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      Histopathological and immunohistochemical study of the protective effect of triptorelin on the neurocytes of the hippocampus and the cerebral cortex of male albino rats after short-term exposure to cyclophosphamide

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          Abstract

          Chemotherapy treats many types of cancer effectively but it often causes side effects. Chemotherapy works on active cells, such as cancer cells, and some healthy cells. Side effects happen when chemotherapy damages these healthy cells. Today, many more drugs are available to treat side effects than in the past. Triptorelin (Decapeptyl) is a gonadotropin-releasing hormone agonist that is reported to have many therapeutic effects besides being an anti-cancer agent. In the current study, intraperitoneal cyclophosphamide (65 mg/kg/day) was administered for 4 weeks to induce marked dystrophic changes in the cerebral cortex and hippocampus of male albino rats. After 4 weeks, we observed significant degeneration of neurocytes with dystrophic changes. Subcutaneous triptorelin (0.05 mg/kg/day) for 4 weeks significantly improved histological signs of degeneration and apoptosis. Anti-Bcl2 staining of sections of the cerebral cortex and hippocampus showed that the apoptotic index was increased. This finding was confirmed by the anti-p53 staining, which showed a significant decrease in the apoptotic index. Ultimately, such improvements were accompanied by significant restoration of normal brain histology, as revealed by hematoxylin and eosin. In conclusion, triptorelin can reverse the apoptotic changes induced by cyclophosphamide therapy, which is more marked in the hippocampus than cerebral cortex.

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          The cognitive sequelae of standard-dose adjuvant chemotherapy in women with breast carcinoma: results of a prospective, randomized, longitudinal trial.

          Retrospective trials have reported that chemotherapy-induced cognitive dysfunction was experienced by a subset of patients with breast carcinoma. However, recent evidence indicated that a subset also exhibited impaired cognitive function at baseline, before the start of chemotherapy. A prospective, longitudinal trial that incorporates baseline neuropsychologic evaluations is necessary to determine to what extent cognitive dysfunction is attributable to chemotherapy in this population. Eighteen women with breast carcinoma underwent a comprehensive neuropsychologic evaluation before treatment and at short-term and long-term intervals after chemotherapy. The incidence, nature, severity, and chronicity of cognitive dysfunction developing in patients with breast carcinoma treated with a standard dose of adjuvant chemotherapy were assessed. Before the start of systemic therapy, 33% of women in the current cohort exhibited cognitive impairment. At the short-term postchemotherapy time point, 61% of the cohort exhibited a decline relative to baseline in 1 or more domains of cognitive functioning and reported greater difficulty in maintaining their ability to work. The most common domains of cognitive dysfunction were related to attention, learning, and processing speed. At the long-term postchemotherapy time point, approximately 50% of patients who experienced declines in cognitive function demonstrated improvement, whereas 50% remained stable. Self-reported ability to perform work-related activities also improved over this interval. Neither impairment at baseline nor subsequent treatment-related cognitive decline exhibited any statistically significant correlation with affective well-being or with demographic or clinical characteristics. The current study is the first longitudinal trial to report evidence of an association between cognitive dysfunction and chemotherapy in a subgroup of women with nonmetastatic breast carcinoma. The importance of using prospective research designs, appropriate cognitive measures, and statistical methods to evaluate subgroup effects was discussed. Identification of mechanisms associated with cognitive dysfunction and of risk factors contributing to subgroup vulnerability is necessary. Copyright 2004 by the American Cancer Society.
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            CNS progenitor cells and oligodendrocytes are targets of chemotherapeutic agents in vitro and in vivo

            Background Chemotherapy in cancer patients can be associated with serious short- and long-term adverse neurological effects, such as leukoencephalopathy and cognitive impairment, even when therapy is delivered systemically. The underlying cellular basis for these adverse effects is poorly understood. Results We found that three mainstream chemotherapeutic agents – carmustine (BCNU), cisplatin, and cytosine arabinoside (cytarabine), representing two DNA cross-linking agents and an antimetabolite, respectively – applied at clinically relevant exposure levels to cultured cells are more toxic for the progenitor cells of the CNS and for nondividing oligodendrocytes than they are for multiple cancer cell lines. Enhancement of cell death and suppression of cell division were seen in vitro and in vivo. When administered systemically in mice, these chemotherapeutic agents were associated with increased cell death and decreased cell division in the subventricular zone, in the dentate gyrus of the hippocampus and in the corpus callosum of the CNS. In some cases, cell division was reduced, and cell death increased, for weeks after drug administration ended. Conclusion Identifying neural populations at risk during any cancer treatment is of great importance in developing means of reducing neurotoxicity and preserving quality of life in long-term survivors. Thus, as well as providing possible explanations for the adverse neurological effects of systemic chemotherapy, the strong correlations between our in vitro and in vivo analyses indicate that the same approaches we used to identify the reported toxicities can also provide rapid in vitro screens for analyzing new therapies and discovering means of achieving selective protection or targeted killing.
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              Frontal gray matter reduction after breast cancer chemotherapy and association with executive symptoms: a replication and extension study.

              Cognitive changes related to cancer and its treatment have been intensely studied, and neuroimaging has begun to demonstrate brain correlates. In the first prospective longitudinal neuroimaging study of breast cancer (BC) patients we recently reported decreased gray matter density one month after chemotherapy completion, particularly in frontal regions. These findings helped confirm a neural basis for previously reported cognitive symptoms, which most commonly involve executive and memory processes in which the frontal lobes are a critical component of underlying neural circuitry. Here we present data from an independent, larger, more demographically diverse cohort that is more generalizable to the BC population. BC patients treated with (N=27) and without (N=28) chemotherapy and matched healthy controls (N=24) were scanned at baseline (prior to systemic treatment) and one month following chemotherapy completion (or yoked intervals for non-chemotherapy and control groups) and APOE-genotyped. Voxel-based morphometry (VBM) showed decreased frontal gray matter density after chemotherapy, as observed in the prior cohort, which was accompanied by self-reported difficulties in executive functioning. Gray matter and executive symptom changes were not related to APOE ε4 status, though a somewhat greater percentage of BC patients who received chemotherapy were ε4 allele carriers than patients not treated with chemotherapy or healthy controls. These findings provide confirmatory evidence of frontal morphometric changes that may be a pathophysiological basis for cancer and treatment-related cognitive dysfunction. Further research into individual risk factors for such changes will be critical for development of treatment and prevention strategies. Copyright © 2012 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                J Microsc Ultrastruct
                J Microsc Ultrastruct
                JMAU
                Journal of Microscopy and Ultrastructure
                Medknow Publications & Media Pvt Ltd (India )
                2213-879X
                2213-8803
                Jul-Sep 2016
                15 December 2015
                : 4
                : 3
                : 123-132
                Affiliations
                [a ] Department of Anatomy, Faculty of Medicine, Umm Al-Qura University, Makkah, Saudi Arabia
                [b ] Department of Anatomy, Faculty of Medicine, Mansoura University, Mansoura, Egypt
                [c ] Department of Anatomy, Batterjee Medical College, Jeddah, Saudi Arabia
                [d ] Department of Anatomy, Faculty of Medicine, Ain Shams University, Cairo, Egypt
                [e ] Department of Anatomy, Almaarefa College of Medicine, Riyadh, Saudi Arabia
                Author notes
                [* ] Corresponding author at: P.O. Box 71666, Riyadh-Diriyah, Kingdom of Saudi Arabia. E-mail address: Mohh.elsherbiny@ 123456gmail.com (M. El-Sherbiny).
                Article
                JMAU-4-123
                10.1016/j.jmau.2015.12.002
                6014199
                30023218
                62b8f80d-2643-4c3f-b062-388fc3603cd5
                Copyright: © 2015 Saudi Society of Microscopes

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 13 May 2015
                : 29 October 2015
                : 02 December 2015
                Categories
                Experimental Study

                cerebral cortex,cyclophosphamide,hippocampus,p53,triptorelin

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