34 research outputs found

    Real‐world clinical effectiveness and safety of CT‐P10 in patients with diffuse large B‐cell lymphoma: An observational study in Europe

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    The rituximab biosimilar CT‐P10 is approved for the treatment of non‐Hodgkin lymphoma. Previous studies have demonstrated clinical similarity between CT‐P10 and reference rituximab. However, real‐world data relating to treatment in patients with DLBCL with rituximab biosimilars are limited. This study collected real‐world data relating to the effectiveness and safety of CT‐P10 treatment from the medical records of 389 patients with DLBCL (24 centers, five European countries). For the primary outcome (clinical effectiveness), overall survival (OS), progression‐free survival (PFS), and best response (BR) were assessed. The percentage (95% confidence interval [95% CI]) of patients alive at 12‐, 18‐, and 30 months postindex (initiation of CT‐P10) was 86% (82.4%–89.4%), 81% (76.9%–84.9%), and 76% (71.2%–80.1%), respectively. The PFS rate (percent, [95% CI]) at 12‐, 18‐, and 30 months postindex was 78% (74.2%–82.5%), 72% (67.9%–76.9%), and 67% (61.9%–71.7%), respectively. Median OS/PFS was not reached. For 82% (n = 312) of patients, the BR to CT‐P10 was a complete response. Adverse events were consistent with known effects of chemotherapy. This international, multicenter study provides real‐world data on the safety and effectiveness profile of CT‐P10 for DLBCL treatment and supports the adoption of CT‐P10 for the treatment of DLBCL

    Impact of treatment with iron chelation therapy in patients with lower-risk myelodysplastic syndromes participating in the European MDS registry

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    Iron overload due to red blood cell transfusions is associated with morbidity and mortality in lower-risk myelodysplastic syndrome patients. Many studies suggested improved survival after iron chelation therapy, but valid data are limited. The aim of this study was to assess the effect of iron chelation on overall survival and hematological improvement in lower-risk myelodysplastic syndrome patients in the European MDS registry. We compared chelated patients with a contemporary, non-chelated control group within the European MDS registry, that met the eligibility criteria for starting iron chelation. A Cox proportional hazards model was used to assess overall survival, treating receipt of chelation as a time-varying variable. Additionally, chelated and non-chelated patients were compared using a propensity-score matched model. Of 2200 patients, 224 received iron chelation. The hazard ratio and 95% confidence interval for overall survival for chelated patients, adjusted for age, sex, comorbidity, performance status, cumulative red blood cell transfusions, IPSS-R, and presence of ringed sideroblasts was 0.50 (0.34-0.74). The propensity-score analysis, matched for age, sex, country, red blood cell transfusion intensity, ferritin level, comorbidity, performance status, and IPSS-R and additionally corrected for cumulative red blood cell transfusions and presence of ringed sideroblasts, demonstrated a significantly improved overall survival for chelated patients with a hazard ratio of 0.42 (0.27-0.63) compared to non-chelated patients. Up to 39% of chelated patients reached an erythroid response. In conclusion, our results suggest that iron chelation may improve overall survival and hematopoiesis in transfused lower-risk myelodysplastic syndrome patients. This trial was registered at www.clinicaltrials.gov as #NCT00600860

    Exome sequencing identifies germline variants in DIS3 in familial multiple myeloma

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    [Excerpt] Multiple myeloma (MM) is the third most common hematological malignancy, after Non-Hodgkin Lymphoma and Leukemia. MM is generally preceded by Monoclonal Gammopathy of Undetermined Significance (MGUS) [1], and epidemiological studies have identified older age, male gender, family history, and MGUS as risk factors for developing MM [2]. The somatic mutational landscape of sporadic MM has been increasingly investigated, aiming to identify recurrent genetic events involved in myelomagenesis. Whole exome and whole genome sequencing studies have shown that MM is a genetically heterogeneous disease that evolves through accumulation of both clonal and subclonal driver mutations [3] and identified recurrently somatically mutated genes, including KRAS, NRAS, FAM46C, TP53, DIS3, BRAF, TRAF3, CYLD, RB1 and PRDM1 [3,4,5]. Despite the fact that family-based studies have provided data consistent with an inherited genetic susceptibility to MM compatible with Mendelian transmission [6], the molecular basis of inherited MM predisposition is only partly understood. Genome-Wide Association (GWAS) studies have identified and validated 23 loci significantly associated with an increased risk of developing MM that explain ~16% of heritability [7] and only a subset of familial cases are thought to have a polygenic background [8]. Recent studies have identified rare germline variants predisposing to MM in KDM1A [9], ARID1A and USP45 [10], and the implementation of next-generation sequencing technology will allow the characterization of more such rare variants. [...]French National Cancer Institute (INCA) and the Fondation Française pour la Recherche contre le Myélome et les Gammapathies (FFMRG), the Intergroupe Francophone du Myélome (IFM), NCI R01 NCI CA167824 and a generous donation from Matthew Bell. This work was supported in part through the computational resources and staff expertise provided by Scientific Computing at the Icahn School of Medicine at Mount Sinai. Research reported in this paper was supported by the Office of Research Infrastructure of the National Institutes of Health under award number S10OD018522. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The authors thank the Association des Malades du Myélome Multiple (AF3M) for their continued support and participation. Where authors are identified as personnel of the International Agency for Research on Cancer / World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer / World Health Organizatio

    DEFICIT EN PYRUVATE KINASE.

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    AIX-MARSEILLE2-BU MĂ©d/Odontol. (130552103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

    Complications cardiovasculaires et infection Ă  VIH (Ă©tude de cas sur l'hĂŽpital d'Avigon de 1996 Ă  2005)

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    AIX-MARSEILLE2-BU MĂ©d/Odontol. (130552103) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

    Rendre les cancers évitables. Recherches sur le travail cancérogÚne et ses conséquences

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    International audienceFrance now counts nearly 400,000 new cancer cases per year. Yet, even though this epidemic is shaped by strong inequalities, the role of work as a cause of cancer remains underacknowledged, if not ignored. In the GISCOP 84 cohort study on blood cancer patients taken care of at Avignon Central Hospital, each cancer is considered as a "sentinel event" giving access to the patients’ past (and present) occupational exposures to carcinogens, as well as to the obstacles to – and levers of action for – the prevention of occupational cancers and their compensation as occupational diseases. This article presents the GISCOP approach and the type of knowledge it produces. It also analyzes the institutional resistances this action research encounters. Indeed, although the ongoing cancer epidemic is a major public-health crisis requiring a strong response, the prevention of occupational cancers is intricately related to social relations of production – and thus politically sensitive.Avec prĂšs de 400 000 nouveaux cas par an, la France est en pleine Ă©pidĂ©mie de cancer. Or, malgrĂ© la nature fortement inĂ©galitaire de cette Ă©pidĂ©mie, le rĂŽle du travail dans la survenue des cancers demeure peu ou pas pris en compte. Dans le cadre de l’enquĂȘte de cohorte du GISCOP 84 auprĂšs de patients atteints de cancer hĂ©matologique pris en charge au centre hospitalier d’Avignon, chaque cancer est considĂ©rĂ© comme un « Ă©vĂ©nement-sentinelle » donnant accĂšs aux expositions professionnelles aux cancĂ©rogĂšnes subies par les patients, mais aussi aux freins et leviers d’action pour la reconnaissance en maladie professionnelle et la prĂ©vention. L’article prĂ©sente cette dĂ©marche de recherche pour l’action et le type de connaissances qu’elle permet de produire, tout en analysant les rĂ©sistances institutionnelles auxquelles elle se heurte. En effet, si la crise sanitaire majeure qu’est l’épidĂ©mie de cancers appelle des rĂ©ponses fortes, la prĂ©vention des cancers professionnels est en prise directe avec les rapports sociaux de production – et donc politiquement sensible

    Poly-exposition aux cancĂ©rogĂšnes et reconnaissance en maladie professionnelle : le cas des patients atteints de lymphome non hodgkinien. Premiers rĂ©sultats de l’enquĂȘte GISCOP 84

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    International audienceAlors que les constats d’une sous-reconnaissance massive et structurelle des cancers d’origine professionnelle se multiplient, le nombre de cancers reconnus en maladies professionnelles baisse. Dans ce contexte, cet article prĂ©sente les premiers rĂ©sultats de l’enquĂȘte du groupement d’intĂ©rĂȘt scientifique sur les cancers d’origine professionnelle dans le Vaucluse (GISCOP 84) auprĂšs de patients atteints d’hĂ©mopathies malignes. Ces rĂ©sultats soulignent l’importance, y compris rĂ©cente, de la poly-exposition aux cancĂ©rogĂšnes dans lesactivitĂ©s de travail, ainsi que les obstacles persistants rencontrĂ©s par les patients dans l’accĂšs au droit Ă  rĂ©paration. Cet article montre comment une dĂ©marche de recherche-action pluriprofessionnelle arrive Ă  partiellement briser l’invisibilitĂ© des cancers professionnels et discute l’inadaptation – et les Ă©volutions possibles – du systĂšme de reconnaissance actuel
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