Factors influencing clinician-educators' assessment practice in varied Southern contexts: a health behaviour theory perspective.

In many contexts, responsibility for exit-level assessment design and implementation in undergraduate medical programmes lies with individuals who convene clinical clerkships. Their assessment practice has significant consequences for students' learning and the patients and communities that graduates will serve. Interventions to enhance assessment must involve these assessors, yet little is known about factors influencing their assessment practice. The purpose of this study was to explore factors that influence assessment practice of clerkship convenors in three varied low-and-middle income contexts in the global South. Taking assessment practice as a behaviour, Health Behaviour Theory (HBT) was deployed as a theoretical framework to explore, describe and explain assessor behaviour. Thirty-one clinician-educators responsible for designing and implementing high-stakes clerkship assessment were interviewed in South Africa and Mexico. Interacting personal and contextual factors influencing clinician-educator assessment intention and action were identified. These included attitude, influenced by impact and response appraisal, and perceived self-efficacy; along with interpersonal, physical and organisational, and distal contextual factors. Personal competencies and conducive environments supported intention to action transition. While previous research has typically explored factors in isolation, the HBT framing enabled a systematic and coherent account of assessor behaviour. These findings add a particular contextual perspective to understanding assessment practice, yet also resonate with and extend existing work that predominantly emanates from high-income contexts in the global North. These findings provide a foundation for the planning of assessment change initiatives, such as targeted, multi-factorial faculty development.

Medical education in the United Arab Emirates: Challenges and opportunities.

Medical education (ME) in the United Arab Emirates (UAE) has a relatively short history that begins with the inception of the UAE almost 50 years ago. The UAE has made great strides in widening access to ME through the rapid implementation of national agendas aimed at advancing healthcare and expanding higher education, in addition to the presence of a strong infrastructure for privatization and business development. While progress is being made at all levels of ME, complex challenges for both undergraduate and postgraduate ME remain. Going forward, issues of standardization, quality, sustainability of academic and healthcare workforces, and research must continue to be addressed.

How to do decolonial research.

The imperative for decolonial research in health professions education (HPE) is rooted in a resistance to coloniality, which characterises modern medicine and HPE. Coloniality is a residual effect of colonialism, which upholds White, Western, Eurocentric knowledge systems while simultaneously marginalising diverse epistemologies. We outline the problematic nature of coloniality in HPE typified in unequal research partnerships, skewed student exchanges and poor representation of diverse authors. Decoloniality advocates for the active disruption and dismantling of colonial hierarchies to promote epistemic justice. We suggest a practical framework for applying decolonial principles in research, emphasising awareness (critical consciousness), deliberation (reflexivity) and action (transformative praxis). Practical steps for decolonial practice include interrogating research conceptualisation, sharing power and diversifying research teams, adopting participatory and reciprocal (mutually beneficial) methodologies, (re)centring marginalised voices and amplifying 'Other' knowledges, and disrupting hegemonic dissemination practices. By employing decolonial strategies, researchers can produce equitable, socially accountable and epistemically just scholarship, ultimately enhancing the relevance and impact of HPE research for all people globally.

Targeting the oncogenic TBX3:nucleolin complex to treat multiple sarcoma subtypes.

Sarcomas are diverse cancers of mesenchymal origin, with compromised clinical management caused by insufficient diagnostic biomarkers and limited treatment options. The transcription factor TBX3 is upregulated in a diverse range of sarcoma subtypes, where it plays a direct oncogenic role, and it may thus represent a novel therapeutic target. To identify versatile ways to target TBX3, we performed affinity purification coupled by mass spectrometry to identify putative TBX3 protein cofactors that regulate its oncogenic activity in sarcomas. Here we identify and validate the multifunctional phosphoprotein nucleolin as a TBX3 cofactor. We show that nucleolin is co-expressed with TBX3 in several sarcoma subtypes and their expression levels positively correlate in sarcoma patients which are associated with poor prognosis. Furthermore, we demonstrate that nucleolin and TBX3 interact in chondrosarcoma, liposarcoma and rhabdomyosarcoma cells where they act together to enhance proliferation and migration and regulate a common set of tumor suppressor genes. Importantly, the nucleolin targeting aptamer, AS1411, exhibits selective anti-cancer activity in these cells and mislocalizes TBX3 and nucleolin to the cytoplasm which correlates with the re-expression of the TBX3/nucleolin target tumor suppressors CDKN1A (p21CIP1) and CDKN2A (p14ARF). Our findings provide the first evidence that TBX3 requires nucleolin to promote features of sarcomagenesis and that disruption of the oncogenic TBX3-nucleolin interaction by AS1411 may be a novel approach for treating sarcomas.

The c-Myc/AKT1/TBX3 Axis Is Important to Target in the Treatment of Embryonal Rhabdomyosarcoma.

Rhabdomyosarcoma is a highly aggressive malignant cancer that arises from skeletal muscle progenitor cells and is the third most common solid tumour in children. Despite significant advances, rhabdomyosarcoma still presents a therapeutic challenge, and while targeted therapy has shown promise, there are limited options because the molecular drivers of rhabdomyosarcoma are poorly understood. We previously reported that the T-box transcription factor 3 (TBX3), which has been identified as a druggable target in many cancers, is overexpressed in rhabdomyosarcoma patient samples and cell lines. To identify new molecular therapeutic targets to treat rhabdomyosarcoma, this study investigates the potential oncogenic role(s) for TBX3 and the factors responsible for upregulating it in this cancer. To this end, rhabdomyosarcoma cell culture models in which TBX3 was either stably knocked down or overexpressed were established and the impact on key hallmarks of cancer were examined using growth curves, soft agar and scratch motility assays, as well as tumour-forming ability in nude mice. Our data show that TBX3 promotes substrate-dependent and -independent proliferation, migration and tumour formation. We further reveal that TBX3 is upregulated by c-Myc transcriptionally and AKT1 post-translationally. This study identifies c-Myc/AKT1/TBX3 as an important axis that could be targeted for the treatment of rhabdomyosarcoma.