33 research outputs found
MRI Appearance of Prostatic Stromal Sarcoma in a Young Adult
Prostatic stromal sarcoma (PSS) is quite rare. Herein, we describe magnetic resonance imaging (MRI) features of a PSS identified in a 26-year-old man with dysuria and hematuria. MRI clearly depicted the extent and multinodular appearance of the tumor, which was mainly located in the central zone of the prostate. The tumor appeared as a heterogeneously signal-hyperintense mass with a pseudocapsule on T2-weighted imaging. Contrast-enhanced T1-weighted MRI showed necrotic portions in the gradually enhanced solid mass, and diffusion-weighted imaging permitted the accurate assessment of the local extent of the tumor. Thus, the appearance on MRI was quite different from that of adenocarcinoma of the prostate
First Case of Cytokine Release Syndrome after Nivolumab for Gastric Cancer
Introduction: Cytokine release syndrome (CRS) is a potentially life-threatening systemic disease that has been observed after treatment with antibodies and adoptive T cell therapies. In this case, we observed nivolumab-induced CRS in a patient with gastric cancer. Case Presentation: A 43-year-old male with advanced gastric cancer was treated with nivolumab as a third-line chemotherapy. He had no history of allergies. Eight days after the first administration of nivolumab, fever, tachycardia, appetite loss and increases in liver and biliary enzymes were observed. Computed tomography revealed neither bile duct obstruction nor progression of liver metastases but showed that there was edema of the Gleason sheath. Histopathological analysis of the liver revealed cholestatic liver injury with CD8+ T lymphocyte and macrophage infiltration. Neither viral infection nor autoimmune disease was revealed. His symptoms were similar to those of CRS observed after T cell therapy. We diagnosed his disease as nivolumab-induced liver injury and cholangitis accompanied by CRS based on his serum cytokine levels. Discussion/Conclusion: To the best of our knowledge, this is the first report of nivolumab-induced CRS in a patient with gastric cancer
Preferential antitumor effect of the Src inhibitor dasatinib associated with a decreased proportion of aldehyde dehydrogenase 1-positive cells in breast cancer cells of the basal B subtype
<p>Abstract</p> <p>Background</p> <p>Recent studies have suggested that the Src inhibitor dasatinib preferentially inhibits the growth of breast cancer cells of the basal-like subtype. To clarify this finding and further investigate combined antitumor effects of dasatinib with cytotoxic agents, a panel of breast cancer cell lines of various subtypes was treated with dasatinib and/or chemotherapeutic agents.</p> <p>Methods</p> <p>Seven human breast cancer cell lines were treated with dasatinib and/or seven chemotherapeutic agents. Effects of the treatments on c-Src activation, cell growth, cell cycle, apoptosis and the proportion of aldehyde dehydrogenase (ALDH) 1-positive cells were examined.</p> <p>Results</p> <p>The 50%-growth inhibitory concentrations (IC<sub>50</sub>s) of dasatinib were much lower in two basal B cell lines than those in the other cell lines. The IC<sub>50</sub>s of chemotherapeutic agents were not substantially different among the cell lines. Dasatinib enhanced antitumor activity of etoposide in the basal B cell lines. Dasatinib induced a G1-S blockade with a slight apoptosis, and a combined treatment of dasatinib with etoposide also induced a G1-S blockade in the basal B cell lines. Dasatinib decreased the expression levels of phosphorylated Src in all cell lines. Interestingly, dasatinib significantly decreased the proportion of ALDH1-positive cells in the basal B cell lines but not in the other cell lines.</p> <p>Conclusions</p> <p>The present study indicates that dasatinib preferentially inhibits the growth of breast cancer cells of the basal B subtype associated with a significant loss of putative cancer stem cell population. A combined use of dasatinib with etoposide additively inhibits their growth. Further studies targeting breast cancers of the basal B subtype using dasatinib with cytotoxic agents are warranted.</p
Changes in synaptic transmission of substantia gelatinosa neurons after spinal cord hemisection revealed by analysis using in vivo patch-clamp recording
Background After spinal cord injury, central neuropathic pain develops in the majority of spinal cord injury patients. Spinal hemisection in rats, which has been developed as an animal model of spinal cord injury in humans, results in hyperexcitation of spinal dorsal horn neurons soon after the hemisection and thereafter. The hyperexcitation is likely caused by permanent elimination of the descending pain systems. We examined the change in synaptic transmission of substantia gelatinosa neurons following acute spinal hemisection by using an in vivo whole-cell patch-clamp technique. Results An increased spontaneous action potential firings of substantia gelatinosa neurons was detected in hemisected rats compared with that in control animals. The frequencies and amplitudes of spontaneous excitatory postsynaptic currents and of evoked excitatory postsynaptic currentss in response to non-noxious and noxious stimuli were not different between hemisected and control animals. On the contrary, the amplitude and frequency of spontaneous inhibitory postsynaptic currents of substantia gelatinosa neurons in hemisected animals were significantly smaller and lower, respectively, than those in control animals (P?<?0.01). Large amplitude and high-frequency spontaneous inhibitory postsynaptic currents, which could not be elicited by mechanical stimuli, were seen in 44% of substantia gelatinosa neurons in control animals but only in 17% of substantia gelatinosa neurons in hemisected animals. In control animals, such large amplitude spontaneous inhibitory postsynaptic currents were suppressed by spinal application of tetrodotoxin (1??M). Cervical application of lidocaine (2%, 10??l) also inhibited such large amplitude of inhibitory postsynaptic currents. The proportion of multi-receptive substantia gelatinosa neurons, which exhibit action potential firing in response to non-noxious and noxious stimuli, was much larger in hemisected animals than in control animals. Conclusions These suggest that substantia gelatinosa neurons receive tonic inhibition by spinal inhibitory interneurons which generate persistent action potentials. Spinal hemisection results in hyperexcitation of substantia gelatinosa neurons at least in part by eliminating the tonic descending control of spinal inhibitory interneurons from supraspinal levelsArticleMOLECULAR PAIN.12:1744806916665820(2016)journal articl
c-Myb and GATA-3 Cooperatively Regulate IL-13 Expression via Conserved GATA-3 Response Element and Recruit Mixed Lineage Leukemia (MLL) for Histone Modification of the IL-13 Locus
Real-time Monitoring and Detection of Primer Generation-Rolling Circle Amplification of DNA Using an Ethidium Ion-selective Electrode
Dimorphic variant of ductal carcinoma in situ of the breast
We report a case of dimorphic variant of ductal carcinoma in situ (dimorphic DCIS), composed of an epithelium intermixed with columnar cells and dimorphic cells. The findings of typical DCIS architecture support categorization as DCIS on a low-power view. Furthermore, there was no difference in the nuclear morphology of the two cell types on the high-power view. The two cell types comprising dimorphic DCIS were negative for p63, CK 5/6 and 14. On the contrary, both cell types were diffusely positive for nuclear ER and AR, as well as marked membrane-associated staining for E-cadherin and cytoplasmic staining for GCDFP-15. These immunohistochemical marker results are similar to conventional DCIS and there were no differences in expression patterns between the columnar epithelial cells and dimorphic cells. The morphological features of dimorphic cells may be confused with cells of other origins if the features of dimorphic DCIS are not recognized. Careful observation of morphological architecture and expression of immunohistochemical markers may support diagnosis. Keywords: Dimorphic cell, Ductal carcinoma in situ, Breast carcinom