CD58 (CD58 Molecule)

In this cohort, 5‑color flow cytometry provided practical MRD assessment in B‑ALL, whereas 10‑color flow cytometry offered greater immunophenotypic detail and improved recognition of low‑level residual disease. These findings support the routine use of flow cytometry‑based MRD evaluation alongside morphology for post‑induction response assessment and risk‑adapted management in B‑ALL.

The CD2 cytoplasmic tail, in combination with CD3z, delivers balanced costimulation that couples brisk tumor debulking to T cell persistence. CD2z therefore may provide a simple, versatile alternative to canonical CD28 and 4-1BB modules for next-generation CAR T therapies.

Collectively, we studied the role of CD2 both as a target for CAR T cell therapy and as a critical costimulatory protein, whose signaling can be rescued using the PD-1:CD2 switch receptor. This receptor can be incorporated into CAR T-cells and provides an effective strategy to overcome CD2-signaling deficiencies.

CD97, CD73, CD86, and CD58 are the best amongst newer markers in B-ALL MRD assessment. Our findings support integrating these into MRD panels to enhance post-therapy MRD detection, thus improving prognostication and guiding treatment decisions.

It serves as an independent prognostic biomarker and a potential therapeutic target. Targeting the CD58-PD-L1 axis may enhance immunotherapy efficacy in gliomas.

The CD2 receptor is an attractive costimulation target owing to its association with T cell receptor signaling and favorable expression profile...We demonstrate that ULBP2-targeted trispecifics with integrated CD2 costimulation and optimized CD3 affinity are superior to higher-affinity CD3 molecules in in vivo mouse efficacy studies. This integrated CD2 costimulation platform, which we termed EVOLVE, represents a next-generation TCE platform to increase T cell effector function in the tumor microenvironment and has the potential to address unmet patient needs by improving the depth and durability of clinical antitumor T cell responses.

This study supplements the current knowledge of the underlying mechanism behind acquired chemoresistance in OVCA. Four differentially methylated genes identified in this study may have the potential to serve as promising epigenetic clinical biomarkers for HGSC chemotherapy resistance.

In this case, the IPE cysts were likely associated with ALL. This rare occurrence may raise awareness of a potential link between IPE cysts and hematological malignancies, and could pave the way for future research to elucidate the underlying pathogenesis and treatment implications.

Patients with high CAMSig scores demonstrated reduced responsiveness to immune checkpoint blockade (ICB) therapy but increased sensitivity to chemotherapeutic agents, such as temozolomide. This study highlights the multifaceted role of CAMs in LGG and their potential impact across cancers, establishing the CAMSig score as a robust tool for prognostic assessment and personalized therapy guidance. By integrating insights into tumor progression, immune modulation, and therapeutic response, this research offers novel strategies for advancing the clinical management of LGG.

This study uncovers a novel vicious crosstalk among macrophages, T/NK cells, and PDAC cells within the tumor microenvironment. Macrophages drive the expressional separation of CD58 via the TGF-β/Smad2/3 signaling pathway. This shift suppresses T/NK-cell activity, allows tumor cells to evade immune killing, and accelerates PDAC progression. In addition, serum sCD58 emerges as a promising diagnostic and prognostic biomarker for PDAC.

In vivo studies showed that CD2-deficient CTLs promoted tumor growth and brain metastasis while affecting metabolic reprogramming by altering key enzyme expressions in pyrimidine biosynthesis and arginine metabolism pathways. The findings suggest that CD2 enhances CTL function against tumor cells and influences their metabolic states, highlighting the role of CD2 in remodeling the brain metastatic microenvironment in breast cancer.

Chemotherapy regimens included vincristine (VCR), methotrexate (MTX), and doxorubicin (DOXO). The constitutive overexpression of ADAM10 in CLL suggests its involvement in chronic leukemic pathogenesis. These findings highlight CD58 and ADAM10 as potential therapeutic targets for overcoming chemoresistance in lymphoid malignancies.