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Cinzia Maria Chinnici Giovanna Russelli Matteo Bulati Vitale Miceli Alessia Gallo Rosalia Bus Rosaria Tinnirello Pier Giulio Conaldi Gioacchin Iannolo 《World journal of gastroenterology : WJG》2021,27(17):1905-1919
Due to their immunomodulatory potential and release of trophic factors that promote healing, mesenchymal stromal cells (MSCs) are considered important players in tissue homeostasis and regeneration. MSCs have been widely used in clinical trials to treat multiple conditions associated with inflammation and tissue damage. Recent evidence suggests that most of the MSC therapeutic effects are derived from their secretome, including the extracellular vesicles, representing a promising approach in regenerative medicine application to treat organ failure as a result of inflammation/fibrosis. The recent outbreak of respiratory syndrome coronavirus, caused by the newly identified agent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has forced scientists worldwide to use all available instruments to fight the infection, including the inflammatory cascade caused by this pandemic disease. The use of MSCs is a valid approach to combat organ inflammation in different compartments. In addition to the lungs, which are considered the main inflammatory target for this virus, other organs are compromised by the infection. In particular, the liver is involved in the inflammatory response to SARS-CoV-2 infection, which causes organ failure, leading to death in coronavirus disease 2019 (COVID-19) patients. We herein summarize the current implications derived from the use of MSCs and their soluble derivatives in COVID-19 treatment, and emphasize the potential of MSC-based therapy in this clinical setting. 相似文献
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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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Renée T. Fortner Anika Hüsing Laure Dossus Anne Tjønneland Kim Overvad Christina C. Dahm Patrick Arveux Agnès Fournier Marina Kvaskoff Matthias B. Schulze Manuela Bergmann Antonia Trichopoulou Anna Karakatsani Carlo La Vecchia Giovanna Masala Valeria Pala Amalia Mattiello Rosario Tumino Fulvio Ricceri Carla H. van Gils Evelyn M. Monninkhof Catalina Bonet José Ramón Quirós Maria-Jose Sanchez Daniel-Ángel Rodríguez-Palacios Aurelio B Gurrea Pilar Amiano Naomi E. Allen Ruth C. Travis Marc J. Gunter Vivian Viallon Elisabete Weiderpass Elio Riboli Rudolf Kaaks 《International journal of cancer. Journal international du cancer》2020,147(5):1325-1333
Endometrial cancer (EC) incidence rates vary ~10-fold worldwide, in part due to variation in EC risk factor profiles. Using an EC risk model previously developed in the European EPIC cohort, we evaluated the prevention potential of modified EC risk factor patterns and whether differences in EC incidence between a European population and low-risk countries can be explained by differences in these patterns. Predicted EC incidence rates were estimated over 10 years of follow-up for the cohort before and after modifying risk factor profiles. Risk factors considered were: body mass index (BMI, kg/m2), use of postmenopausal hormone therapy (HT) and oral contraceptives (OC) (potentially modifiable); and, parity, ages at first birth, menarche and menopause (environmentally conditioned, but not readily modifiable). Modeled alterations in BMI (to all ≤23 kg/m2) and HT use (to all non-HT users) profiles resulted in a 30% reduction in predicted EC incidence rates; individually, longer duration of OC use (to all ≥10 years) resulted in a 42.5% reduction. Modeled changes in not readily modifiable exposures (i.e., those not contributing to prevention potential) resulted in ≤24.6% reduction in predicted EC incidence. Women in the lowest decile of a risk score based on the evaluated exposures had risk similar to a low risk countries; however, this was driven by relatively long use of OCs (median = 23 years). Our findings support avoidance of overweight BMI and of HT use as prevention strategies for EC in a European population; OC use must be considered in the context of benefits and risks. 相似文献
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Iñaki Comino-Méndez Luis J Leandro-García Guillermo Montoya Lucía Inglada-Pérez Aguirre A. de Cubas María Currás-Freixes Carolyn Tysoe Louise Izatt Rocío Letón Álvaro Gómez-Graña Veronika Mancikova María Apellániz-Ruiz Massimo Mannelli Francesca Schiavi Judith Favier Anne-Paule Gimenez-Roqueplo Henri J. L. M. Timmers Giovanna Roncador Juan F. Garcia Cristina Rodríguez-Antona Mercedes Robledo Alberto Cascón 《Journal of molecular medicine (Berlin, Germany)》2015,93(11):1247-1255