Publications

Metabolic Crosstalk in the Tumor Microenvironment)

tThis review explores how leukemia thrives in the bone marrow, where adipocytes supply vital nutrients and send signals that support cancer growth. In response, leukemia cells hijack these adipocytes, reshaping them to boost their survival, evade treatment, and undergo fuel relapse.

By integrating single-cell dissection of the tumor landscape and an in-depth, single-cell–based off-tumor antigen prediction, we identify CD86 as a promising therapeutic target in cHL. CD86 is highly expressed on Hodgkin and Reed-Sternberg cancer cells and cHL-specific tumor-associated macrophages.

A retrospective multicentric study was conducted across 31 French Innovative Leukemia Organization (FILO-CLL) affiliated centers in France, including patients diagnosed between 1998 and 2023.

This is the first documented confirmation of Mycosis fungoides (MF) involvement to the kidneys through specific IHC and T-cell PCR-confirmed clonality testing. It highlights advances in therapy for localized disease and underscores the importance of confirming T-cell clonality, especially in atypical sites like the kidneys, illustrating its potential to enhance targeted therapy in disseminated MF.

We retrospectively analysed bortezomib–dexamethasone–rituximab (BDR) combination in patients with Waldenström macroglobulinaemia (WM) in a real world setting.

Inflammatory form of Waldenström macroglobulinemia (iWM) predicts outcomes after immuno-chemotherapy and Bruton tyrosine kinase inhibitors, but its origin is unknown. Here, we unravel increased clonal hematopoiesis in patients with iWM (61% vs 23% in noninflammatory WM), suggesting a contribution of environmental cells to iWM.

The development of organ-on-chip and 3D culture systems, such as spheroids, have revealed the importance of mechanical cues in regulating signaling pathways to organize cell adhesion and survival.

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In this study, we assessed the impact of nine recurrently mutated genes (BIRC3, EGR2, MYD88, NFKBIE, NOTCH1, POT1, SF3B1, TP53, and XPO1) in pre-treatment samples from 4580 patients with CLL, using time-to-first-treatment (TTFT) as the primary end-point in relation to IGHV gene SHM status.

In the present study, we have identified the dihydroorotate dehydrogenase (DHODH), an essential enzyme for the de novo biosynthesis of pyrimidine-based nucleotides, to be overexpressed in MCL in comparison to healthy peripheral blood mononuclear cells (PBMC).

Mutant Ikzf3 alters DNA binding specificity and target selection, leading to hyperactivation of B cell receptor (BCR) signaling, overexpression of nuclear factor κB (NF-κB) target genes, and development of CLL-like disease in elderly mice with a penetrance of ~40%.