CD37 (CD37 Molecule)

This study provides the first characterization of CD371 expression patterns in PMF, showing significantly different expression profiles compared to controls. While CD371 demonstrated comparable performance to standard markers (CD34/CD38/CD13/CD33) and showed better discrimination than CD123/HLA-DR, these preliminary findings suggest its potential utility for: (1) identifying abnormal CD34+CD117+ populations in PMF, and (2) possible integration into routine clinical workflows, pending further validation in larger cohorts.

This pilot study highlights the activity of low-dose IL-18 "armored" CAR T-cells against refractory AML and their potential to promote CAR T-cell cytotoxicity and innate endogenous anti-tumor immunity. NCT06017258.

While validated across multiple cohorts, experimental studies are warranted to unravel CD37's mechanistic role. Our findings highlight the potential of neutrophil-centric biomarkers in guiding personalized AML therapy.

In TCL models with dependence on MCL-1, combining CAR-37 T cells and the MCL-1 inhibitor AZD5991 increases anti-TCL response and prolongs survival of xenografted mice. These findings suggest that personalized selection of BH3 mimetic/CAR-T combinations could maximize the therapeutic index for patients with TCL and possibly other diseases.

As previously reported, both CD2 and CD371 were positive in all cases with DUX4::IGH fusion, suggesting that the combination of CD2 and CD371 could be a more reliable marker for detecting the presence of this fusion. Identification of DUX4::IGH fusion in ALL could be possible more easily by a simple multiplex PCR strategy.

Anti-IL6 antibody tocilizumab improved the ADC's cytotoxic activity in CD37+ cells...Adding idelalisib or venetoclax overcame resistance in the resistant derivative and improved the cytotoxic activity in the parental cells. In conclusion, targeting B-cell lymphoma with the naratuximab emtansine showed vigorous anti-tumor activity as a single agent, which was also observed in models bearing genetic lesions associated with inferior outcomes, such as MYC translocations and TP53 inactivation or R-CHOP resistance. Resistant DLBCL models identified active combinations of naratuximab emtansine with drugs targeting IL6, PI3Kδ, and BCL2.

Our work revealed that the clinically relevant anti-CD37 antibody drug conjugate (ADC) Debio 1562 (αCD37-DM1) is highly cytotoxic to AML blasts, but not normal hematopoietic stem cells. We found that αCD37-DM1 improved clinical outcomes and overall survival in multiple in vivo models of AML. Together, these data demonstrate that targeting CD37 with an ADC such as αCD37-DM1 is a feasible and promising therapeutic option for the treatment of AML.

β(2)-MG (>2.3 μg/L) , Follicular lymphoma international prognostic index-1 (FLIPI-1) score (3-5 points) , negative CD37 expression, positive c-Myc expression, and TLG (>2 342.55 g) were all independent risk factors for PFS in the FL patients (HR=3.609, 2.509, 0.255, 3.506, 13.531, all P value<0.05) . (18)F-FDG PET-CT is a powerful complement to FL histopathological grading and the combination of the two may better predict the prognosis of FL patients.

Finally, qRT-PCR, WB and IHC were performed to confirm the elevated expression of RASGRP2 and the decreased expression of TTC9, CD37, DPM3 and ARHGAP4, consistent with the DEG analysis. Conclusively, our findings provide insights into the novel prognostic biomarkers of NPC by mega-data bioinformatics analysis, which suggests that they may serve special targets in the treatment of NPC.

Rituximab (RTX) plus chemotherapy (R-CHOP) applied as a first-line therapy for lymphoma leads to a relapse in approximately 40% of the patients...Importantly, even a major downregulation in CD37 levels does not hamper the efficacy of CD37-directed chimeric antigen receptor (CAR) T cells. In summary, we present here a novel mechanism of CD37 regulation with further implications for the use of anti-CD37 immunotherapies.

Three patients experienced prolonged and severe pancytopenia, and in two of these patients, efforts to ablate CAR-37 T-cells (which were engineered to co-express truncated EGFR) with cetuximab, were unsuccessful. In conclusion, CAR-37 T-cells exhibited anti-tumor activity, with significant CAR expansion and cytokine production. CAR-37 T-cells may be an effective therapy in hematologic malignancies as a bridge to hematopoietic stem cell transplant.

ALA and ELK1 are found to regulate both human granulopoiesis and erythropoiesis via RNA spliceosome, and ALA-ELK1 signal might be the target of human leukemia therapy.