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Enfants d'empires coloniaux et postmémoires européennes révèle les souvenirs intergénérationnels des enfants de ceux qui ont vécu les derniers jours du colonialisme et les luttes pour l'indépendance dans les territoires colonisés par la Belgique, la France et le Portugal. Dans ce recueil de postmémoires, des récits d'Algérie, du Congo, d'Angola, du Cap-Vert, de Guinée-Bissau, du Mozambique et de São Tomé et-Príncipe résonnent à travers les mots de trente-sept citoyen·ne·s européen·ne·s, dont les histoires et les réflexions interrogent ce passé, ses ombres et ses silences, mais expriment aussi ses joies et ses accomplissements dans le présent européen. À partir de ces mémoires personnelles, nous pouvons tisser les fils qui associent les relations coloniales du passé aux phénomènes contemporains de migrations, de nostalgie, de racisme, de discrimination ou d'hypocrisie politique des relations entre les anciennes métropoles colonisatrices et les anciennes colonies. Dès lors, des questions telles que la citoyenneté, l'appartenance, l'héritage, mais aussi la réparation, la restitution et la dénonciation sont abordées, produisant une dialectique intergénérationnelle complexe et nouvelle qui refuse de poursuivre la retraumatisation, tout en rejetant les logiques de l'oubli. Ce sont des regards attentifs sur d'autres versants de l'histoire, forcément subjectifs et riches du vécu des autres, générateurs de multiples liens affectifs, familiaux et politiques, qui contribuent à éclairer et à comprendre le présent européen et les liens entre l'Europe et l'Afrique. Pour conclure cet ouvrage, un texte de l'écrivain portugais Paulo Faria ouvre sur de nouvelles constellations de mémoires européennes et suggère d'autres questions

Vol. 1: Informe general y costos de la discriminación. - XI,135 S. - ISBN 99922-909-1-9; Vol. 2: Marco jurídico y políticas comparadas. - XII,133 S. - ISBN 99922-909-0-0; Vol. 3: Prácticas discriminatorias y construcción colectiva de conceptos. - 164 S. - ISBN 99922-909-2-7; Vol. 4: Perspectivas y visiones ciudadanas. - XVII,191 S. - ISBN 99922-909-4-3; Vol. 5: Análisis crítico del discurso periodístico racista. - XI,106 S. - ISBN 99922-909-3-5; Vol. 6: Historias de vida. - VIII,92 S. - ISBN 978-99922-909-5-8

Non-small cell lung adenocarcinoma (NSCLC) bearing K-RasG12D mutations is one of the most prevalent types of lung cancer worldwide. Aryl hydrocarbon receptor (AHR) expression varies in human lung tumors and has been associated with either increased or reduced lung metastasis. In the mouse, Ahr also adjusts lung regeneration upon injury by limiting the expansion of resident stem cells. Here, we show that the loss of Ahr enhances K-RasG12D-driven NSCLC in mice through the amplification of stem cell subpopulations. Consistent with this, we show that K-RasG12D;Ahr−/− lungs contain larger numbers of cells expressing markers for both progenitor Clara (SCGB1A1 and CC10) and alveolar type-II (SFTPC) cells when compared to K-RasG12D;Ahr+/+-driven tumors. They also have elevated numbers of cells positive for pluripotent stem cells markers such as SOX2, ALDH1, EPCAM, LGR5 and PORCN. Typical pluripotency genes Nanog, Sox2 and c-Myc were also upregulated in K-RasG12D;Ahr−/− lung tumors as found by RNAseq analysis. In line with this, purified K-RasG12D/+;Ahr−/− lung cells generate larger numbers of organoids in culture that can subsequently differentiate into bronchioalveolar structures enriched in both pluripotency and stemness genes. Collectively, these data indicate that Ahr antagonizes K-RasG12D-driven NSCLC by restricting the number of cancer-initiating stem cells. They also suggest that Ahr expression might represent a good prognostic marker to determine the progression of K-RasG12D-positive NSCLC patients. ; This work was supported by grants to P.M.F.-S. from the Spanish Ministry of Economy and Competitiveness (SAF2017-82597-R and PID2020-114846RB-I00) and from the Junta de Extremadura (GR18006, IB160210 and IB20014). A.N.-P. was supported by the Ministry of Economy and Competitiveness and the Junta de Extremadura. C.M.R.-G. was a predoctoral F.P.U. fellow of the Ministry of Economy and Competitiveness. All Spanish funding was co-sponsored by the European Union FEDER program.

Recent experimental evidences from cellular systems and from mammalian and non-mammalian animal models highlight novel functions for the aryl hydrocarbon/dioxin receptor (AhR) in maintaining cell differentiation and tissue homeostasis. Notably, AhR depletion stimulates an undifferentiated and pluripotent phenotype likely associated to a mesenchymal transition in epithelial cells and to increased primary tumorigenesis and metastasis in melanoma. In this work, we have used a lung model of epithelial regeneration to investigate whether AhR regulates proper tissue repair by adjusting the expansion of undifferentiated stem-like cells. AhR-null mice developed a faster and more efficient repair of the lung bronchiolar epithelium upon naphthalene injury that required increased cell proliferation and the earlier activation of stem-like Clara, Basal and neuroepithelial cells precursors. Increased basal content in multipotent Sca1/CD31/CD4 cells and in cells expressing pluripotency factors NANOG and OCT4 could also improve re-epithelialization in AhR-null lungs. The reduced response of AhR-deficient lungs to Sonic Hedgehog (Shh) repression shortly after injury may also help their improved bronchiolar epithelium repair. These results support a role for AhR in the regenerative response against toxins, and open the possibility of modulating its activation level to favor recovery from lesions caused by environmental contaminants. ; This work was supported by grants to P.M.F-S. from the Spanish Ministry of Economy and Competitiveness (SAF2014-51813-R) and from the Junta de Extremadura (GR15008 and IB16210). Research at P.M.F-S. laboratory was also funded by the Red Temática de Investigación Cooperativa en Cáncer (RTICC), Carlos III Institute, Spanish Ministry of Economy and Competitiveness (RD12/0036/0032). A.M.-H. was supported by the Junta de Extremadura and N.M.-M. and A.N.-P. by the Ministerio de Economía y Competitividad. B.P. was supported by Junta de Extremadura. All Spanish funding is co-sponsored by the European Union FEDER program. ; Peer Reviewed