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Little is understood about how campus educators within Academic Affairs and Student Affairs use institutional websites to articulate what their institutional commitments to diversity, inclusion, and social justice are and how they are enacted. Through an exploratory content analysis using LePeau’s (2015) framework on pathways to partnership (i.e., complementary, coordinated, and pervasive) to address diversity, inclusion, and social justice aims, we examined 23 institutional websites to determine what types of Academic Affairs and Student Affairs partnerships institutions employed. Findings revealed predominantly complementary partnerships, which means maintaining the distinct cultures of Academic Affairs and Student Affairs in diversity, inclusion, and social justice efforts.

Cyclin E, in conjunction with its catalytic partner cyclin-dependent kinase 2 (CDK2), regulates cell cycle progression as cells exit quiescence and enter S-phase. Multiple mechanisms control cyclin E periodicity during the cell cycle, including phosphorylation-dependent cyclin E ubiquitylation by the SCFFbw7 ubiquitin ligase. Serine 384 (S384) is the critical cyclin E phosphorylation site that stimulates Fbw7 binding and cyclin E ubiquitylation and degradation. Because S384 is autophosphorylated by bound CDK2, this presents a paradox as to how cyclin E can evade autocatalytically induced degradation in order to phosphorylate its other substrates. We found that S384 phosphorylation is dynamically regulated in cells and that cyclin E is specifically dephosphorylated at S384 by the PP2A-B56 phosphatase, thereby uncoupling cyclin E degradation from cyclin E-CDK2 activity. Furthermore, the rate of S384 dephosphorylation is high in interphase but low in mitosis. This provides a mechanism whereby interphase cells can oppose autocatalytic cyclin E degradation and maintain cyclin E-CDK2 activity while also enabling cyclin E destruction in mitosis, when inappropriate cyclin E expression is genotoxic.

Researchers, policymakers, and administrations have shown great concern over the efficacy of college remediation, which has prompted some states to eliminate remedial programs from public 4–year institutions. However, research suggests that eliminating these programs may have unintended consequences on college access and opportunity for underrepresented minority students, particularly African Americans. This study explores the impact of a remedial program on 11 African-American male students at a public 4–year historically Black institution. Findings illuminate the importance of college remediation in promoting college access and opportunity for underprepared Black male students, and how remedial programs increase academic and social integration for these students.

Macroautophagy is a dynamic process whereby portions of the cytosol are encapsulated in double-membrane vesicles and delivered to the lysosome for degradation. Phosphatidylinositol-3-phosphate (PtdIns3P) is concentrated on autophagic vesicles and recruits effector proteins that are crucial for this process. The production of PtdIns3P by the class III phosphatidylinositol 3-kinase Vps34, has been well established; however, protein phosphatases that antagonize this early step in autophagy remain to be identified. To identify such enzymes, we screened human phosphatase genes by RNA interference and found that loss of PTPσ, a dual-domain protein tyrosine phosphatase (PTP), increases levels of cellular PtdIns3P. The abundant PtdIns3P-positive vesicles conferred by loss of PTPσ strikingly phenocopied those observed in cells starved of amino acids. Accordingly, we discovered that loss of PTPσ hyperactivates both constitutive and induced autophagy. Finally, we found that PTPσ localizes to PtdIns3P-positive membranes in cells, and this vesicular localization is enhanced during autophagy. We therefore describe a novel role for PTPσ and provide insight into the regulation of autophagy. Mechanistic knowledge of this process is crucial for understanding and targeting therapies for several human diseases, including cancer and Alzheimer's disease, in which abnormal autophagy might be pathological.

Recent research has shown a nexus between active out-of-class engagement and the accrual of unique race/gender-specific educational outcomes among Black male undergraduates. Yet, rarely explored are the racialized experiences of those who become actively engaged and assume leadership positions on campuses where racial diversity is low, hence the purpose of this study. Focus group interviews were conducted with 52 Black male Resident Assistants (RAs) at six large, predominantly White universities. Racist stereotypes and racial microaggressions, the complexities associated with “onlyness” in the RA position, and heightened scrutiny from White supervisors are among the findings reported in this article. Also offered are implications for addressing racial toxins that dissuade Black male student leadership in residence halls and other out-of-class engagement venues.

This qualitative study of 11 Black male students who entered a public historically Black college and university (HBCU) as academically underprepared and persisted to graduation, provides insight into the ways in which family promotes academic success for Black male students at a public HBCU. The study’s findings encourage practitioners at HBCUs to reassess the relationship between family involvement and academic success for Black male students. Further, the findings affirm the justification to revise Tinto’s theory of student departure to account for relationships minority students have with support networks outside the campus milieu.

African American Men in College, edited by Michael J. Cuyjet. San Francisco: Jossey-Bass, 2006. 384 pp. ISBN 978-0-7879-6460-3. Nationally, African American male students hold the lowest college completion rate (32.8%) among both sexes and among all racial/ethic groups in higher education (Chronicle of Higher Education Almanac, 2006), and no reform effort has been able to abolish this trend. Clearly, a comprehensive but concentrated plan of action is needed to deconstruct this persistent problem. In 1997, University of Louisville Professor Michael J. Cuyjet offered insight on ways to minimize Black male college attrition and to address this crisis in his edited book, Helping African American Men Succeed in College. Nearly one decade later, Cuyjet has assembled African American Men in College, which he describes as the "sequel" to the former edition (p. ix). This 21-chapter volume is appropriately divided into two parts. The first section includes a collection of empirical studies that illuminate issues and ideas impeding or facilitating Black male college success. The second section describes nine exemplary programs designed for campus administrators to help improve the staggering completion rate noted above. Pieced together, this book is aimed at helping Black men "surmount and reduce these challenges such that the journey for these young men is made easier and the numbers of those succeeding increases significantly" (p. x). In chapter 1, Cuyjet employs U.S. Census data and other national sources to highlight the status of Black men in higher education and society by unraveling the numerous economic, cultural, historical, and political issues that surround them. He points out interventions that undercut Black male college success. This introduction sets the tone for the 11 chapters that follow in part 1. In chapter 2, Fred Bonner and Kevin Bailey describe some underlying elements that affect Black male academic achievement, including the role of peer influence, family support, faculty relationships, self-esteem, and institutional environment. These factors alone often determine the fate of Black male college success but remain complex and disconnected in many cases. The next two chapters, authored separately by Charles Brown and Shaun Harper, use qualitative methods to explore the benefits of cocurricular engagement on Black men in college, specifically by way of participation in student activities and student organizations. In chapter 5, Michael Sutton emphasizes the role of mentorship for Black male college students, using the Student African American Brotherhood (SAAB.) as an example of good practice. Chapter 6, written by Lemuel Watson, uses survey data to uncover the social construct of spirituality and religion in the lives of Black men while pursing a college education. Chapters 7 and 8 arguably address two of the most well-known, intricate issues that affect Black male undergraduates--that is, the current state of Black fraternities and athletes in the American higher education. Shaun Harper and Frank Harris explain the gains associated with holding membership in Black fraternities and evenhandedly discuss the current issues that threaten the existence of these organizations. Next, in her review of literature, Kenya LeNoir Messer compiles the factors that impinge upon college success among Black male college athletes. These factors include academic underpreparedness, stressors ignited by negative stereotypes from faculty and peers, and alarmingly high attrition rates. Jamie Washington and Vernon Wall, two prominent experts on multiculturalism and inclusion in higher education, use the limited research that exists on homosexuality in general to unveil the specific concerns of gay and bisexual African American college men. Washington and Wall posit that most Black gay and bisexual men, as an oppressed subgroup in the backdrop of campus culture and more specifically within Black culture, "are not only dealing with the confusion as it relates to their attraction to other men, but what that means for them in the context of the Black community, the church, and the eyes of God" (p. …

Cyclin E, in conjunction with its catalytic partner cyclin-dependent kinase 2 (CDK2), regulates cell cycle progression as cells exit quiescence and enter S-phase. Multiple mechanisms control cyclin E-CDK2 activity during the cell cycle, including phosphorylation-dependent cyclin E ubiquitylation by the SCFFbw7 ubiquitin ligase. Serine 384 (S384) is the critical cyclin E phosphorylation site that stimulates Fbw7 binding and subsequent cyclin E degradation. Because S384 is autophosphorylated by CDK2, cyclin E therefore instigates its own degradation in an autocatalytic manner. This presents a paradox as to how cyclin E-CDK2 is able to phosphorylate its numerous substrates prior to cyclin E autophosphorylation-catalyzed degradation. Here we find that the PP2A-B56 phosphatase specifically dephosphorylates cyclin E at S384, thereby uncoupling cyclin E degradation from cyclin E-CDK2 activity. Furthermore, the rate of S384 dephosphorylation is high in interphase and low in mitosis, allowing PP2A-B56 to oppose autocatalytic cyclin E degradation and maintain cyclin E-CDK2 activity at the G1/S transition. Citation Format: Ryan J. Davis, Jherek Swanger, Bruce E. Clurman. The PP2A-B56 phosphatase opposes cyclin E autocatalytic degradation via site-specific dephosphorylation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 308. doi:10.1158/1538-7445.AM2017-308

Fbw7 is an evolutionary conserved F box protein that functions as a substrate adapter for the Skp1-Cullin 1-F box (SCF) E3 ubiquitin ligase complex. Fbw7 is also a tumor suppressor gene that is mutated in diverse human cancers. Many Fbw7 substrates are oncogenic transcription factors, including c-Myc, Notch, and Jun. Cancer-associated Fbw7 mutations diminish its ability to interact with substrates, which results in inappropriate oncoprotein accumulation. One of the significant challenges for understanding the consequences of Fbw7 mutations in tumors is that Fbw7 coordinately regulates approximately two dozen broadly-acting transcription factors. To address this problem, we used novel computational methods to analyze TCGA gene expression datasets to derive transcriptional signatures that could predict a tumor’s Fbw7 mutational status; these signatures were then analyzed for enrichment of genes involved in specific biological processes. We found that genes associated with mitochondrial function were highly predictive of Fbw7 mutations across several tumor types, suggesting that metabolic reprogramming is a crucial oncogenic consequence of Fbw7 mutations. We validated this prediction by creating isogenic colorectal cancer cells with normal or mutant Fbw7 alleles. We found that mitochondrial signature genes are elevated in Fbw7 mutant cells, which also exhibit increased oxidative metabolism. Moreover, metabolomic studies revealed deregulation of other metabolic pathways in Fbw7-mutant cells, including amino acid and nucleotide biosynthesis. These data suggest that metabolic vulnerabilities may represent novel therapeutic targets in Fbw7-associated cancers. Citation Format: Ryan J. Davis, Mehmet Gonen, David Hockenbery, Adam Margolin, Bruce E. Clurman. Metabolic reprogramming caused by mutations of the Fbw7 ubiquitin ligase in colorectal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1030. doi:10.1158/1538-7445.AM2017-1030

Glioblastoma multiforme (GBM) is the most aggressive and common form of brain cancer in adults. There are currently no effective therapies for GBM. Even with standard of care treatments, such as surgery, radiation, and chemotherapy, ∼90% of adult patients die within 2 years of diagnosis. To identify therapeutic targets for Glioblastoma (GBM), we performed genome-wide CRISPR-Cas9 “knockout” (KO) screens in patient-derived GBM stem-like cells (GSCs) and human neural stem/progenitors (NSCs), non-neoplastic stem cell controls, for genes required for their in vitro growth. Surprisingly, the vast majority GSC-lethal hits were found outside of molecular networks commonly altered in GBM and GSCs (e.g., oncogenic drivers). In vitro and in vivo validation of GSC-specific targets revealed several strong hits, including the wee1-like kinase, PKMYT1/Myt1. Mechanistic studies demonstrated that PKMYT1 acts redundantly with WEE1 to inhibit Cyclin B-CDK1 activity via CDK1-Y15 phosphorylation and to promote timely completion of mitosis in NSCs. However, in GSCs, this redundancy is lost, likely as a result of oncogenic signaling, causing GBM-specific lethality. From a biological standpoint, our results help re-discover PKMYT1 function in human cells. From a cancer standpoint, these results suggest that targeting PKMYT1 is a glioma-lethal gene and that tandem or sequential use of PKMYT1 and WEE1 inhibitors may illicit therapeutic responses in GBM. In addition to these results we will also present retest data for other candidate glioma-lethal genes and networks in multiple patient samples. Citation Format: Chad Toledo, Ding Yu, Pia Hoellerbauer, Ryan Davis, Ryan Basom, Emily Girard, Philip Corrin, Hamid Bolouri, Jerry Davison, Qing Zhang, Do-Hyun Nam, Jeongwu Lee, Steven Pollard, Jeffery Delrow, Bruce Clurman, James Olson, Patrick Paddison. Genome-wide CRISPR-Cas9 screens reveal loss of redundancy between PKMYT1 and WEE1 in patient-derived glioblastoma stem-like cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 4370.

Precision oncology is currently based on the notion that genomic analysis of descriptive molecular signatures from patient tumors will lead to actionable therapeutic targets following the patient's arrival into the clinic. However, this approach has failed to deliver new effective treatments for glioblastoma multiforme (GBM), which is the most common and aggressive form of brain cancer; and thus, ∼90% of adult GBM patients receiving standard of care therapies continue to die within 2 years of diagnosis. In addition, this approach has neglected the importance for using functional genetics in precision oncology. To identify new therapeutic targets for GBM, we applied functional genetics to perform lethal genome-wide CRISPR-Cas9 knockout screens in patient-derived GBM stem-like cells (GSCs) and also non-transformed human neural stem cells (NSCs), non-neoplastic tissue of origin controls. Here, we present our latest findings from these screens, which include multiple novel GBM-specific lethal genes that were validated by both in vitro and in vivo preclinical studies. Knockout of GBM-specific lethal genes, including the WEE1-like kinase, PKMYT1/Myt1, lead to lethality in GSCs, but not NSCs. Focused mechanistic studies revealed that PKMYT1 acts redundantly with WEE1 to phosphorylate CDK1-Y15 and to promote timely completion of mitosis in NSCs, but that this redundancy is lost in most GBM isolates and in NSCs harboring activated alleles of EGFR and AKT1, which are commonly altered signaling pathways in GBM. Moreover, PKMYT1 depletion in GSCs and genetically altered NSCs requiring PKMYT1 lead to cytokinesis failure and cell death during mitosis. In addition to lethal genes, genes promoting in vitro expansion of NSCs upon knockout were examined. For this category, we validated multiple genes that are candidate tumor suppressors and involved in: the negative regulation of Hippo signaling, TP53 signaling, epigenetic regulation, promoting neural development, and other cellular functions. Knockout of these genes caused shortened cell cycle transit times and drastic growth advantages in NSCs, and in the case of CREBBP knockout, caused precious entry into S-phase and deregulation of cell cycle gene expression. The identification of these potential tumor suppressors here reveal new genetic drivers in glioma/GBM, which contributes to a growing body of work that will help redefine GBM gene signatures. Furthermore, we found that the molecular signatures of pathways and genes commonly altered in GBM are not ideal GBM therapeutic targets since most of these targets failed to score as GBM-specific lethal hits in our knockout screens and likely are non-essential or essential in both the GSCs and NSCs. Nonetheless, these common GBM alterations give rise to cancer-specific vulnerabilities, which then lead to genes, such as PKMYT1, that are required to overcome functional impairments in cancer cells. Taken together, we demonstrated here that genomics and functional genetics are equally important for precision oncology, as the combination of both tools can identify genetically altered genes, cancer-specific therapeutic targets, and tumor suppressors. These results are part of a rapidly growing body of work by the science community that will one day allow oncologists to tailor therapies for each patient based upon his or her tumor genetic profile and characteristics. Citation Format: Chad M. Toledo, Yu Ding, Pia Hoellerbauer, Ryan J. Davis, Ryan Basom, Emily J. Girard, Eunjee Lee, Philip Corrin, Hamid Bolouri, Jerry Davison, Qing Zhang, Do-Hyun Nam, Jeongwu Lee, Steven M. Pollard, Jun Zhu, Jeffery J. Delrow, Bruce E. Clurman, James M. Olson, Patrick J. Paddison. Genome-wide CRISPR-Cas9 screens uncover therapeutic targets and tumor suppressor genes in glioblastoma multiforme. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl 2):Abstract nr C159.

The purpose of this study was to identify factors that influenced the college choice process for high-achieving, low-income African American students, and to understand the effect of the Gates Millennium Scholarship on their college choice. Drawing from the Gates Millennium Scholar Tracking Database, a College Choice Survey, and the Integrated Postsecondary Education Data System, 231 high-achieving, low-income African American students who were selected as part of the 2012 cohort of Gates Millennium Scholars were surveyed. Data revealed the role of financial aid and college costs in the college choice process, and that being selected as a Gates Millennium Scholars enabled students to choose colleges that were more prestigious and institutions with more academic offerings. Implications research, policy, and practice are presented in the summary of the article.Keywords: Gates Millennium Scholars, low-income students, high-achieving students, grant aid, college choiceIntroductionFor several decades, policymakers and the constituents they serve have been deeply concerned about the rising cost of American higher education. Students and their families have also been affected by the shift in less grant aid to more loans (Lillis, 2008). Although the Obama administration has enacted federal policies over the past few years that have increased federal student aid (Baum & Payea, 2012), the average annual percentage increase for tuition and fees across all institutional types over the last decade has been 5.2% after controlling for inflation (Baum & Ma, 2012). Given these increases have consistently outpaced the rate of inflation, the role of federal, state, institutional, and private grant aid has been increasingly important for students from low- and moderate-incomes to attend the college of their choice.The role of grant aid in expanding college access and choice is particularly important for lowincome African American students given they disproportionately come from lower socioeconomic contexts and represent the racial/ethnic group that is most sensitive to the cost of higher education (Pema & Titus, 2005). Understanding how the timing, packaging, marketing, and actual distribution of grant aid affects different types of students is fundamentally important to expand college access and choice for all groups of students (Litten, 1982). However, much remains to be known about the role of grant aid in the college choice processes of different subgroups of collegegoing students. Granted that high-achieving, low-income African American students are substantially more likely to face socioeconomic challenges (Pema & Titus, 2005), but have more postsecondary options than their lower-performing peers (Hurtado, Inkelas, Briggs, & Rhee, 1997), a clearer understanding about how this subgroup of students choose their college of choice can help policymakers, college admissions officers, high school counselors, and community leaders understand the most effective methods to market, package, and distribute grant aid to this highly-qualified group of college-going students.OVERVIEW OF THE GATES MILLENNIUM SCHOLARS PROGRAMOne of the largest and most widely distributed forms of private grant aid created to assist lowincome, high-achieving African Americans (and other students of color) is the Gates Millennium Scholars (GMS) Program, chiefly administered by UNCF (United Negro College Fund). While higher education has shifted from grants to loans in recent decades, the GMS Program was established in 1999 with a 20-year $1.6 billion grant from the Bill and Melinda Gates Foundation to reduce the financial constraints of low-income, high-achieving students who aspire to earn a postsecondary education. While the GMS Program offers leadership development, academic empowerment, and mentorship to its Scholars, perhaps the most appealing component of the GMS Program is its national scholarship, which provides up to 10 years of renewable grant aid that covers the full cost of attendance for 1,000 high-achieving, low-income students of color each year to enroll in their college of choice and earn their undergraduate and graduate degrees. …

Macroautophagy is a dynamic process whereby portions of the cytosol are encapsulated in double-membrane vesicles and delivered to the lysosome for degradation. Phosphatidylinositol-3-phosphate (PI(3)P) is concentrated on autophagic vesicles and recruits effector proteins critical for this process. The production of PI(3)P by the class III phosphatidylinositol 3-kinase (PI3K), Vps34, has been well established; however, protein phosphatases which antagonize this early step in autophagy remain to be identified. To identify such enzymes, we screened human phosphatase genes by RNA interference (RNAi) and found that loss of PTPsigma, a dual-domain protein tyrosine phosphatase (PTP), increases cellular PI(3)P. The abundant PI(3)P-positive vesicles conferred by PTPsigma loss strikingly phenocopied those observed in amino acid-starved cells. Accordingly, we discovered that loss of PTPsigma hyperactivates both constitutive and induced autophagy. Finally, we found that PTPsigma localizes to PI(3)P-positive membranes in cells and this vesicular localization is enhanced during autophagy. Our findings propose a novel role for PTPsigma and provide insight into the regulation of autophagy. Mechanistic knowledge of this process is critical for understanding and targeting therapies for several human diseases, including cancer and Alzheimer's disease, in which abnormal autophagy may be pathological. 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 3836. doi:10.1158/1538-7445.AM2011-3836

SummaryTo identify therapeutic targets for glioblastoma (GBM), we performed genome-wide CRISPR-Cas9 knockout (KO) screens in patient-derived GBM stem-like cells (GSCs) and human neural stem/progenitors (NSCs), non-neoplastic stem cell controls, for genes required for their in vitro growth. Surprisingly, the vast majority GSC-lethal hits were found outside of molecular networks commonly altered in GBM and GSCs (e.g., oncogenic drivers). In vitro and in vivo validation of GSC-specific targets revealed several strong hits, including the wee1-like kinase, PKMYT1/Myt1. Mechanistic studies demonstrated that PKMYT1 acts redundantly with WEE1 to inhibit cyclin B-CDK1 activity via CDK1-Y15 phosphorylation and to promote timely completion of mitosis in NSCs. However, in GSCs, this redundancy is lost, most likely as a result of oncogenic signaling, causing GBM-specific lethality.