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Background: No specific safety data concerning systemic oncological treatments were available at time of COVID-19 outbreak in Belgium. In our hospital we decided to maintain adjuvant and early line treatments for metastatic disease in patients under 65 and without specific comorbidities and to apply a shared decision approach in other patients while following closely the safety of these treatments. Method(s): Real time safety monitoring was proposed to all patients treated for solid tumours in our day-care unit starting March 1st, 2020. After signing informed consent patients were asked questions concerning protective measures at home, signs of SARS-CoV-2 infection and hospitalisation. Patients' charts were reviewed for outcome, including death, after suspected or proven SARS-CoV-2 infection. Minimum follow-up was 5 weeks after day care unit attendance. Result(s): 387 patients were included in our registry between March 1st and March 31st, 2020. Median age was 64 years-old (range 27-90). Most patients suffered from lung (n=96), breast (n=93), gastrointestinal (n=87), gynaecological (n=38) or urological (n=33) cancers. 131 patients received (neo)adjuvant treatments, 256 patients were treated for metastatic disease. Patients received chemotherapy (n=170), immunotherapy (n=103), targeted therapy (n=68) or other combinations (n=46). Although Belgium had one of the highest infection rates in the world, safety data concerning risk of SARS-CoV-2 infection and outcomes were rather reassuring. A total of 11 patients had either suspected (n=5, 1.3%) or proven (n=6, 1.6%) SARS-CoV-2 infection. Only one 74 years old patient died of COVID-19, another 51 years old patient died of progressive disease but presented also suspicion of SARS-CoV-2 infection at the time of death. Conclusion(s): Analysis of our data for patients treated in March 2020 in the day-care unit are reassuring and suggest higher risk related to under-treatment compared to risk related to continuation of systemic therapy at time of COVID-19 outbreak. Patients' follow-up will be updated and additional analyses and data in particular for April 2020, when the infection rate was still extremely high in Belgium, will be presented. Legal entity responsible for the study: The authors. Funding(s): Fondation Leon Fredericq. Disclosure: A. Rorive: Travel/Accommodation/Expenses: BMS;MSD. B. Sautois: Advisory/Consultancy, Travel/Accommodation/Expenses: Janssen;Advisory/Consultancy: Clovis;Sanofi;Astellas. J. Collignon: Advisory/Consultancy, Travel/Accommodation/Expenses: Roche;Amgen;Pfizer;Advisory/Consultancy: Servier;Bayer;Merck;Lilly;Sanofi;Sirtex;Celgene;Ipsen;Novartis. P. Freres: Advisory/Consultancy: Ipsen;Merck;BMS. C. Gennigens: Advisory/Consultancy, Research grant/Funding (institution): Astra-Zeneca;Advisory/Consultancy: BMS;GSK;Lilly;MSD;Advisory/Consultancy, Travel/Accommodation/Expenses: Ipsen;Pfizer;Pharmamar;Roche. G. Jerusalem: Advisory/Consultancy, Research grant/Funding (institution), Travel/Accommodation/Expenses: Novartis;Roche;Pfizer;Speaker Bureau/Expert testimony, Travel/Accommodation/Expenses: Lilly;Advisory/Consultancy, Research grant/Funding (institution): Amgen;Advisory/Consultancy, Travel/Accommodation/Expenses: BMS;AstraZeneca;Daiichi Sankyo;Advisory/Consultancy: Abbvie;Travel/Accommodation/Expenses: Medimmune;MerckKGaA. All other authors have declared no conflicts of interest.Copyright © 2020

Non-coding RNAs (ncRNA) represent 1/5 of the mammalian transcript number, and 90% of the genome length is transcribed. Many ncRNAs play a role in cancer. Among them, non-coding natural antisense transcripts (ncNAT) are RNA sequences that are complementary and overlapping to those of either protein-coding (PCT) or non-coding transcripts. Several ncNATs were described as regulating protein coding gene expression on the same loci, and they are expected to act more frequently in cis compared to other ncRNAs that commonly function in trans. In this work, 22 breast cancers expressing estrogen receptors and their paired adjacent non-malignant tissues were analyzed by strand-specific RNA sequencing. To highlight ncNATs potentially playing a role in protein coding gene regulations that occur in breast cancer, three different data analysis methods were used: differential expression analysis of ncNATs between tumor and non-malignant tissues, differential correlation analysis of paired ncNAT/PCT between tumor and non-malignant tissues, and ncNAT/PCT read count ratio variation between tumor and non-malignant tissues. Each of these methods yielded lists of ncNAT/PCT pairs that were enriched in survival-associated genes. This work highlights ncNAT lists that display potential to affect the expression of protein-coding genes involved in breast cancer pathology.

Over the last 5 years, immunotherapy has become one of the backbones for cancer treatment, showing significant improvement in prognosis for several malignancies. Currently, in clinical practice, we have several immune checkpoint inhibitors targeting cytotoxic T lymphocyte associated antigen 4 (CTLA4), programmed cell death 1 (PD-1) and programmed death ligand 1 (PD-L1), while several other drugs, directed toward different co-inhibitory or co-stimulatory molecules, are under evaluation (1).

Background The BRCA1 gene plays a key role in triple negative breast cancers (TNBCs), in which its expression can be lost by multiple mechanisms: germinal mutation followed by deletion of the second allele; negative regulation by promoter methylation; or miRNA-mediated silencing. This study aimed to establish a correlation among the BRCA1-related molecular parameters, tumor characteristics and clinical follow-up of patients to find new prognostic factors. Methods BRCA1 protein and mRNA expression was quantified in situ in the TNBCs of 69 patients. BRCA1 promoter methylation status was checked, as well as cytokeratin 5/6 expression. Maintenance of expressed BRCA1 protein interaction with BARD1 was quantified, as a marker of BRCA1 functionality, and the tumor expression profiles of 27 microRNAs were determined. Results miR-548c-5p was emphasized as a new independent prognostic factor in TNBC. A combination of the tumoral expression of miR-548c and three other known prognostic parameters (tumor size, lymph node invasion and CK 5/6 expression status) allowed for relapse prediction by logistic regression with an area under the curve (AUC) = 0.96. BRCA1 mRNA and protein in situ expression, as well as the amount of BRCA1 ligated to BARD1 in the tumor, lacked any associations with patient outcomes, likely due to high intratumoral heterogeneity, and thus could not be used for clinical purposes. Conclusions In situ BRCA1-related expression parameters could be used for clinical purposes at the time of diagnosis. In contrast, miR-548c-5p showed a promising potential as a prognostic factor in TNBC. Electronic supplementary material The online version of this article (doi:10.1186/s12885-015-1740-9) contains supplementary material, which is available to authorized users.

Background Germline mutations in breast cancer susceptibility gene 1 (BRCA1) increase the risk of breast and ovarian cancers. However, no association between BRCA1 germline mutation and glioblastoma malignancy has ever been highlighted. Here we report two cases of BRCA1 mutated patients who developed a glioblastoma multiform (GBM). Cases presentation Two patients diagnosed with triple negative breast cancer (TNBC) were screened for BRCA1 germline mutation. They both carried a pathogenic mutation introducing a premature STOP codon in the exon 11 of the BRCA1 gene. Few years later, both patients developed a glioblastoma and a second breast cancer. In an attempt to clarify the role played by a mutated BRCA1 allele in the GBM development, we investigated the BRCA1 mRNA and protein expression in breast and glioblastoma tumours for both patients. The promoter methylation status of this gene was also tested by methylation specific PCR as BRCA1 expression is also known to be lost by this mechanism in some sporadic breast cancers. Conclusion Our data show that BRCA1 expression is maintained in glioblastoma at the protein and the mRNA levels, suggesting that loss of heterozygosity (LOH) did not occur in these cases. The protein expression is tenfold higher in the glioblastoma of patient 1 than in her first breast carcinoma, and twice higher in patient 2. In agreement with the high protein expression level in the GBM, BRCA1 promoter methylation was not observed in these tumours. In these two cases, despite of a BRCA1 pathogenic germline mutation, the tumour-suppressor protein expression is maintained in GBM, suggesting that the BRCA1 mutation is not instrumental for the GBM development.