CD123 (Interleukin 3 Receptor Subunit Alpha)

P1, N=10, Active, not recruiting, City of Hope Medical Center | Trial completion date: Nov 2025 --> Jan 2027 | Trial primary completion date: Nov 2025 --> Jan 2027

PVEK, with convenient dosing, led to high, durable responses, especially in frontline BPDCN, and a manageable safety profile.

In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets.

The t(16;21)(p11;q22) FUS::ERG fusion gene is rare in pediatric AML and associated with poor prognosis. Allo-HSCT may mitigate the adverse prognostic impact of the FUS::ERG fusion gene and contribute to prolonged survival.

NXP900 also synergized with gemcitabine/cisplatin chemotherapy, enhancing antitumor efficacy in both in vitro and in vivo models. IL13RA-AKT signaling was upregulated in resistant models; NXP900 sensitivity could be restored with AKT or IL13RA2 inhibition. Together, these findings demonstrate the therapeutic potential of NXP900 as a novel YAP inhibitor in CCA and support further investigation in a clinical trial.

We demonstrate that DISCERN can track phenotypic plasticity in leukemia cells and identify stem-like subsets in leukemia xenograft models. This cost-effective and robust platform provides a promising tool for AML risk stratification, relapse prediction, and precision therapy.

Validation of the prognostic FCM-PS in an independent patient cohort confirmed good discrimination performance (AUC: 0.70). We introduce a unique, easy-to-use prognostic FCM-PS score (panel: CD45/CD34/CD117/CD33/CD19/CD123/HLA-DR) for OS in MDS, allowing refined risk stratification for IPSS-R subgroups.

AML with KMT2A-PTD shows distinctive immunophenotypic features with increased CD123 and aberrant CD25 expression, both associated with FLT3-ITD. These markers may have diagnostic and therapeutic relevance in this AML subtype.

We propose the "Hamburger Sign" to describe characteristic imaging findings of the blastic plasmacytoid dendritic cell neoplasm, that is, the dermal T2-dark "patty" is sandwiched by tumor "buns" and the superficial and deep tumor components. Early recognition of this sign may prompt appropriate immunohistochemical work-up (plasmacytoid dendritic markers of TCF4, CD123, and TCL1) and expedite diagnosis, particularly when initial biopsy suggests undifferentiated carcinoma.

Serial assessments were performed before and during treatment with bortezomib and dexamethasone for MM, and later with daunorubicin/cytarabine for AML. It demonstrates the earliest events in pDC-AML evolution. Furthermore, the immature immunophenotype raises the question of appropriate treatment, since a diagnosis of acute undifferentiated leukemia can be established.

Disruption of the secretion of secreted cytokines in serum and peritoneal fluid in patients with ovarian cancer may lead to their pro-inflammatory activation, indicating that modulation of cytokines of the IL-1 family may affect the course of the inflammatory process that accompanies the development of cancer. The observed perturbations involving the cytokines studied may represent one of the more important immune mechanisms that promote the development of this cancer, indicating the need for new complex therapies targeting a wide variety of immune response mechanisms, but this requires further, more advanced research.

The 4-year overall survival (OS) and event-free survival (EFS) rates for the entire cohort were 94.4% ± 5.4% (95% CI, 83.8%-100.0%) and 87.7% ± 8.2% (95% CI, 71.6%-100.0%), respectively. Paediatric patients with BPDCN who receive allogeneic HSCT-particularly haploidentical HSCT-during CR following ALL-like induction chemotherapy appear to have favorable outcomes in this limited cohort.