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In this article, we examine the existing policy and academic literature on punitive responses to gender-based and family violence, focusing, in particular, on women’s police stations. Specialist women’s police stations have been a feature of policing in Argentina, Brazil, and other South American as well as Central American countries since the late 1980s. They are considered to be a phenomenon of ‘the global South’, having also been set up in some African and Asian countries including Sierra Leone and India. In this article, we critique research on women’s police stations as well as the public discourse within which women’s police stations are being proposed as a solution to domestic violence – looking at questions of research design, methodology, empiricism, ethics, and criminological claims to knowledge or ‘truth’. We reflect on the significant dangers posed by the potential transfer of women’s police stations to the Australian context, especially for sovereign Indigenous women and girls. Finally, we critique what we see as deep-seated contradictions and anomalies inherent in ‘southern theory’ and white feminist carceralism.

In Australia, those who talk of non-Indigenous sovereignty must offer accounts of Indigenous and non-Indigenous sovereignties and relations between them. In this chapter, we address these concerns through the histories and jurisprudence of rulership, relationship and responsibility, and through a number of historic and contemporary examples. Our purpose in doing so is to describe some practices of sovereignty that shape thinking with sovereignty in Australia. Describing these practices matters because the continual disavowal of Indigenous sovereignty by the Australian state is oppressive and limits the understanding of what it means to take responsibility for the relations between peoples and laws.

Lung squamous cell carcinoma (LSCC) is a considerable global health burden, with an incidence of over 600,000 cases per year. Treatment options are limited, and patient’s 5-year survival rate is less than 5%. The ubiquitin-specific protease 28 (USP28) has been implicated in tumourigenesis through its stabilization of the oncoproteins c-MYC, c-JUN, and Δp63. Here, we show that genetic inactivation of Usp28-induced regression of established murine LSCC lung tumours. We developed a small molecule that inhibits USP28 activity in the low nanomole range. While displaying cross-reactivity against the closest homologue USP25, this inhibitor showed a high degree of selectivity over other deubiquitinases. USP28 inhibitor treatment resulted in a dramatic decrease in c-MYC, c-JUN, and Δp63 proteins levels and consequently induced substantial regression of autochthonous murine LSCC tumours and human LSCC xenografts, thereby phenocopying the effect observed by genetic deletion. Thus, USP28 may represent a promising therapeutic target for the treatment of squamous cell lung carcinoma.

In contemporary Australia Aboriginal parents, and parents of Aboriginal kids, work to prepare their children for potentially negative encounters with police. Racialised policing practices target an...

The discovery, structure-activity relationships, and optimization of a novel class of fatty acid synthase (FASN) inhibitors is reported. High throughput screening identified a series of substituted piperazines with structural features that enable interactions with many of the potency-driving regions of the FASN KR domain binding site. Derived from this series was FT113, a compound with potent biochemical and cellular activity, which translated into excellent activity in in vivo models.

When a ribosome stalls during translation, it runs the risk of collision with a trailing ribosome. Such an encounter leads to the formation of a stable di-ribosome complex, which needs to be resolved by a dedicated machinery. The initial stalling and the subsequent resolution of di-ribosomal complexes requires activity of Makorin and ZNF598 ubiquitin E3 ligases, respectively, through ubiquitylation of the eS10 and uS10 subunits of the ribosome. We have developed a specific small-molecule inhibitor of the deubiquitylase USP9X. Proteomics analysis, following inhibitor treatment of HCT116 cells, confirms previous reports linking USP9X with centrosome-associated protein stability but also reveals a loss of Makorin 2 and ZNF598. We show that USP9X interacts with both these ubiquitin E3 ligases, regulating their abundance through the control of protein stability. In the absence of USP9X or following chemical inhibition of its catalytic activity, levels of Makorins and ZNF598 are diminished, and the ribosomal quality control pathway is impaired.

Clancy et al. develop a specific chemical inhibitor of USP9X and characterize its effects upon the cellular proteome. This analysis reveals a central role in the regulation of ribosomal stalling through control of critical E3 ligases., When a ribosome stalls during translation, it runs the risk of collision with a trailing ribosome. Such an encounter leads to the formation of a stable di-ribosome complex, which needs to be resolved by a dedicated machinery. The initial stalling and the subsequent resolution of di-ribosomal complexes requires activity of Makorin and ZNF598 ubiquitin E3 ligases, respectively, through ubiquitylation of the eS10 and uS10 subunits of the ribosome. We have developed a specific small-molecule inhibitor of the deubiquitylase USP9X. Proteomics analysis, following inhibitor treatment of HCT116 cells, confirms previous reports linking USP9X with centrosome-associated protein stability but also reveals a loss of Makorin 2 and ZNF598. We show that USP9X interacts with both these ubiquitin E3 ligases, regulating their abundance through the control of protein stability. In the absence of USP9X or following chemical inhibition of its catalytic activity, levels of Makorins and ZNF598 are diminished, and the ribosomal quality control pathway is impaired.

A protein structure-guided drug design approach was employed to develop small molecule inhibitors of the BET family of bromodomains that were distinct from the known (+)-JQ1 scaffold class. These efforts led to the identification of a series of substituted benzopiperazines with structural features that enable interactions with many of the affinity-driving regions of the bromodomain binding site. Lipophilic efficiency was a guiding principle in improving binding affinity alongside drug-like physicochemical properties that are commensurate with oral bioavailability. Derived from this series was tool compound FT001, which displayed potent biochemical and cellular activity, translating to excellent in vivo activity in a mouse xenograft model (MV-4-11).

History, Power, Text: Cultural Studies and Indigenous Studies is a collection of essays on Indigenous themes published between 1996 and 2013 in the journal known first as UTS Review and now as Cultural Studies Review. This journal opened up a space for new kinds of politics, new styles of writing and new modes of interdisciplinary engagement. History, Power, Text highlights the significance of just one of the exciting interdisciplinary spaces, or meeting points, the journal enabled. ‘Indigenous cultural studies’ is our name for the intersection of cultural studies and Indigenous studies showcased here. This volume republishes key works by academics and writers Katelyn Barney, Jennifer Biddle, Tony Birch, Wendy Brady, Gillian Cowlishaw, Robyn Ferrell, Bronwyn Fredericks, Heather Goodall, Tess Lea, Erin Manning, Richard Martin, Aileen Moreton-Robinson, Stephen Muecke, Alison Ravenscroft, Deborah Bird Rose, Lisa Slater, Sonia Smallacombe, Rebe Taylor, Penny van Toorn, Eve Vincent, Irene Watson and Virginia Watson—many of whom have taken this opportunity to write reflections on their work—as well as interviews between Christine Nicholls and painter Kathleen Petyarre, and Anne Brewster and author Kim Scott. The book also features new essays by Birch, Moreton-Robinson and Crystal McKinnon, and a roundtable discussion with former and current journal editors Chris Healy, Stephen Muecke and Katrina Schlunke. Timothy Neale is a research fellow at the Institute for Culture and Society, University of Western Sydney. He completed his doctorate at the University of Melbourne in 2014 and his research concerns environmental politics, settler-colonialism and critical theory. His writing has been published in Australian Humanities Review, Continuum and Griffith Law Review. Crystal McKinnon lectures in Indigenous Studies at the University of Melbourne. She is a doctoral candidate in the Department of Historical and European Studies at Latrobe University. Her thesis examines Indigenous resistance to oppression through the use of the creative arts, including music and literature. She is an Amangu woman from the Yamatji nation on the west coast of Australia. Her work has been published in Making Settler Colonial Space: Perspectives on Race, Place and Identity (Palgrave, 2010) and Alternative Law Journal. Eve Vincent is a lecturer in the Department of Anthropology at Macquarie University. Her doctoral thesis, completed in 2013, examined one mob’s lived experience of a divisive native title claims process. Her writing has been published in places such as Australian Humanities Review, Australian Journal of Human Rights, Sydney Review of Books, Meanjin and Overland.

Members of the Bromodomain and Extra-Terminal (BET) family of bromodomain-containing proteins (BRD2, BRD3, BRD4, and BRDT) bind to acetylated lysine residues on histone tails and act as epigenetic readers to regulate chromatin structure and gene expression. In particular, BET family member BRD4 has been shown to positively regulate the expression of MYC and other critical cancer-associated genes through the localization of BRD4 to super-enhancer regulatory elements. Results from preclinical studies conducted using the small molecule tool BET inhibitor (+)-JQ1, and emerging data from clinical trials of BET inhibitors in leukemia and lymphoma patients, have provided support for the therapeutic potential of BET inhibitors in hematologic malignancies. A protein structure-guided drug design approach was employed to explore small molecule acetyl lysine mimetics and led to the identification of the BET inhibitor FT-1101, which is structurally unrelated to reported clinical-stage BET inhibitors in the (+)-JQ1 class. In biochemical binding assays, FT-1101 displayed equipotent inhibition of binding of both bromodomains in all four BET family members to a known bromodomain ligand (Kd ≤ 20 nM). In vitro, FT-1101 displayed potent anti-proliferative activity across a broad panel of human leukemia, lymphoma, and multiple myeloma cell lines, with 66 out of 123 cell lines having IC50 values < 500 nM. For the MV-4-11 acute myeloid leukemia cell line, the anti-proliferative activity of FT-1101 (IC50 = 40 nM) correlated with down-regulation of MYC gene and protein expression, suggesting that its anti-proliferative activity was at least in part due to suppression of MYC. Additionally, genome-wide mapping of BRD4 super-enhancer binding sites in MV-4-11 cells by ChIP-sequencing identified several potential pharmacodynamic biomarkers outside of the MYC signaling network. In vivo, in the MV-4-11 xenograft model, oral treatment with FT-1101 at its maximum tolerated dose resulted in significant tumor growth inhibition, including tumor regressions, on schedules ranging from once daily to once weekly, and similar activity was also observed in the THP-1 AML xenograft model. Superior in vivo efficacy in the MV-4-11 model was observed for FT-1101 relative to BET inhibitors of the (+)-JQ1 class. In vivo efficacy was associated with prolonged drug exposure and a >75% decrease in MYC gene expression in tumors that was sustained for at least 12 hours. FT-1101 also crossed the blood-brain barrier in mice, achieving a pharmacologically relevant free drug concentration in the brain. The promising preclinical profile of FT-1101 warranted its rapid progression into human clinical trials, and a Phase 1 study in patients with relapsed refractory acute leukemia or high-risk myelodysplastic syndrome is currently underway. Disclosures No relevant conflicts of interest to declare.

In the late 1970s in the inner city suburbs of Melbourne, such as Fitzroy, Carlton and Richmond, Indigenous peoples often had problems getting into local pubs, bars, general nightlife and music venues. As Uncle Alf Bamblett states: ‘we finished off being barred from all the places around, purely on the base of race’.2 Not content with this situation he, along with others such as Tony Lovett, approached the Eastern Hill Public Bar, and stated they wanted to put a night on themselves, ‘somewhere for our own mobs to go and enjoy themselves’.3 They ‘scratched together a band’, with members including at the time Uncle Alf Bamblett, Tony Lovett, Tony Gorrie and Janice Johnstone.4 What they would create through their music was more than a band. Rather, their performance, the places they performed, and the spaces they and their audience created when they performed would generate critical sites of Indigenous resistance.