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Simona Coco Simona Boccardo Marco Mora Vincenzo Fontana Irene Vanni Carlo Genova Angela Alama Sandra Salvi Maria Giovanna Dal Bello Silvia Bonfiglio Erika Rijavec Claudio Sini Giulia Barletta Federica Biello Franca Carli Zita Cavalieri Giovanni Burrafato Luca Longo Francesco Grossi 《Clinical breast cancer》2021,21(3):218-230.e6
IntroductionBreast cancer survivors are at increased risk of developing unrelated primary cancers, particularly lung cancer. Evidence indicates that sex hormones as well as a deregulation of DNA-repair pathways may contribute to lung cancer onset. We investigated whether the hormone status and expression of markers involved in DNA repair (BRCA1/2, ERCC1, and P53R2), synthesis (TS and RRM1), and cell division (TUBB3) might be linked to lung cancer risk.Patients and MethodsThirty-seven breast cancer survivors with unrelated lung cancer and 84 control subjects comprising women with breast cancer (42/84) or lung cancer (42/84) were enrolled. Immunohistochemistry on tumor tissue was performed. Geometric mean ratio was used to assess the association of marker levels with patient groups.ResultsEstrogen receptor was expressed in approximately 90% of the breast cancer group but was negative in the majority of the lung cancer group, a result similar to the lung cancer control group. Likewise, ER isoform β was weakly expressed in the lung cancer group. Protein analysis of breast cancer versus control had a significantly lower expression of BRCA1, P53R2, and TUBB3. Likewise, a BRCA1 reduction was observed in the lung cancer group concomitant with a BRCA2 increase. Furthermore, BRCA2 and TUBB3 increased in ipsilateral lung cancer in women who had previously received radiotherapy for breast cancer.ConclusionThe decrease of DNA-repair proteins in breast cancer could make these women more susceptible to therapy-related cancer. The increase of BRCA2 and TUBB3 in lung cancer from patients who previously received radiotherapy for breast cancer might reflect a tissue response to exposure to ionizing radiation. 相似文献
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Simona Petrucci MD PhD Monia Ginevrino PhD Ilaria Trezzi MD Edoardo Monfrini MD Lucia Ricciardi MD PhD Alberto Albanese MD Micol Avenali MD Paolo Barone MD Anna Rita Bentivoglio MD PhD Vincenzo Bonifati MD PhD Francesco Bove MD Laura Bonanni MD PhD Livia Brusa MD Cristina Cereda PhD Giovanni Cossu MD Chiara Criscuolo MD Giovanna Dati BSc Anna De Rosa MD PhD Roberto Eleopra MD Giovanni Fabbrini MD Laura Fadda MD PhD Manuela Garbellini BSc Brigida Minafra MD Marco Onofrj MD Claudio Pacchetti MD Ilaria Palmieri BSc Maria Teresa Pellecchia MD PhD Martina Petracca MD Marina Picillo MD PhD Antonio Pisani MD PhD Annamaria Vallelunga PhD Roberta Zangaglia MD Alessio Di Fonzo MD PhD Francesca Morgante MD PhD Enza Maria Valente MD PhD ITA-GENE-PD Study Group 《Movement disorders》2020,35(11):2106-2111
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Francesca Zoratto Clelia Buccheri Romina Mura Luisa Altabella Marion Vanneste Marie Villotte Giovanni Laviola Francois Dauphin Eleni Paizanis Walter Adriani Rossella Canese 《Synapse (New York, N.Y.)》2020,74(4):e22138
We aimed at the further characterization of rats in which SERT gene silencing was achieved by hippocampal injection of a lentiviral vector, carrying three si-RNA to block SERT mRNA at 66% of normal levels. Improved self-control and reduced restlessness were already demonstrated in these rats. Present further studies consisted of male adult rats, bilaterally inoculated within the hippocampus; control rats received lentivirus particles inactivated with heat. Both groups were maintained in isolation for 5 months, starting from inoculation. Neurochemical changes were studied by proton magnetic resonance spectroscopy (1H-MRS): we found increased hippocampal viability and bioenergetic potential; however, rats showed a behaviorally depressive pattern, also characterized by enhanced affiliation. Based on the extent of such effects, the whole lenti-SERT group was divided into two subgroups, termed intermediate- and extreme- phenotype profiles. While all rats had a widespread modification within dorsal/ventral striatum, amygdala, and hypothalamus, only the former subgroup showed an involvement of Raphé medialis, while, for the latter subgroup, an increase of SERT within hippocampus was unexpectedly caused. Within the less-affected “intermediate” rats, hippocampal 5-HT7 receptors were down-modulated, and also similarly within substantia nigra, septum, and neocortex. This picture demonstrates that additional rather than fewer neurobiological changes accompany a lower phenotypic expression. Overall, tapping hippocampal SERT affected the balance between habits versus strategies of coping by promoting morphogenetic processes indicative of a serotonergic fiber plasticity. Supplementary studies about serotonergic dynamics and neurogenesis within fronto-striatal circuits are needed. 相似文献
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