient underwent a resection of tumor, and the pathological diagnosis was a benign mixed tumor of soft tissue without high vascularity, characterized by histological features similar to pleomorphic adenomas in the salivary glands. Immunohistochemical study proved expression of Na(+)/K(+)-ATPase of tumor cells. Overexpression of Na(+)/K(+)-ATPase of the tumor might be responsible for the early uptake of Tl-201, and poor vascular structure in this tumor might lead to continuous accumulation. The Tl-201 scintigraphic features of mixed tumor of soft tissue are assessed to resemble those of malignant soft tissue tumors

    Relative Dose Intensity of Induction-Phase Pazopanib Treatment of Soft Tissue Sarcoma: Its Relationship with Prognoses of Pazopanib Responders

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    The approved standard dose of pazopanib is 800 mg per day, but the appropriate dose of pazopanib to treat soft tissue sarcoma (STS) patients in real-world practice is controversial. Of 124 STS patients treated with pazopanib, we retrospectively analyzed the cases of STS patients who achieved progression-free survival at 12 weeks by pazopanib treatment as pazopanib responders, and we evaluated their relative dose intensity (RDI) in the initial 12 weeks (12W-RDI). We enrolled 78 STS patients in the analyses as pazopanib responders, and 54 patients of the 78 pazopanib responders (69%) were able to maintain 12W-RDI ≥80%. In landmark analyses, patients with 12W-RDI of 80% ≥80% had significantly longer progression-free survival compared to those with 12W-RDI <80% (30.7 weeks vs. 22.0 weeks, hazard ratio [HR]: 0.56 [95%CI: 0.33–0.94], p = 0.026). The most frequently observed reasons of treatment interruption and/or dose reduction of pazopanib during the initial 12 weeks were anorexia and liver function disorders. Liver toxicity was the adverse event most frequently observed in the 12W-RDI <80% patients throughout the treatment periods. Based on our results, it appears that maintaining as high a dose intensity as possible that is tolerable—at least during the initial 12 weeks—is likely to be the better option in pazopanib treatment for STS patients

    EPSIN 3, A Novel p53 Target, Regulates the Apoptotic Pathway and Gastric Carcinogenesis

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    BACKGROUND & AIM: p53 activation by cellular stresses induces the transcription of hundreds of its target genes. To elucidate the entire picture of its downstream pathway, we screened a cDNA microarray dataset of adriamycin-treated HCT116 p53−/− or p53+/+ cells and identified EPSIN 3 as a novel p53 target. METHODS: Potential p53 binding sequences in the EPSIN 3 locus were evaluated by reporter and CHIP assays. To investigate the role of EPSIN 3 in the p53 downstream pathway, we assessed DNA damage-induced apoptosis in EPSIN 3-knockdown HCT116 cells or Epsin 3-deficient mice. In addition, we evaluated EPSIN 3 expression levels in various tissues, including gastric adenocarcinoma, human gastric mucosa with or without Helicobacter pylori infection, and mouse acute gastritis tissues induced by indomethacin. RESULTS: In response to DNA damage, p53 induced the expression of EPSIN 3 through the p53 binding elements in the EPSIN 3 promoter and the first intron. Knockdown of EPSIN 3 resulted in resistance to DNA damage-induced apoptosis both in vitro and in vivo. EPSIN 3 expression was down-regulated in gastric cancer tissues compared with normal tissues. In addition, Helicobacter pylori infection and indomethacin-induced acute gastritis repressed EPSIN 3 expression in gastric mucosa. CONCLUSIONS: EPSIN 3 is a novel p53 target and a key mediator of apoptosis. Chronic or acute mucosal inflammation as well as p53 inactivation induced down-regulation of EPSIN 3 and subsequently caused apoptosis resistance, which is a hallmark of cancer cells

    A retrospective study of residual myomas following laparoscopic myomectomy

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    Background: With the development of laparoscopic instruments such as the morcellator, a large number of gynecologists have performed laparoscopic myomectomies. In this study, we reviewed all cases in which residual myomas were identified by follow-up magnetic resonance imaging in order to evaluate why any myomas would remain after a laparoscopic myomectomy and to find their most common location and depth within the uterus. Methods: Patients (n = 128) with uterine myomas who underwent a laparoscopic myomectomy between 2008 and 2011 and received follow-up magnetic resonance imaging 3 months afterward were reviewed retrospectively. We analyzed the influence of preoperative gonadotrophin-releasing hormone agonist treatment, as well as the location and depth of the residual myomas within the uterus. The pregnancy rate in all cases was also investigated. Results: The duration of the preoperative administration of gonadotrophin-releasing hormone agonist was statistically longer in cases where multiple residual myomas were found, compared with cases where a single residual myoma was present. There was no statistical difference in the rate and size of the residual myomas among five different locations within the uterus. The rate of residual subserosal myomas was lowest, compared with two other types, and was statistically lower than residual intramuscular myomas (p < 0.05). The pregnancy rate in cases of residual myomas revealed no statistical difference compared with nonresidual cases. Conclusion: Because the completion of laparoscopic myomectomy without any residual myomas is difficult, informed consent regarding the possibility of their occurrence is necessary, regardless of the number of myomas detected preoperatively. Moreover, intramuscular residual myomas should be given particular attention due to their higher rate of incidence

    Successful Complete Response of Tumor Thrombus after Combined with Chemotherapy and Irradiation for Ewing Sarcoma

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    Pelvic Ewing sarcoma is associated with a worse prognosis. Thromboembolic events are relatively common in pediatric patients with cancers including sarcomas. We have presented a case of Ewing sarcoma arising from the left iliac bone with tumor thrombus of inferior vena cava (IVC) which was obtained complete response by both chemotherapy and irradiation. Magnetic resonance imaging (MRI) scan demonstrated that the tumor arising from the left iliac bone extended into the left side of sacral bone, suggesting the difficulty of surgical resection. Computed tomography (CT) revealed the existence of the tumor thrombus of IVC. We performed irradiation (31.2 Gy) and chemotherapy (combination of VCR, Act-D, IFM, and ADR). The tumor was controlled successfully, and the tumor thrombus of IVC has completely vanished. Four years after the treatment, coin lesion in the left upper lung appeared. Suspected of metastasis, segmental resection of the left upper lung was performed. Fourteen years after the surgery, the patient has been remained free of recurrence. It is clinically significant for surgeons to treat pelvic Ewing sarcoma with tumor thrombus

    Pre-Treatment Neutrophil-to-Lymphocyte Ratio (NLR) as a Predictive Marker of Pazopanib Treatment for Soft-Tissue Sarcoma

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    Pazopanib with trabectedin and eribulin is widely used to treat soft-tissue sarcoma (STS). We have shown that baseline neutrophil-to-lymphocyte ratio (NLR) may predict the efficacy and patient prognosis of eribulin. Changes in NLR, but not baseline NLR, can predict patient prognosis of trabectedin. However, prognostic factors of pazopanib for STS have not been identified. We present a retrospective analysis of 141 patients treated with pazopanib for recurrent or metastatic non-round cell STS. Univariate and multivariate analyses were performed to determine the predictive factors of durable clinical benefit (DCB), overall survival (OS), and progression-free survival. L-sarcoma histology (odds ratio [OR] = 0.31, 95% CI = 0.12&ndash;0.79; p = 0.014) and pre-treatment NLR &lt; 3.0 (OR = 2.03, 95% CI = 1.02&ndash;6.67; p = 0.045) were independent predictive factors of DCB. Pre-treatment NLR &lt; 3.0 (hazard ratio [HR] = 0.55, 95% CI = 0.36&ndash;0.84; p = 0.0057), liposarcoma histology (HR = 1.78, 95% CI = 1.09&ndash;2.91; p = 0.022), primary extremity site (HR = 0.48, 95% CI = 0.31&ndash;0.75; p = 0.0010), ECOG PS &ge; 1 (HR = 1.62, 95% CI = 1.08&ndash;2.42; p = 0.019), and CRP &lt; 0.3 (HR = 0.52, 95% CI = 0.33&ndash;0.82; p = 0.0050) were independent predictive factors of OS. These findings indicate that baseline NLR predicts the efficacy and patient prognosis of pazopanib for STS
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