BACKGROUND: Vesical Imaging-Reporting And Data System (VI-RADS) was proposed to detect muscle-invasive bladder cancer (MIBC). OBJECTIVE: To evaluate the performance of VI-RADS and additional value of apparent diffusion coefficient (ADC) values measured on diffusion-weighted magnetic resonance imaging (MRI) for detecting MIBC. METHODS: A total of 176 patients undergoing MRI (multiparametric in 97 [55%] and biparametric in 79 [45%]) before transurethral resection of bladder tumor for primary bladder cancer were retrospectively identified. MRI findings were scored according to VI-RADS. The standardized tumor ADC (sT-ADC: tumor ADC/gluteus maximus ADC) was calculated and used to account for the incompatibility among different MRI protocols. The accuracy of VI-RADS, sT-ADC and their combination to detect MIBC was assessed using the AUC of the ROC curve. RESULTS: MIBC was pathologically confirmed in 46 patients (26%). AUC of VI-RADS to detect MIBC was 0.86. When cut-off of VI-RADS was set at≥3 and≥4, sensitivity/specificity were 78% /70% and 63% /96%, respectively. A lower sT-ADC (≤0.894) was significantly associated with muscle invasion (p < 0.01, AUC 0.79) with sensitivity 78% and specificity 79%. Combination of VI-RADS and sT-ADC improved the accuracy (AUC 0.94); sensitivity was 100% when VI-RADS≥3 or sT-ADC≤0.894 was considered positive, and specificity was 99% when VI-RADS≥4 and sT-ADC≤0.894 was considered positive. Incorporation of sT-ADC reduced under-staging of MIBC as VI-RADS < 3 by 100% and over-staging of non-MIBC as VI-RADS≥4 by 80%. CONCLUSIONS: Incorporation of ADC values into VI-RADS improves accuracy to detect MIBC in primary bladder cancer patients.
A 37-year-old Burmese woman presented with an incidentally found retroperitoneal fat-containing tumor. The tumor was 9 cm in the longest diameter, surrounding the right kidney, and composed of homogenous adipose tissue with thickened septum-like structures and spotty nonadipose structures, which were enhanced on contrast-enhanced computed tomography and magnetic resonance imaging. The tumor did not show either a beak sign or synchronous angiomyolipoma-like lesion in the kidneys. The tumor had irregular septa, thin blood vessels, and spotty small soft-tissue nodules. The tumor did not contain any heterogeneously enhanced solid lesions suspicious for dedifferentiated liposarcomas. Based on these imaging findings, a clinical diagnosis of a well-differentiated liposarcoma was made. Under the consensus of a multidisciplinary cancer board, she was recommended to undergo core-needle biopsy to confirm the clinical diagnosis. However, she declined to undergo biopsy for financial reasons. She underwent kidney-sparing retroperitoneal tumor resection. Histopathologically, the tumor was an angiomyolipoma with positive immunostaining for HMB45 and Melan A. The present case suggests the importance of core-needle biopsy prior to surgical intervention for retroperitoneal fat-containing tumors.
<div>Abstract<p>In two-stage skin chemical carcinogenesis, phorbol ester 12-<i>O</i>-tetradecanoylphorbol-13-acetate (TPA) acts as a promoter essential for clonal expansion of the initiated cells carrying the activated <i>ras</i> oncogenes. Although protein kinase C (PKC) isozymes are the main targets of TPA, their role in tumor promotion remains controversial. We previously reported that mice lacking a Ras/Rap effector phospholipase Cε (<i>PLCε<sup>−/−</sup></i> mice) exhibited marked resistance to tumor formation in the two-stage skin carcinogenesis. <i>PLCε<sup>−/−</sup></i> mice also failed to exhibit basal layer cell proliferation and epidermal hyperplasia induced by TPA, suggesting a role of PLCε in tumor promotion. Here, we show that <i>PLCε<sup>−/−</sup></i> mice exhibit resistance to TPA-induced skin inflammation as assessed by reduction in edema, granulocyte infiltration, and expression of a proinflammatory cytokine, interleukin-1α (IL-1α). On the other hand, the proliferative potentials of keratinocytes or dermal fibroblasts in culture remain unaffected by the <i>PLCε</i> background, suggesting that the PLCε's role in tumor promotion may be ascribed to augmentation of inflammatory responses. In dermal fibroblast primary culture, TPA can induce activation of the PLCε lipase activity, which leads to the induction of IL-1α expression. Experiments using small interfering RNA–mediated knockdown indicate that this activation is mediated by Rap1, which is activated by a TPA-responsive guanine nucleotide exchange factor RasGRP3. Moreover, TPA-induced activation of Rap1 and PLCε is inhibited by a PKC inhibitor GF109203X, indicating a crucial role of PKC in signaling from TPA to PLCε. These results imply that two TPA targets, RasGRP3 and PKC, are involved in TPA-induced inflammation through PLCε activation, leading to tumor promotion. [Cancer Res 2008;68(1):64–72]</p></div>
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