Marker-negative pheochromocytoma is uncommon, representing 9% of cases in our series. Of patients with adrenal masses or presentation suggesting catecholamine excess with normal labs, those with vertigo/dizziness may warrant a metaiodobenzylguanidine scan or repeat testing to avoid missing pheochromocytoma. Clinicians may need a high degree of suspicion for pheochromocytoma in patients with negative testing and elevated BMI.
BACKGROUND African–American men with prostate cancer (PCa) present with higher-grade and -stage tumors compared to Caucasians. While the disparity may result from multiple factors, a biological basis is often strongly suspected. Currently, few well-characterized experimental model systems are available to study the biological basis of racial disparity in PCa. We report a validated in vitro cell line model system that could be used for the purpose. METHODS We assembled a PCa cell line model that included currently available African–American PCa cell lines and LNCaP (androgen-dependent) and C4-2 (castration-resistant) Caucasian PCa cells. The utility of the cell lines in studying the biological basis of variance in a malignant phenotype was explored using a multiplex biomarker panel consisting of proteins that have been proven to play a role in the progression of PCa. The panel expression was evaluated by Western blot and RT-PCR in cell lines and validated in human PCa tissues by RT-PCR. As proof-of-principle to demonstrate the utility of our model in functional studies, we performed MTS viability assays and molecular studies. RESULTS The dysregulation of the multiplex biomarker panel in primary African–American cell line (E006AA) was similar to metastatic Caucasian cell lines, which would suggest that the cell line model could be used to study an inherent aggressive phenotype in African–American men with PCa. We had previously demonstrated that Protein kinase D1 (PKD1) is a novel kinase that is down regulated in advanced prostate cancer. We established the functional relevance by over expressing PKD1, which resulted in decreased proliferation and epithelial mesenchymal transition (EMT) in PCa cells. Moreover, we established the feasibility of studying the expression of the multiplex biomarker panel in archived human PCa tissue from African–Americans and Caucasians as a prelude to future translational studies. CONCLUSION We have characterized a novel in vitro cell line model that could be used to study the biological basis of disparity in PCa between African–Americans and Caucasians.
Background Influenza B is generally regarded as a less severe counterpart to influenza A, typically causing mild upper respiratory symptoms. Myocardial involvement with influenza B is a rare complication, better described in children than adults. However, when it occurs, it can lead to profound myocarditis with progression to shock requiring aggressive supportive care. Case Presentation We present a case of cardiac tamponade in the setting of influenza B infection in a previously healthy 57-year-old woman, with progression to refractory shock and death. Autopsy revealed myocardial necrosis with infiltration of CD3+ lymphocytes, and little evidence of viral pneumonia. Conclusions Myocarditis is a rare complication of influenza B in adults, and subsequent pericardial effusion with tamponade physiology is a previously unreported event in an otherwise healthy adult without other medical comorbidities. While rare, this is a serious and potentially fatal complication that clinicians should be aware of when evaluating a patient with suspected viral illness who is exhibiting shock physiology.
Background: Prostate Cancer (PCa) exhibits striking racial disparity and is presented more aggressively in African Americans (AAs) than Caucasians (CAs). We have previously reported that the dysregulation of PKD1-centered signaling in primary AA prostate cancer cell line E006AA is akin to more aggressive Caucasian cell line C4-2. As PKD1 plays a central role in several cellular mechanisms that contribute in aggressive malignant phenotype, we defined a PKD1 related biomarker panel consisting of 11 biomarkers and explored whether PKD1 centered signaling would be differentially regulated in AA compared to CA PCa. Methods: PKD1 related biomarker panel consisted of PKD1, AR, HSP27, N-Cadherin, Snail, Vimentin, MMP-2, MMP-9, MT-1, E-cadherin, beta-Catenin. The validity of the PKD1 related biomarker panel in PCa was evaluated on available microarray databases (cbioportal.org). The differential expression of the biomarker panel was quantified on PCa tissue samples from15 AA and 15 CA men with matching Gleason score obtained from tumor tissue bank of Comprehensive Cancer Center of Wake Forest University. Results: The cbioportal consisted of six different PCa databases with approximately 662 human PCa samples in total. In average, PKD1 related biomarker panel was altered 47.7% in available cases. Quantification of the PKD1 related biomarker panel regarding gene expression demonstrated a trend toward higher expression of majority of biomarkers in AA samples in compare to CAs. However, only variances in expression of MMP2 (P<0.0001) and MT1A (P = 0.03) were significantly different between AAs and CAs. The results obtained from human PCa samples showed a moderate correlation with previously reported cell line data which showed significantly higher expression of EMT markers N-Cadherin, Vimentin and Snail in AA cell line in compare to CA cell lines. Conclusion: The differential expression of PKD1 related biomarker panel in AAs in compare to CAs suggests a biological basis for disparity in PCa. Besides, relatively high altered PKD1 related biomarker panel in available microarray databases suggests the potential of the panel as a tool in diagnosis of aggressive phenotype in PCa. Citation Format: Bita Nickkholgh, Xiaolan Fang, Shira M. Winters, Nora Fino, KC. Balaji. Differential expression of novel PKD1 related biomarker panel in African American men with prostate cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4342. doi:10.1158/1538-7445.AM2015-4342
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