RESUMO
For decades, our nation has called upon higher education to create a more competitively-trained and diverse STEM workforce. While recent efforts to improve undergraduate STEM education have been successful, they have largely focused on "fixing" students and been devoid of the kind of effort needed to build institutional change capacity, moderate STEM departmental climate, and/or provide professional development for faculty. As a result, U. S. global preeminence in science and technology remains threatened, and the prevailing systems of oppression that continue to marginalize students from underrepresented groups remain intact. Redressing this particular trend calls not only for a deeper understanding of what works in STEM higher education reform, but also for an understanding of what works best for whom and under what conditions. To this end, my presentation for the 2017 FUN Workshop at Dominican University explored the most important advances in culturally responsive undergraduate STEM teaching, as well as the outcomes thereof. Attendees were invited to interrogate their own motivations for teaching and training future generations of diverse neuroscientists, and to contribute to developing both immediate and future next steps for national STEM higher education reform.
RESUMO
The unequal burden of cancer in minority and underserved communities nationally and in Maryland is a compelling crisis. The Maryland Special Populations Cancer Research Network (MSPN) developed an infrastructure covering Maryland's 23 jurisdictions and Baltimore City through formal partnerships between the University of Maryland School of Medicine, University of Maryland Statewide Health Network, University of Maryland Eastern Shore, and community partners in Baltimore City, rural Eastern Shore, rural Western Maryland, rural Southern Maryland, and Piscataway Conoy Tribe and statewide American Indians. Guided by the community-based participatory framework, the MSPN undertook a comprehensive assessment (of needs, strengths, and resources available) that laid the foundation for programmatic efforts in community-initiated cancer awareness and education, research, and training. The MSPN infrastructure was used to implement successful and innovative community-based cancer education interventions and technological solutions; conduct education and promotion of clinical trials, cancer health disparities research, and minority faculty cancer research career development; and leverage additional resources for sustainability. MSPN engaged in informed advocacy among decision- and policymakers at state and national levels, and its community-based clinical trials program was recognized by the U.S. Department of Health and Human Services as a Best Practice Award. The solutions to reduce and eliminate cancer health disparities are complex and require comprehensive and focused multidisciplinary cancer health disparities research, training, and education strategies implemented through robust community-academic partnerships. Cancer 2006. (c) American Cancer Society.
Assuntos
Redes Comunitárias/organização & administração , Educação em Saúde , Acessibilidade aos Serviços de Saúde , Área Carente de Assistência Médica , Grupos Minoritários , Qualidade da Assistência à Saúde , Pesquisa Biomédica , Humanos , Relações Interinstitucionais , MarylandRESUMO
BACKGROUND: Esophageal cancer rate disparities are pronounced for blacks and whites. This study presents black-white esophageal cancer incidence, mortality, relative survival rates, histology and trends for two five-year time periods--1991-1995 and 1996-2000--and for the time period 1991-2000. METHODS: The study used data from the National Cancer Institute's population-based Surveillance Epidemiology End Results (SEER) program with submission dates 1991-2000. Age-adjusted incidence, mortality, relative survival rates and histology for esophageal carcinoma were calculated for nine SEER cancer registries for 1991-2000. Rates were analyzed by race and gender for changes over specified time periods. RESULTS: Esophageal cancer age-adjusted incidence of blacks was about twice that of whites (8.63 vs. 4.39/100,000, p < 0.05). Age-adjusted mortality for blacks, although showing a declining trend, was nearly twice that of whites (7.79 vs. 3.96, p < 0.05). Although survival was poor for all groups, it was significantly poorer in blacks than in whites. Squamous cell carcinoma was more commonly diagnosed in blacks and white females, whereas adenocarcinoma was more common among white males (p < 0.001). CONCLUSIONS: Racial disparities in esophageal cancer incidence, mortality, survival and histology exist. Survival rates from this disease have not significantly improved over the decade. These data support the need for advances in prevention, early detection biomarker research and research on new, more effective treatment modalities for this disease.
Assuntos
População Negra/estatística & dados numéricos , Neoplasias Esofágicas/etnologia , População Branca/estatística & dados numéricos , Adenocarcinoma/etnologia , Carcinoma de Células Escamosas/etnologia , Neoplasias Esofágicas/mortalidade , Neoplasias Esofágicas/patologia , Feminino , Humanos , Incidência , Masculino , Distribuição por Sexo , Análise de Sobrevida , Estados Unidos/epidemiologiaRESUMO
Protein phosphatase 2A (PP2A) is a ubiquitously expressed member of the serine-threonine phosphatase family that is involved in regulation of many cellular processes including transcription, translation, cellular metabolism, and apoptosis. Because of a correlation between PP2A and estrogen receptor alpha (ER) expression in several human breast cancer cell lines, the effect of PP2A on regulation of ER expression in the human breast cancer cell line MCF-7 was studied. Inhibition of PP2A using the pharmacologic inhibitor okadaic acid at 250 nm for 16 h resulted in a 60% reduction in PP2A activity in MCF-7 cells concurrent with a 75% reduction in ER mRNA and protein expression. Similar results were obtained with a small interfering RNA probe that specifically inhibited PP2A expression. ER promoter studies showed that regulation of ER through the PP2A pathway did not occur through transcriptional activation. Rather, PP2A mediated ER expression through modulation of ER mRNA stability through degradation of ER mRNA, reversible with concomitant treatment with the proteasomal inhibitor MG 132. These data suggest a novel pathway controlling ER expression resulting from the activation of PP2A, potentially providing a novel therapeutic target.
Assuntos
Receptor alfa de Estrogênio/genética , Regulação da Expressão Gênica , Fosfoproteínas Fosfatases/fisiologia , RNA Mensageiro/metabolismo , Regiões 3' não Traduzidas/fisiologia , Linhagem Celular Tumoral , Humanos , Ácido Okadáico/farmacologia , Regiões Promotoras Genéticas , Complexo de Endopeptidases do Proteassoma/fisiologia , Proteína Fosfatase 2 , RNA Interferente Pequeno/farmacologiaRESUMO
Cancer in Maryland is a serious health concern for minority and underserved populations in rural and urban areas. This report describes the National Cancer Institute (NCI) supported Maryland Special Populations Cancer Network (MSPN), a community-academic partnership. The MSPN's priority populations include African Americans, Native Americans, and other medically underserved residents of rural and urban areas. The MSPN has established a community infrastructure through formal collaborations with several community partners located in Baltimore City, the rural Eastern Shore, and Southern and Western Maryland, and among the Piscataway Conoy Tribe and the other 27 Native American Tribes in Maryland. Key partners also include the University of Maryland Eastern Shore and the University of Maryland Statewide Health Network. The MSPN has implemented innovative and successful programs in cancer health disparities research, outreach, and training; clinical trials education, health disparities policy, and resource leveraging. The MSPN addresses the goal of the NCI and the Department of Health and Human Services (DHHS) to reduce and eventually eliminate cancer health disparities. Community-academic partnerships are the foundation of this successful network.
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Grupos Minoritários , Neoplasias/etnologia , Neoplasias/terapia , Programas Médicos Regionais/organização & administração , Telemedicina , Populações Vulneráveis , Negro ou Afro-Americano , Relações Comunidade-Instituição , Acessibilidade aos Serviços de Saúde , Hispânico ou Latino , Humanos , Indígenas Norte-Americanos , Maryland , Modelos Organizacionais , National Institutes of Health (U.S.) , Neoplasias/epidemiologia , Serviços de Saúde Rural/organização & administração , Fatores Socioeconômicos , Estados Unidos , Universidades , Serviços Urbanos de Saúde/organização & administraçãoRESUMO
Although smallpox was globally eradicated in 1977, the current threat of smallpox as a bioterrorism agent is unknown. Based on intelligence reports, the U.S. government and public health sectors have recommended smallpox vaccination for very select individuals. Patients with cancer are at particular risk for complications from the smallpox vaccine because of potential immunosuppression. Vaccinated nurses caring for these patients also need to take special precautions because of the possibility of secondary transmission of this live vaccine to patients. This article reviews background information on bioterrorism, the presentation and clinical features of smallpox, contraindications to the smallpox vaccine, and implications for oncology nurses.
Assuntos
Bioterrorismo/prevenção & controle , Papel do Profissional de Enfermagem , Enfermagem Oncológica/métodos , Vacina Antivariólica , Varíola/prevenção & controle , Varicela/diagnóstico , Contraindicações , Diagnóstico Diferencial , Humanos , Hospedeiro Imunocomprometido , Neoplasias/complicações , Neoplasias/imunologia , Neoplasias/enfermagem , Fatores de Risco , Varíola/diagnóstico , Vacina Antivariólica/efeitos adversos , Vacinação/efeitos adversos , Vacinação/métodos , Vacinação/enfermagemRESUMO
Absence of the estrogen receptor alpha (ER) in human breast cancer cells is an indicator of poor prognosis, and predictive of lack of response to hormonal therapy. Previous studies in our laboratory and others have shown that epigenetic regulation, including DNA methylation and histone deacetylation, are common mechanisms leading to ER gene silencing. Through the use of pharmacologic inhibitors, 5-aza 2'deoxycytidine (AZA) and Trichostatin A (TSA), we have shown that alterations in both of these mechanisms results in synergistic reexpression of ER mRNA and functional protein. These alterations may play a larger role in stimulation of cell signaling pathways leading to ER expression. We have utilized newly developed genome wide screening microarray techniques to identify gene(s) contributing to the hormone independent phenotype and AZA/TSA mediated ER expression. From this screen, we identified and confirmed expression of 4 candidate genes (PP2A, XCL1, THY1 and NBC4) as potential regulators of the hormone independent phenotype. Expression of two genes, XCL1 and PP2A, appeared to be correlated with ER expression. PP2A expression was not changed with ER degradation using ICI 182,780 whereas XCL1 expression decreased in the presence of AZA/TSA and ICI 182,780. This suggests that PP2A may be a determinant of ER expression while XCL1 appears to be ER responsive and downstream of ER expression. These gene products may be novel targets to be further explored in the development of new therapeutics for ER negative breast cancer.
Assuntos
Azacitidina/análogos & derivados , Neoplasias da Mama/genética , Metilação de DNA , Epigênese Genética , Receptor alfa de Estrogênio/genética , Linfocinas/genética , Fosfoproteínas Fosfatases/genética , Sialoglicoproteínas/genética , Acetilação/efeitos dos fármacos , Azacitidina/farmacologia , Neoplasias da Mama/tratamento farmacológico , Neoplasias da Mama/metabolismo , Quimiocinas C , Metilases de Modificação do DNA/antagonistas & inibidores , Decitabina , Receptor alfa de Estrogênio/metabolismo , Feminino , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Inibidores de Histona Desacetilases , Humanos , Ácidos Hidroxâmicos , Linfocinas/metabolismo , Análise de Sequência com Séries de Oligonucleotídeos , Fosfoproteínas Fosfatases/metabolismo , Proteína Fosfatase 2 , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , RNA Neoplásico/genética , RNA Neoplásico/metabolismo , Receptores de Progesterona/genética , Receptores de Progesterona/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Sialoglicoproteínas/metabolismo , Células Tumorais CultivadasRESUMO
Epigenetic mechanisms, such as DNA methylation and histone deacetylation, may play a role in loss of estrogen receptor alpha (ER) expression in ER negative human breast cancer cells. Our previous studies showed that pharmacologic inhibition of these mechanisms using the DNA methyltransferase inhibitor, 5-aza-2'-deoxycytidine (AZA), and the histone deacetylase (HDAC) inhibitor, Trichostatin A (TSA), resulted in expression of functional ER mRNA and protein. Therefore, we sought to characterize the effects of a recently described HDAC inhibitor, Scriptaid, on cell growth and ER expression and function in ER negative human breast cancer cell lines. Scriptaid treatment of three ER negative cell lines, MDA-MB-231, MDA-MB-435 and Hs578t, resulted in significant growth inhibition and increased acetylation of H3 and H4 histone tails. Quantitative Real Time PCR showed 2000-20,000-fold increase of ER mRNA transcript in all three cell lines after 48 h of Scriptaid treatment. Further, dose dependent re-expression of an estrogen responsive gene, the progesterone receptor (PR), indicated that induced ER is functional. As seen with TSA and AZA, Scriptaid and AZA co-treatment was more effective in inducing ER than Scriptaid or AZA alone. In vivo analysis using a xenograft mouse model bearing MDA-MB-231 tumors showed decreased tumor growth following Scriptaid or TSA treatment. Our results indicate that the novel HDAC inhibitor, Scriptaid, inhibits tumor growth in vitro and in vivo and, in conjunction with AZA, acts to re-express functional ER. These data suggest that Scriptaid or related HDAC inhibitors are candidates for further study in breast cancer.