BackgroundCancer seems to have an independent adverse prognostic effect on COVID-19-related mortality, but uncertainty exists regarding its effect across different patient subgroups. We report a population-based analysis of patients hospitalised with COVID-19 with prior or current solid cancer versus those without cancer.MethodsWe analysed data of adult patients registered until 24 May 2020 in the Belgian nationwide database of Sciensano. The primary objective was in-hospital mortality within 30 days of COVID-19 diagnosis among patients with solid cancer versus patients without cancer. Severe event occurrence, a composite of intensive care unit admission, invasive ventilation and/or death, was a secondary objective. These endpoints were analysed across different patient subgroups. Multivariable logistic regression models were used to analyse the association between cancer and clinical characteristics (baseline analysis) and the effect of cancer on in-hospital mortality and on severe event occurrence, adjusting for clinical characteristics (in-hospital analysis).ResultsA total of 13 594 patients (of whom 1187 with solid cancer (8.7%)) were evaluable for the baseline analysis and 10 486 (892 with solid cancer (8.5%)) for the in-hospital analysis. Patients with cancer were older and presented with less symptoms/signs and lung imaging alterations. The 30-day in-hospital mortality was higher in patients with solid cancer compared with patients without cancer (31.7% vs 20.0%, respectively; adjusted OR (aOR) 1.34; 95% CI 1.13 to 1.58). The aOR was 3.84 (95% CI 1.94 to 7.59) among younger patients (<60 years) and 2.27 (95% CI 1.41 to 3.64) among patients without other comorbidities. Severe event occurrence was similar in both groups (36.7% vs 28.8%; aOR 1.10; 95% CI 0.95 to 1.29).ConclusionsThis population-based analysis demonstrates that solid cancer is an independent adverse prognostic factor for in-hospital mortality among patients with COVID-19. This adverse effect was more pronounced among younger patients and those without other comorbidities. Patients with solid cancer should be prioritised in vaccination campaigns and in tailored containment measurements.
The present systematic review was performed under the auspices of the European Lung Cancer Working Party (ELCWP) in order to determine the role of early intermediate criteria (surrogate markers), instead of survival, in determining treatment efficacy in patients with lung cancer. Initially, the level of evidence for the use of overall survival to evaluate treatment efficacy was reviewed. Nine questions were then formulated by the ELCWP. After reviewing the literature with experts on these questions, it can be concluded that overall survival is still the best criterion for predicting treatment efficacy in lung cancer. Some intermediate criteria can be early predictors, if not surrogates, for survival, despite limitations in their potential application: these include time to progression, progression-free survival, objective response, local control after radiotherapy, downstaging in locally advanced nonsmall cell lung cancer (NSCLC), complete resection and pathological TNM in resected NSCLC, and a few circulating markers. Other criteria assessed in these recommendations are not currently adequate surrogates of survival in lung cancer.
Because of their substantial in vitro synergy, we conducted a dose-escalation study of cyclophosphamide (CP) added to 2-chloro-2′-deoxyadenosine (CdA) in patients with previously treated chronic lymphocytic leukemia and non-Hodgkin's lymphoma. CdA was given at a fixed dose (5.6 mg/m 2 /day) as a 2-h intravenous (i.v.) infusion, immediately followed by a 1-h i.v. infusion of CP, for 3 days. The initial daily CP dose was 200 mg/m 2 , and was escalated by 100 mg/m 2 increments in successive cohorts of three to six patients to determine the maximum-tolerated dose (MTD). Additional patients were included at the MTD to extend toxicity and response analysis. Twenty-six patients received 68 cycles of chemotherapy. The MTD of CP after CdA 5.6 mg/m 2 , was 300 mg/m 2 . Acute neutropenia was the dose-limiting toxicity of this regimen, which was otherwise well tolerated. Delivery of repeated cycles was not feasible in eight patients (31%) because of prolonged thrombocytopenia. Severe infections were seen in three of 68 cycles (4%). The overall response rate was 58% (15 of 26; 95% CI, 36-76%), with 15% complete responses and 42% partial responses. These data show the feasibility of the association of CdA with CP. Given the response rate observed, further studies of this regimen are warranted in untreated patients, in particular with chronic lymphocytic leukemia and with Waldenströ m macroglobulinemia. Leukemia (2000) 14, 1136-1142. Keywords: 2-chloro-2′-deoxyadenosine; cladribine; cyclophosphamide; chronic lymphocytic leukemia; non-Hodgkin's lymphomaThe purine nucleoside analogs 2-chloro-2′-deoxyadenosine (CdA) and fludarabine have established activity in the treatment of B cell chronic lymphocytic leukemia (CLL) and indolent non-Hodgkin's lymphoma (NHL). The hallmark of these compounds is their ability to kill both non-dividing and dividing cells via an apoptotic pathway. This may explain why they are effective in indolent lymphoproliferative disorders that usually have a low growth fraction rate and acquired resistance to apoptosis, together with the potential to accumulate active phosphorylated derivatives of purine analogs. 1In B-CLL, purine analogs yield an unprecedented rate of complete remissions (CR) compared to alkylating agents at standard dose.2,3 CdA and fludarabine are also active in follicular lymphoma (FL), Waldenströ m macroglobulinemia (WM), mantle-cell lymphoma (MCL), and lymphoplasmacytic lymphoma. [4][5][6][7][8] To date however, these drugs have not been shown to confer a survival advantage over standard therapy. 9-11In an attempt to increase the rate of CRs -as a step towards prolonged survival -one approach is to incorporate purine analogs into regimens that include agents such as chlorambuCorrespondence: E Van Den Neste, Hematology, Cliniques Universitaires Saint-Luc, 10, Av. Hippocrate, 1200 Brussels, Belgium; Fax: 32 2 764 8959 Received 17 November 1999; accepted 25 January 2000 cil (CLB) or cyclophosphamide (CP). This strategy relies on a variety of rationales including the individual activity of ...
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