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This research examines the experiences of individuals diagnosed with chronic mental illnesses and how they navigated the mental healthcare system in New Orleans, Louisiana. To realize the main research objective, I analyzed how individuals with chronic mental illnesses perceive mental illness and stigma; the services individuals use to address their mental health needs and the barriers they face in this process; who individuals disclose their mental illness to and under what contexts; and how individuals diagnosed with mental illness and their caregivers understand and embody recovery. Situated between medical anthropology and urban anthropology, it examines the challenges individuals diagnosed with chronic mental illness and caregivers encounter in utilizing mental health services. Using critical race theory and studies on whiteness, I analyze the intersectional identities of individuals to understand how various axes of identities such as race, gender, age, and religion affect how people utilize mental health services, conceptualize stigma, how this is related to disclosure, and what recovery means to them. While I use stigma scales to measure various types of stigma, I triangulate this data with observations from participant-observation and interviews to reconceptualize stigma in what Tyler and Slater (2018) argue for approaching the social and political dynamics of stigma and acknowledging history. I do this through the use of stigma syndemics. Central to this is the role of mental health professionals and other key stakeholders, and how they interact with individuals utilizing community mental health services. I examine how past experiences such as trauma and incarceration limit access to housing programs, employment, and how this affects recovery. Lastly, I argue that for effective advocacy on mental health to occur, synergistic activism through coalition building needs to transpire between all the entities that affect individuals who have mental illnesses.

Background A subset of patients with ductal carcinoma in situ (DCIS) experience recurrence or progression to invasive cancer. Current clinical practice is not reliably guided by DCIS recurrence prediction, although recurrence risk for invasive breast cancer can now be assessed. We analyzed a panel of biomarkers (estrogen receptor, Her2, Ki67, p53, cyclin D1, COX-2, caveolin-1, survivin, and PPAR-γ) and DCIS histologic and clinical features to determine associations with DCIS recurrence. Materials and methods Seventy DCIS cases diagnosed between 1995 and 2010 were divided into 2 groups: 52 had DCIS without known recurrence after excision and 18 had DCIS with subsequent recurrence after excision as DCIS or invasive carcinoma in the ipsilateral or contralateral breast. Tissue microarrays were prepared, immunohistochemistry performed, and expression of the biomarkers scored semiquantitatively. Variables analyzed included age, tumor size, margin status, DCIS grade, necrosis, histologic type, and immunohistochemistry scores. Differences between groups were evaluated using t tests for continuous variables and Fisher exact tests for categorical variables. Results Intraductal necrosis was associated with increased recurrence risk: 46% of nonrecurrent cases showed necrosis compared with 83% of those who recurred (P=0.007). Her2 (human epidermal growth factor receptor 2) and Ki67 expression distributions were significantly different between nonrecurrent and recurrent cases. Her2 was overexpressed in 14% of nonrecurrent cases compared with 50% in the recurrent cases (P=0.03). A total of 87% of nonrecurrent cases had low Ki67 staining (0% to 10%) compared with 50% among the recurrent cases (P=0.002). Conclusion Our results suggest that Her2 and Ki67 immunohistochemistry and the presence of intraductal necrosis aid in DCIS risk stratification.

Gliomas are highly invasive, lethal brain tumors. Tumor-associated proteases play an important role in glioma progression. Annexin A2 is overexpressed in many cancers and correlates with increased plasmin activity on the tumor cell surface, which mediates degradation of extracellular matrix and promotes neoangiogenesis to facilitate tumor growth. In this study, we used two glioma cell lines, mouse GL261–EGFP and rat C6/LacZ, as well as stable clones transfected with an annexin A2 knockdown construct. We find that the annexin A2 knockdown decreased glioma cell migrationin vitroand decreased membrane-bound plasmin activity.In vivo, we injected the glioma cells into the rodent brain and followed glioma progression. Knockdown of annexin A2 in glioma cells decreased tumor size and slowed tumor progression, as evidenced by decreased invasion, angiogenesis, and proliferation, as well as increased apoptosis in the tumor tissue of the annexin A2 knockdown group. Moreover, we report that the levels of expression of annexin A2 in human glioma samples correlate with their degree of malignancy. Together, our findings demonstrate that inhibition of annexin A2 expression in glioma cells could become a new target for glioma therapy.

Background We have previously shown that miR-215 suppressed the expression of key targets such as thymidylate synthase (TS), dihydrofolate reductase, and denticleless protein homolog (DTL) in colon cancer. miR-215 is a tumor suppressor candidate due to the upregulation of p53 and p21 by targeting DTL. However, high levels of miR-215 conferred chemoresistance due to cell cycle arrest and reduced cell proliferation by suppressing DTL. In this study, the clinical significance of miR-215 was further investigated as a potential prognostic biomarker in colon cancer patients. Methods Total RNAs were extracted from 34 paired normal and colon (stage II and III) tumor specimens using the Trizol-based approach. The levels of miR-215 and a closely related miR-192 were quantified using quantitative real-time polymerase chain reaction (qRT-PCR) expression analysis. The expression of DTL mRNA and protein were quantified by real time qRT-PCR and immunohistochemistry. Results The expression levels of miR-192 (P = .0008) and miR-215 (P < .0001) were significantly decreased in colon tumors compared with normal tissues. DTL was significantly over-expressed and was inversely correlated with miR-215, further suggesting an in vivo physiologic relevance of miR-215 mediated DTL suppression. Kaplan-Meier survival analysis by Cox regression revealed that high levels of miR-215 expression (hazard ratio, 3.516; 95% confidence interval, 1.007-12.28, P = .025) are closely associated with poor patient's overall survival. Furthermore, an elevated expression of a miR-215 target protein DTL was detected in colon cancer tissues whereas no expression was present in normal tissues. Conclusion miR-215 has a unique potential as a prognostic biomarker in stage II and III colon cancer.

Background: We have previously shown that miR-215 suppressed the expression of key targets such as thymidylate synthase (TS), dihydrofolate reductase (DHFR), and denticleless protein homolog (DTL) in colon cancer. miR-215 is a tumor suppressor candidate due to the up-regulation of p53 and p21 by targeting DTL. However, high levels of miR-215 conferred chemoresistance due to cell cycle arrest and reduced cell proliferation by suppressing DTL. In this study, the clinical significance of miR-215 was further investigated as a potential prognostic biomarker in colon cancer patients. Methods: Total RNAs were extracted from 34 paired normal and colon (stage II and III) tumor specimens using Trizol based approach. The levels of miR-215 and a closely related miR-192 were quantified using real time qRT-PCR expression analysis. The expression of DTL mRNA and protein were quantified by real time qRT-PCR and immunohistochemistry. Results: The expression levels of miR-192 (p=0.0008) and miR-215 (p Conclusion: miR-215 has a unique potential as a prognostic and diagnostic biomarker in stage II and III colon cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2263. doi:10.1158/1538-7445.AM2011-2263

Background: microRNAs (miRNAs) have emerged as key regulators of gene expression, and their altered expression has been associated with tumorigenesis and tumor progression. As a result, miRNAs represent important diagnostic biomarkers for the advancement of cancer and potential therapeutic approaches. They may be up-regulated or down-regulated in various tumor types, thus act as oncogenes or tumor suppressors. Although accumulating evidence suggests the role of aberrant miRNA expression in endometrial carcinogenesis, there is still limited data available about the endrometrial miRNAs. Endometrial cancer is characterized by frequently infiltrating tumors, and one of the most important molecular alterations in this process is through epithelial-mesencymal transition (EMT). Several studies implicated the role of miRNAs targeting the critical players during EMT. The goal of this study is to investigate the clinical utility of selected key miRNAs in archival FFPE tissue samples of patients with endometrial cancer. In this study, the expression of miR-26a, miR-205, miR-200c, miR-192, miR-215, let-7g, miR-21, miR-181b were quantified from 20 stage I, 2 stage II, 5 stage III, 8 stage IV endometrial cancer patients (endometrioid-type endometrial cancer (EEC), endometrial serous carcinoma(ESC), clear cell carcinoma(CCC) undifferentiated carcinoma (UDC), malignant mullerian mixed tumor (MMMT)) with up to 15 years clinical follow up information. Methods: Using archival FFPE tissues, areas of tumor and normal tissues were identified according to the corresponding hematoxylin and eosin stained sections, and cores of 1.5 mm in diameter were extracted. Total RNAs were isolated from 35 paired endometrial tumor and adjacent normal tissue specimens by using Trizol based approach. The expression levels of miRNAs were quantified by using real-time qRT-PCR analysis. Results: The expression of miR-205 (p=0.0002) and miR-200c (p Conclusions: miR-205 holds a great potential as a prognostic biomarker in endometrial cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 158. doi:10.1158/1538-7445.AM2011-158

3586 Background: Translational control mediated by noncoding microRNAs plays a key role in resistance to anticancer drug treatment. As a result, non-coding microRNAs hold great potential as new pro...