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      Cognitive impairment in hodgkin lymphoma survivors

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          Candidate mechanisms for chemotherapy-induced cognitive changes.

          The mechanism(s) for chemotherapy-induced cognitive changes are largely unknown; however, several candidate mechanisms have been identified. We suggest that shared genetic risk factors for the development of cancer and cognitive problems, including low-efficiency efflux pumps, deficits in DNA-repair mechanisms and/or a deregulated immune response, coupled with the effect of chemotherapy on these systems, might contribute to cognitive decline in patients after chemotherapy. Furthermore, the genetically modulated reduction of capacity for neural repair and neurotransmitter activity, as well as reduced antioxidant capacity associated with treatment-induced reduction in oestrogen and testosterone levels, might interact with these mechanisms and/or have independent effects on cognitive function.
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            Reduced-intensity chemotherapy and PET-guided radiotherapy in patients with advanced stage Hodgkin's lymphoma (HD15 trial): a randomised, open-label, phase 3 non-inferiority trial.

            The intensity of chemotherapy and need for additional radiotherapy in patients with advanced stage Hodgkin's lymphoma has been unclear. We did a prospective randomised clinical trial comparing two reduced-intensity chemotherapy variants with our previous standard regimen. Chemotherapy was followed by PET-guided radiotherapy. In this parallel group, open-label, multicentre, non-inferiority trial (HD15), 2182 patients with newly diagnosed advanced stage Hodgkin's lymphoma aged 18-60 years were randomly assigned to receive either eight cycles of BEACOPP(escalated) (8×B(esc) group), six cycles of BEACOPP(escalated) (6×B(esc) group), or eight cycles of BEACOPP(14) (8×B(14) group). Randomisation (1:1:1) was done centrally by stratified minimisation. Non-inferiority of the primary endpoint, freedom from treatment failure, was assessed using repeated CIs for the hazard ratio (HR) according to the intention-to-treat principle. Patients with a persistent mass after chemotherapy measuring 2·5 cm or larger and positive on PET scan received additional radiotherapy with 30 Gy; the negative predictive value for tumour recurrence of PET at 12 months was an independent endpoint. This trial is registered with Current Controlled Trials, number ISRCTN32443041. Of the 2182 patients enrolled in the study, 2126 patients were included in the intention-to-treat analysis set, 705 in the 8×B(esc) group, 711 in the 6×B(esc) group, and 710 in the 8×B(14) group. Freedom from treatment failure was sequentially non-inferior for the 6×B(esc) and 8×B(14) groups as compared with 8×B(esc). 5-year freedom from treatment failure rates were 84·4% (97·5% CI 81·0-87·7) for the 8×B(esc) group, 89·3% (86·5-92·1) for 6×B(esc) group, and 85·4% (82·1-88·7) for the 8×B(14) group (97·5% CI for difference between 6×B(esc) and 8×B(esc) was 0·5-9·3). Overall survival in the three groups was 91·9%, 95·3%, and 94·5% respectively, and was significantly better with 6×B(esc) than with 8×B(esc) (97·5% CI 0·2-6·5). The 8×B(esc) group showed a higher mortality (7·5%) than the 6×B(esc) (4·6%) and 8×B(14) (5·2%) groups, mainly due to differences in treatment-related events (2·1%, 0·8%, and 0·8%, respectively) and secondary malignancies (1·8%, 0·7%, and 1·1%, respectively). The negative predictive value for PET at 12 months was 94·1% (95% CI 92·1-96·1); and 225 (11%) of 2126 patients received additional radiotherapy. Treatment with six cycles of BEACOPP(escalated) followed by PET-guided radiotherapy was more effective in terms of freedom from treatment failure and less toxic than eight cycles of the same chemotherapy regimen. Thus, six cycles of BEACOPP(escalated) should be the treatment of choice for advanced stage Hodgkin's lymphoma. PET done after chemotherapy can guide the need for additional radiotherapy in this setting. Deutsche Krebshilfe and the Swiss Federal Government. Copyright © 2012 Elsevier Ltd. All rights reserved.
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              Is there a dysexecutive syndrome?

              The role of the frontal lobes has often been described as a 'paradox' or a 'riddle'. Ascribed to this region has been the loftiest of functions (e.g. executive; seat of wisdom); others contested that the frontal lobes played no special role. There has also been controversy about the unity or diversity of functions related to the frontal lobes. Based on the analysis of the effects of lesions of the frontal lobes, we propose that there are discrete categories of functions within the frontal lobes, of which 'executive' functioning is one. Within the executive category, the data do not support the concept of an undifferentiated central executive/supervisory system. The results are better explained as impairments in a collection of anatomically and functionally independent but interrelated attentional control processes. Evidence for three separate frontal attentional processes is presented. For each process, we present an operational description, the data supporting the distinctiveness of each process and the evidence for impairments of each process after lesions in specific frontal regions. These processes and their coarse frontal localizations are energization-superior medial, task setting-left lateral and monitoring-right lateral. The strength of the findings lies in replication: across different tasks; across different cognitive modalities (e.g. reaction time paradigms, memory); and across different patient groups. This convergence minimizes the possibility that any of the findings are limited to a specific task or to a specific set of patients. Although distinct, these processes are flexibly assembled in response to context, complexity and intention over real time into different networks within the frontal regions and between frontal and posterior regions.
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                Author and article information

                Journal
                British Journal of Haematology
                Br J Haematol
                Wiley
                00071048
                September 2018
                September 2018
                July 05 2018
                : 182
                : 5
                : 670-678
                Affiliations
                [1 ]Bruce Rappaport Faculty of Medicine; Technion; Haifa Israel
                [2 ]Quality Assurance Unit; Rambam Health Care Campus; Haifa Israel
                [3 ]Department of Cognitive Neurology; Rambam Health Care Campus; Haifa Israel
                [4 ]Haematology Unit; Bnai Zion Medical Centre; Haifa Israel
                [5 ]Department of Haematology and Bone Marrow Transplantation; Rambam Health Care Campus; Haifa Israel
                Article
                10.1111/bjh.15448
                29974933
                4db8f690-b6b4-4fe4-9acc-5f63e8c596b8
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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