Publications by authors named "R Chabanon"
Article Synopsis
- Desmoplastic small round cell tumor (DSRCT) is an aggressive form of cancer linked to a specific genetic factor called EWS-WT1, and treatment options have not improved significantly in over 20 years.
- Researchers conducted a comprehensive drug sensitivity test on DSRCT cells and found that they respond well to PARP and ATR inhibitors, both alone and in combination, showcasing these treatments across various models.
- The study reveals that the combination of these inhibitors causes significant DNA damage and activates immune responses, suggesting that targeting EWS-WT1 could be an effective strategy in treating DSRCT.
Desmoplastic small round cell tumor (DSRCT) is a rare, aggressive sarcoma driven by the EWSR1::WT1 chimeric transcription factor. Despite this unique oncogenic driver, DSRCT displays a polyphenotypic differentiation of unknown causality. Using single-cell multi-omics on 12 samples from five patients, we find that DSRCT tumor cells cluster into consistent subpopulations with partially overlapping lineage- and metabolism-related transcriptional programs.
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- * Research revealed two patterns of immune response: one with reduced HLA-I expression linked to a suppressive tumor environment and poor prognosis, and another with preserved HLA-I that showed signs of effective immune activity and better outcomes.
- * The study suggests that HLA-I expression at relapse is a result of immune subversion initiated by BCG, rather than just a consequence of immune editing, highlighting the importance of HLA-I testing for guiding treatment options.
The MYC proto-oncogene family encompasses three related transcription factors (MYC, MYCL, and MYCN), which are master regulators of cellular programs orchestrating multiple hallmarks of cancer, including proliferation, metabolism, invasiveness, and immune surveillance. MYC activation is one of the most frequent alterations in cancer, induced by genetic, epigenetic, or posttranslational alterations of MYC itself, or of MYC-related proteins or pathways. Sun and colleagues found a unique function of the rate-limiting nucleotide synthesis enzyme CTP synthase 1 (CTPS1) in the survival of MYC-driven cancer cells.
View Article and Find Full Text PDFImmunotherapy has revolutionized cancer treatment and substantially improved patient outcome with regard to multiple tumour types. However, most patients still do not benefit from such therapies, notably because of the absence of pre-existing T cell infiltration. DNA damage response (DDR) deficiency has recently emerged as an important determinant of tumour immunogenicity.
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