Publisher Correction: Truncated FGFR2 is a clinically actionable oncogene in multiple cancers.

This paper was originally published under a standard Springer Nature license

Undernutrition in nursing home rehabilitation patients

OBJECTIVE: To examine the prevalence of undernutrition, received dietetic treatment and self-perception of nutritional status in older patients admitted to Dutch nursing home rehabilitation wards. METHODS: Between December 2012-February 2014, we included 190 patients (≥65 y) admitted to seven nursing home rehabilitation wards. Nutritional status in the first week of admission was characterized as: severely undernourished (>10% unintentional weight loss in the past six months and/or >5% unintentional weight loss in the past month and/or BMI 28 kg/m(2)). Primary diagnosis was categorized as: trauma, elective orthopaedics, stroke and other. Perceived nutritional status was determined with the question: 'Do you currently consider yourself undernourished?' (yes/no). Information regarding dietetic treatment was obtained from medical records. RESULTS: A complete dataset was obtained from 179 patients (70% female, age 81 ± 8 y). 26% of the patients was found to be severely undernourished and 14% moderately undernourished. Prevalence of undernutrition did not differ by sex or age. Of all undernourished patients, 56% had been treated by a dietitian. Only one out of five of undernourished patients considered themselves undernourished. Elective orthopaedics patients had the lowest prevalence of undernutrition (19%) while patients categorised as 'other' had the highest prevalence (51%). CONCLUSION: More than one in three older patients in Dutch nursing home rehabilitation wards are moderately to severely undernourished. Out of these patients the majority does not consider themselves undernourished and almost half has not received dietetic treatment. More attention to undernutrition in nursing home rehabilitation patients seems necessary

Truncated FGFR2 is a clinically actionable oncogene in multiple cancers.

Somatic hotspot mutations and structural amplifications and fusions that affect fibroblast growth factor receptor 2 (encoded by FGFR2) occur in multiple types of cancer1. However, clinical responses to FGFR inhibitors have remained variable1-9, emphasizing the need to better understand which FGFR2 alterations are oncogenic and therapeutically targetable. Here we apply transposon-based screening10,11 and tumour modelling in mice12,13, and find that the truncation of exon 18 (E18) of Fgfr2 is a potent driver mutation. Human oncogenomic datasets revealed a diverse set of FGFR2 alterations, including rearrangements, E1-E17 partial amplifications, and E18 nonsense and frameshift mutations, each causing the transcription of E18-truncated FGFR2 (FGFR2ΔE18). Functional in vitro and in vivo examination of a compendium of FGFR2ΔE18 and full-length variants pinpointed FGFR2-E18 truncation as single-driver alteration in cancer. By contrast, the oncogenic competence of FGFR2 full-length amplifications depended on a distinct landscape of cooperating driver genes. This suggests that genomic alterations that generate stable FGFR2ΔE18 variants are actionable therapeutic targets, which we confirmed in preclinical mouse and human tumour models, and in a clinical trial. We propose that cancers containing any FGFR2 variant with a truncated E18 should be considered for FGFR-targeted therapies