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Patients were divided into two groups. Group 1 consisted of 29 patients who received radiotherapy combined with CON (RT?+?CON); group 2 had 60 patients who received chemo-radiotherapy (CRT) with cis-platinum. Group 2 was randomly divided into two subgroups, #links# who received CRT plus CON or CRT alone. Biopsy specimens were taken to identify CA9 as a hypoxia marker, vascular endothelial growth factor (VEGF) as an angiogenesis marker, and S-phase fraction (SPF) as a proliferation marker. Analysis was done to evaluate the correlation between the three markers, between the markers and tumour volume, and the benefit of introducing CON. Findings: A significant positive correlation was noted among pre-irradiated tumour volume and two markers: CA9 (r?=?0.514, p?=?0.007) and SPF (r?=?0.422, p?=?0.032), but there was a weak and non-significant correlation between tumour volume and VEGF (r?=?0.422, p?=?0.114). Significant correlations among the markers were also found: CA9 with VEGF (r?=?0.678, p?=?0.000), VEGF with SPF (r?=?0.475, p?=?0.005), and SPF with CA9 (r?=?0.510, p?=?0.002). CON effectiveness was analysed by evaluating treatment response. 69.2% in the RT?+?CON group had a complete response. 90.9% of the CRT?+?CON group and 63.6% of the CRT group had a complete response (statistically significant at p?=?0.031). No significant correlation was found between RT?+?CON and CRT (p?=?0.313). Interpretation: This study shows that hypoxia and cell proliferation increase with tumour volume. The response to radiation increased significantly in the group who received CON as part of treatment. This finding shows that CON has an #links# important role in breaking the cycle that causes radio-chemoresistance. Therefore, CON in combination with #links# RT can be considered for those who are not eligible for or refuse chemotherapy. Funding: Department of Radiotherapy, Cipto Mangunkusumo General Hospital, Jakarta, Indonesia, in collaboration with Radboud University, Nijmegen, Netherlands. The authors declared no conflicts of interest. ""Background: Nischarin, a novel protein, was originally identified as an ��5��1 interacting protein and has been shown to inhibit cell motility through inhibition of the Rac/PAK/LIMK/Coffinin pathway. Nischarin blocks tumour-cell migration and invasion in breast-cancer cell line MCF7. Methods: To further study the role of Nischarin in breast cancer, we evaluated expression levels by immunohistochemistry in 36 breast-cancer and 20 normal-breast tissue sections. We also looked at the expression pattern using the NCBI-GEO database. Findings: Nischarin expression was positive in 27.8% (10/36) breast-cancer tissues, which was significantly lower than the percent expressing the protein in normal breast tissues (55%, 11/20; p?<?0.05). Furthermore, expression of Nischarin in breast cancer was associated with oestrogen-receptor (ER) status.</p>