Heterotopic ossification (HO) is the pathological process of bone formation in non-osseous tissues following trauma and/or surgical intervention. Following traumatic injury, cellular and hormonal signals from the site of injury, a supply of mesenchymal cells and the appropriate tissue microenvironment are all among the potential factors that could contribute to development of HO in injured tissues (1). Prophylactic radiation therapy (RT) is commonly used to reduce the risk of HO after open reduction and internal fixation (ORIF) of traumatic acetabular fractures (TAFs); heterotopic ossification after operative treatment of the hip using a posterior surgical approach has been reported in up to 50% of such patients (2). Radiation therapy presumably decreases the risk of HO by inhibiting the proliferation of pluripotential mesenchymal cells that could potentially differentiate into osteoblastic stem cells and is usually administered postoperatively, within 72 h of surgery (3-5). However, preoperative RT has also been used in these situations (6)(7)(8). In a recent meta-analysis reporting the incidence of HO after TAF status post ORIF, it was reported that the incidence of HO formation after RT prophylaxis 461 This article is freely accessible online.

Head and neck cancers radiotherapy (RT) is associated with inevitable injury to parotid glands and subsequent xerostomia. We investigated the utility of SUV derived from 18 FDG-PET to develop metabolic imaging biomarkers (MIBs) of RT-related parotid injury. Methods: Data for oropharyngeal cancer (OPC) patients treated with RT at our institution between 2005 and 2015 with available planning computed tomography (CT), dose grid, pre-& first post-RT 18 FDG-PET-CT scans, and physician-reported xerostomia assessment at 3-6 months post-RT (Xero 3-6 ms) per CTCAE, was retrieved, following an IRB approval. A CT-CT deformable image co-registration followed by voxel-by-voxel resampling of pre & post-RT 18 FDG activity and dose grid were performed. Ipsilateral (Ipsi) and contralateral (contra) parotid glands were sub-segmented based on the received dose in 5 Gy increments, i.e. 0-5 Gy, 5-10 Gy sub-volumes, etc. Median and dose-weighted SUV were extracted from whole parotid volumes and sub-volumes on pre-& post-RT PET scans, using in-house code that runs on MATLAB. Wilcoxon signed-rank and Kruskal-Wallis tests were used to test differences pre-and post-RT. Results: 432 parotid glands, belonging to 108 OPC patients treated with RT, were sub-segmented & analyzed. Xero 3-6 ms was reported as: non-severe (78.7%) and severe (21.3%). SUV-median values were significantly reduced post-RT, irrespective of laterality (p = 0.02). A similar pattern was observed in parotid sub-volumes, especially ipsi parotid gland sub-volumes receiving doses 10-50 Gy (p < 0.05). Kruskal-Wallis test showed a significantly higher mean RT dose in the contra parotid in the patients with more severe Xero 3-6mo (p = 0.03).

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Background Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer (BC) with ill-defined therapeutic targets. Androgen receptor (AR) and tumour-infiltrating lymphocytes (TILs) had a prognostic and predictive value in TNBC. The relationship between AR, TILs and clinical behaviour is still not fully understood. Methods Thirty-six TNBC patients were evaluated for AR (positive if ≥1% expression), CD3, CD4, CD8 and CD20 by immunohistochemistry. Stromal TILs were quantified following TILs Working Group recommendations. Lymphocyte-predominant breast cancer (LPBC) was defined as stromal TILs ≥ 50%, whereas lymphocyte-deficient breast cancer (LDBC) was defined as <50%. Results The mean age was 52.5 years and 27.8% were ≥60 years. Seven patients (21.2%) were AR+. All AR+ cases were postmenopausal (≥50 years old). LPBC was 32.2% of the whole cohort. Median TILs were 37.5% and 10% ( p = 0.1) and median CD20 was 20% and 7.5% ( p = 0.008) in AR− and AR+, respectively. Mean CD3 was 80.7% and 93.3% ( p = 0.007) and CD8 was 75% and 80.8% ( p = 0.41) in AR− and AR+, respectively. All patients who were ≥60 years old expressed CD20. LDBC was found to be significantly higher in N+ versus N− patients ( p = 0.03) with median TILs of 20% versus 50% in N+ versus N−, respectively ( p = 0.03). LDBC was associated with higher risk of lymph node (LN) involvement (odds ratio = 6; 95% CI = 1.05–34.21; p = 0.04). Conclusions AR expression was evident in older age (≥50 years). Median CD20 was higher in AR− TNBC, while mean CD3 was higher in AR+ tumours. LDBC was associated with higher risk of LN involvement. Larger studies are needed to focus on the clinical impact of the relation between AR and TILs in TNBC.

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