B y early March 2020, the spread of the coronavirus disease 2019 (COVID-19) outbreak had reached the Paris area, France. Since then, all medical resources have been reorganized to handle the pandemic. As a tertiary cancer center, Gustave Roussy has followed two objectives: define processes to safely sustain cancer care in a secured environment and reorganize internally to adapt its capacities to hospitalize patients with cancer and COVID-19 illness. Patients with cancer have been considered at increased risk of COVID-19, on the rationale of the increased systemic immunosuppressive state caused by the underlying malignancy and anticancer treatments. The first report from a retrospective cohort in China suggested that patients with cancer were observed to have a higher risk of severe events (for example, a composite endpoint of intensive care unit (ICU) admission, invasive ventilation or death) compared with patients without cancer (seven (39%) of 18 patients versus 124 (8%) of 1,572 patients; P = 0.0003) and that patients with cancer deteriorated more rapidly than those without cancer 1. While general determinants of COVID-19 severity have emerged from large cohorts from China and Italy 2,3 , limited data are available on the specificity of patients with cancer to help the oncology community to identify patients at risk of severe COVID-19. Furthermore, the impact of COVID-19 infection on ongoing cancer care is unexplored. This study investigated the determinants of clinical worsening and death, as well as the impact on cancer care, for the first patients sequentially managed for COVID-19 and cancer in an academic tertiary cancer center. Results Patient population. From 24 March 2020 until 29 April 2020, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was detected in 196 (12%) of 1,633 tests performed internally at the Gustave Roussy Cancer Centre. Overall, 209 patients were identified (including a few identified by PCR with reverse transcription (RT-PCR) performed at another facility and some diagnosed by computed tomography scan alone) and the final study population included 178 adult patients. The following were reasons for exclusion: pediatric population (six patients); non-cancer patients (19 patients); and COVID-19 ultimately ruled out (six patients). Baseline demographics, comorbidities and underlying cancer characteristics for

Bamlivimab + etesevimab therapy induces SARS-COV-2 immune escape mutations and secondary clinical deterioration in Covid-19 patients with B cell malignancies F.

Five to 10% of desmoid-type fibromatosis (DF) arise in the context of familial adenomatous polyposis (FAP). The beta-catenin gene (CTNNB1) exon 3 mutations are found in 90% of DF (except those associated with FAP) in two codonscodon 41 (p.T41A) and codon 45 (p.S45F and p.S45P) which are serine and threonine phosphorylation sites required for beta-catenin degradation. Mutations p.S45F are associated with a higher risk of recurrence. Among 64 patients with DF and documented CTNNB1 mutational status treated with oral weekly vinorelbine for 6 months, p.S45F or p.S45P mutations were associated with longer time to treatment failure compared to p.T41A or wild type tumors (HR : 2.78, 95%CI: 1.23-6.27), p = 0.04. The functional impact of codons 41 and 45 mutations is certainly different, since the phosphorylation of amino acid 45 targeted by casein kinase-1 serves as a priming phosphorylation for GSK-3β targeting the amino acid 41. Research.