The prizes for the best posters were given this year at the Génopode Retreat in Leysin (September 5 & 6, 2024) to:
1st price: Claire Paltenghi (van Leuwen lab) – Identification of suppressor genes rescuing Mendelian disease-causing genes in HAP1 cells (poster #42)
2nd price: Nathaniel Himmel (Benton lab) – A testis-expressed homologous of insect Gustatory and Odorant receptors (poster #31)
Dear All,
As you know, the CIG takes all forms of workplace discrimination very seriously. To foster working conditions that respect Equality, Diversity & Inclusion (EDI), PIs have recently attended a seminar led by UNIL’s EDI office. Moreover, a CIG EDI committee has been elected.
As one of its first initiatives, the EDI committee has requested that an EDI seminar be presented to all CIG members, including PhDs, Postdocs and all PAT members, including those from central services.
The first EDI seminar will take place during a regular CIG seminar slot on Monday, October 7, 2024, at 12h15 in Genopode’s Auditoire B.
As these topics are relevant to everyone, all CIG members are strongly encouraged to attend.
Discussion during this session and feedback from a questionnaire afterwards will be used to plan future events to ensure that all CIG members can openly discuss and receive training in EDI-related issues.
Best regards,
Frédéric, for the CIG EDI Committee
Develop your skills and contribute to the “savoir vivant”
Graduate Campus (https://courses.unil.ch/graduatecampus) offers a number of workshops specifically designed for doctoral candidates, postdoctoral researchers and supervisors from all faculties (UNIL, CHUV and Unisanté). These workshops are free of charge.
You can register for our workshops in the following four modules:
https://www.unil.ch/ecoledoctoralefbm/en/home.html (until mid October 2024)
https://news.unil.ch/display/1727340583220 (permalink)
Spencer S Watson 1, Anoek Zomer 2, Nadine Fournier 3, Joao Lourenco 3, Manfredo Quadroni 4, Agnieszka Chryplewicz 5, Sina Nassiri 3, Pauline Aubel 1, Simona Avanthay 2, Davide Croci 2, Erik Abels 6, Marike L D Broekman 6, Douglas Hanahan 7, Jason T Huse 8, Roy T Daniel 9, Monika E Hegi 10, Krisztian Homicsko 11, Giulia Cossu 12, Andreas F Hottinger 13, Johanna A Joyce 14
. 2024 Sep 9;42(9):1507-1527.e11.
doi: 10.1016/j.ccell.2024.08.012.
Free article
Glioblastoma recurrence is currently inevitable despite extensive standard-of-care treatment. In preclinical studies, an alternative strategy of targeting tumor-associated macrophages and microglia through CSF-1R inhibition was previously found to regress established tumors and significantly increase overall survival. However, recurrences developed in ∼50% of mice in long-term studies, which were consistently associated with fibrotic scars. This fibrotic response is observed following multiple anti-glioma therapies in different preclinical models herein and in patient recurrence samples. Multi-omics analyses of the post-treatment tumor microenvironment identified fibrotic areas as pro-tumor survival niches that encapsulated surviving glioma cells, promoted dormancy, and inhibited immune surveillance. The fibrotic treatment response was mediated by perivascular-derived fibroblast-like cells via activation by transforming growth factor β (TGF-β) signaling and neuroinflammation. Concordantly, combinatorial inhibition of these pathways inhibited treatment-associated fibrosis, and significantly improved survival in preclinical trials of anti-colony-stimulating factor-1 receptor (CSF-1R) therapy.
Matthew Jensen 1 2, Corrine Smolen 1 2, Anastasia Tyryshkina 1, Lucilla Pizzo 1, Deepro Banerjee 1, Matthew Oetjens 3, Hermela Shimelis 3, Cora M Taylor 3, Vijay Kumar Pounraja 1 2, Hyebin Song 4, Laura Rohan 1, Emily Huber 1, Laila El Khattabi 5, Ingrid van de Laar 6, Rafik Tadros 6, Connie Bezzina 6, Marjon van Slegtenhorst 6, Janneke Kammeraad 6, Paolo Prontera 7, Jean-Hubert Caberg 8, Harry Fraser 9, Siddhartha Banka 9 10, Anke Van Dijck 11, Charles Schwartz 12, Els Voorhoeve 13, Patrick Callier 14, Anne-Laure Mosca-Boidron 14, Nathalie Marle 14, Mathilde Lefebvre 15, Kate Pope 16, Penny Snell 16, Amber Boys 16, Paul J Lockhart 16 17, Myla Ashfaq 18, Elizabeth McCready 19, Margaret Nowacyzk 19, Lucia Castiglia 20, Ornella Galesi 20, Emanuela Avola 20, Teresa Mattina 20, Marco Fichera 20 21, Maria Grazia Bruccheri 20, Giuseppa Maria Luana Mandarà 22, Francesca Mari 23, Flavia Privitera 23, Ilaria Longo 23, Aurora Curró 23, Alessandra Renieri 23, Boris Keren 24, Perrine Charles 24, Silvestre Cuinat 25, Mathilde Nizon 25, Olivier Pichon 25, Claire Bénéteau 25, Radka Stoeva 25, Dominique Martin-Coignard 26, Sophia Blesson 27, Cedric Le Caignec 28 29, Sandra Mercier 27, Marie Vincent 27, Christa Martin 3, Katrin Mannik 30 31, Alexandre Reymond 32, Laurence Faivre 14 15, Erik Sistermans 13, R Frank Kooy 11, David J Amor 13, Corrado Romano 20 21, Joris Andrieux 33, Santhosh Girirajan 1 2 34
[Preprint]. 2024 Aug 28:2024.08.27.24312158.
doi: 10.1101/2024.08.27.24312158.
Variable expressivity of disease-associated variants implies a role for secondary variants that modify clinical features. We assessed the effects of modifier variants towards clinical outcomes of 2,252 individuals with primary variants. Among 132 families with the 16p12.1 deletion, distinct rare and common variant classes conferred risk for specific developmental features, including short tandem repeats for neurological defects and SNVs for microcephaly, while additional disease-associated variants conferred multiple genetic diagnoses. Within disease and population cohorts of 773 individuals with the 16p12.1 deletion, we found opposing effects of secondary variants towards clinical features across ascertainments. Additional analysis of 1,479 probands with other primary variants, such as 16p11.2 deletion and CHD8 variants, and 1,084 without primary variants, showed that phenotypic associations differed by primary variant context and were influenced by synergistic interactions between primary and secondary variants. Our study provides a paradigm to dissect the genomic architecture of complex disorders towards personalized treatment.