Access to higher education for undocumented students: “Outlaws” of social justice, equity, and equality

The status of access to higher education for undocumented students in this country is inconsistent from state to state, region to region, and the nation at large. This inconsistency is reflected in the development of policies and legislation that either provide or limit access to an affordable higher education for these students. Beneath the external debates regarding the application of instate tuition rates for undocumented students exists an underlying struggle embedded within an inherent cultural, societal, and systemic bias around beliefs, power, and privilege. The marginalization of undocumented students in accessing higher education—as evidenced by the absence of social justice, equity, and equality—has created an underground movement that is based in feminist and critical race theory descriptions of “outlaw culture.” This framework encapsulates the phenomenon of outlaw culture within the confines of systemic barriers, whereby those in positions closest to the front lines of service and access to higher education may become “outlaws” in bending, breaking, or circumventing the rules and regulations that perpetuate inequity and inequality and inhibit a socially just process for undocumented students. Implications regarding policy and practices to address socially just, equitable, and equal processes for access to higher education for undocumented students are presented for future consideration

HIC1 (hypermethylated in cancer 1) SUMOylation is dispensable for DNA repair but is essential for the apoptotic DNA damage response (DDR) to irreparable DNA double-strand breaks (DSBs).

The tumor suppressor gene HIC1 (Hypermethylated In Cancer 1) encodes a transcriptional repressor mediating the p53-dependent apoptotic response to irreparable DNA double-strand breaks (DSBs) through direct transcriptional repression of SIRT1. HIC1 is also essential for DSB repair as silencing of endogenous HIC1 in BJ-hTERT fibroblasts significantly delays DNA repair in functional Comet assays. HIC1 SUMOylation favours its interaction with MTA1, a component of NuRD complexes. In contrast with irreparable DSBs induced by 16-hours of etoposide treatment, we show that repairable DSBs induced by 1 h etoposide treatment do not increase HIC1 SUMOylation or its interaction with MTA1. Furthermore, HIC1 SUMOylation is dispensable for DNA repair since the non-SUMOylatable E316A mutant is as efficient as wt HIC1 in Comet assays. Upon induction of irreparable DSBs, the ATM-mediated increase of HIC1 SUMOylation is independent of its effector kinase Chk2. Moreover, irreparable DSBs strongly increase both the interaction of HIC1 with MTA1 and MTA3 and their binding to the SIRT1 promoter. To characterize the molecular mechanisms sustained by this increased repression potential, we established global expression profiles of BJ-hTERT fibroblasts transfected with HIC1-siRNA or control siRNA and treated or not with etoposide. We identified 475 genes potentially repressed by HIC1 with cell death and cell cycle as the main cellular functions identified by pathway analysis. Among them, CXCL12, EPHA4, TGFβR3 and TRIB2, also known as MTA1 target-genes, were validated by qRT-PCR analyses. Thus, our data demonstrate that HIC1 SUMOylation is important for the transcriptional response to non-repairable DSBs but dispensable for DNA repair

Repeatability of Quantitative 18F-NaF PET: A Multicenter Study

PURPOSE In bone-metastatic breast cancer patients, there are no current imaging biomarkers to identify which patients have worst prognosis. The purpose of our study was to investigate if skeletal tumor burden determined by 18F-Fluoride PET/CT correlates with clinical outcomes and may help define prognosis throughout the course of the disease. RESULTS Bone metastases were present in 49 patients. On multivariable analysis, skeletal tumor burden was significantly and independently associated with overall survival (p <0.0001) and progression free-survival (p <0.0001). The simple presence of bone metastases was associated with time to bone event (p = 0.0448). MATERIALS AND METHODS We quantified the skeletal tumor burden on 18F-Fluoride PET/CT images of 107 female breast cancer patients (40 for primary staging and the remainder for restaging after therapy). Clinical parameters, primary tumor characteristics and skeletal tumor burden were correlated to overall survival, progression free-survival and time to bone event. The median follow-up time was 19.5 months. CONCLUSIONS 18F-Fluoride PET/CT skeletal tumor burden is a strong independent prognostic imaging biomarker in breast cancer patients