Professionalism and skills enhancement in the built environment: the role of higher education in a changing policy context in England

Since the election of the Labour Government in 1997 there have been a series of policy initiatives emphasising the importance of co-ordinated and integrated approaches to the delivery of urban regeneration and in particular Sustainable Communities. This changing policy context has given rise to a shortage of practitioners with both the technical skills to deliver specific programmes, and more especially the generic skills to work in multi-disciplinary teams in conjunction with partnership-based management boards. This paper discusses the origins of the debate about skills shortages and deficiencies and reviews the main government reports which have advocated a new approach to the provision of skills for community regeneration. It focuses particularly on the work of the Planning Network which was funded by the Centre for Education in the Built Environment (CEBE) to examine the contribution of higher education to the wider skills debate. It concludes by arguing that higher education has an important part to play in the provision of a more appropriate skills set for professional practice within a broader and more inclusive strategy involving all key stakeholders. However, employers also have a major responsibility in ensuring that key skills are maintained and enhanced within their own organisations.

Engendering a culture of quality enhancement in teaching and learning: lessons learned

Enhancing the quality of learning and teaching in higher education has been on the English national agenda for more than a decade. The Government and funding organisations have enabled universities to focus on creating a culture of excellence in learning and teaching and continuing academic and professional development. This paper describes some of the strategies that have promoted a culture of quality teaching in higher education in England and how one organisation, the University of Westminster has implemented those strategies to engender a culture of quality enhancement and continuing professional development.

Diagnostic value of H3F3A mutations in giant cell tumour of bone compared to osteoclast-rich mimics

Driver mutations in the two histone 3.3 (H3.3) genes, H3F3A and H3F3B, were recently identified by whole genome sequencing in 95% of chondroblastoma (CB) and by targeted gene sequencing in 92% of giant cell tumour of bone (GCT). Given the high prevalence of these driver mutations, it may be possible to utilise these alterations as diagnostic adjuncts in clinical practice. Here, we explored the spectrum of H3.3 mutations in a wide range and large number of bone tumours (n 5 412) to determine if these alterations could be used to distinguish GCT from other osteoclast-rich tumours such as aneurysmal bone cyst, nonossifying fibroma, giant cell granuloma, and osteoclast-rich malignant bone tumours and others. In addition, we explored the driver landscape of GCT through whole genome, exome and targeted sequencing (14 gene panel). We found that H3.3 mutations, namely mutations of glycine 34 in H3F3A, occur in 96% of GCT. We did not find additional driver mutations in GCT, including mutations in IDH1, IDH2, USP6, TP53. The genomes of GCT exhibited few somatic mutations, akin to the picture seen in CB. Overall our observations suggest that the presence of H3F3A p.Gly34 mutations does not entirely exclude malignancy in osteoclast-rich tumours. However, H3F3A p.Gly34 mutations appear to be an almost essential feature of GCT that will aid pathological evaluation of bone tumours, especially when confronted with small needle core biopsies. In the absence of H3F3A p.Gly34 mutations, a diagnosis of GCT should be made with caution.

Distinct H3F3A and H3F3B driver mutations define chondroblastoma and giant cell tumor of bone

It is recognized that some mutated cancer genes contribute to the development of many cancer types, whereas others are cancer type specific. For genes that are mutated in multiple cancer classes, mutations are usually similar in the different affected cancer types. Here, however, we report exquisite tumor type specificity for different histone H3.3 driver alterations. In 73 of 77 cases of chondroblastoma (95%), we found p.Lys36Met alterations predominantly encoded in H3F3B, which is one of two genes for histone H3.3. In contrast, in 92% (49/53) of giant cell tumors of bone, we found histone H3.3 alterations exclusively in H3F3A, leading to p.Gly34Trp or, in one case, p.Gly34Leu alterations. The mutations were restricted to the stromal cell population and were not detected in osteoclasts or their precursors. In the context of previously reported H3F3A mutations encoding p.Lys27Met and p.Gly34Arg or p.Gly34Val alterations in childhood brain tumors, a remarkable picture of tumor type specificity for histone H3.3 driver alterations emerges, indicating that histone H3.3 residues, mutations and genes have distinct functions.