PDGFRB (Platelet Derived Growth Factor Receptor Beta)

Reference inhibitors (osimertinib-EGFR, ibrutinib-BTK, THZ1-CDK7, and THZ531-CDK12) reproduced the expected geometries and served as internal controls. Although no quantitative affinity was inferred, the consistent geometric feasibility supports their potential as structural templates for covalent-binding natural scaffolds. These results provide a qualitative, structure-based rationale for further chemoproteomic and enzymatic validation of NP-derived or hybrid compounds as potential leads in cancer therapy, expanding covalent chemical space beyond existing synthetic scaffolds.

This fusion drives tumorigenesis and forms the basis for imatinib treatment, which acts by blocking platelet-derived growth factor receptor-beta kinase activity...In this editorial commentary, we briefly highlight the ever-growing genomic landscape of DFSP, report rare fusions and their biological implications, and examine the role of expanded molecular diagnostics in refining diagnosis, guiding therapy, and informing prognosis. Incorporating comprehensive fusion analysis into routine workup may be critical for accurate classification, especially in unusual presentations where reliance on morphology alone risks misdiagnosis.

Early clinical experience with [¹⁷⁷Lu]Lu-PSMA radioligands and ongoing trials such as RENALUT and PRadR are exploring the feasibility of radioligand therapy targeting PSMA-positive ccRCC neovasculature. Although biological and kinetic barriers persist, PSMA-based imaging and therapy represent a feasible, rapidly translatable platform that bridges diagnosis and targeted treatment, marking a pivotal step towards personalised, imaging-guided management of advanced ccRCC.

Interventions utilizing a range of inhibitors at the in vitro level, including the PDGFR-β inhibitor AG1296, the PI3K inhibitor LY294002, the AKT inhibitor MK2206, and the FAK inhibitor Y15, demonstrated that E. multilocularis protoscoleces protein (EmP) induces angiogenesis through PDGFR/PI3K/AKT/FAK signaling pathway. Our findings provide new perspectives on how E. multilocularis infection triggers pathological angiogenesis in the host liver, and may provide a novel anti-angiogenic therapeutic strategy against E. multilocularis infection.

LG2 mainly exerts anti-tumor effect on lung cancer by inhibiting the PI3K/AKT signaling pathway, regulating tumor stemness, and ferroptosis. These findings provide a mechanistic rationale and potential therapeutic strategy for the application of LG2 in lung cancer treatment.

Our results also indicate an association between CCT/TRiC chaperonins and the regulation of tubulin/actin, supporting their involvement in cytoskeleton dynamics, the mitotic spindle, chromosome segregation, and autophagy/aggrephagy. Overall, our findings expand the repertoire of chaperone client proteins and provide insights into how chaperone dysregulation influence breast cancer biology, highlighting their potential as therapeutic targets.

Platelet-derived growth factor receptor beta (PDGFRB)-rearranged myeloid/lymphoid neoplasms (MLNs) are rare hematologic malignancies typically responsive to tyrosine kinase inhibitors (TKIs) such as imatinib. The patient progressed to acute myeloid leukemia (AML) within 11 months despite sequential therapies including dasatinib and azacitidine-venetoclax, ultimately succumbing to sepsis. This case highlights the limitations of TKI monotherapy in MLNs with PDGFRB rearrangements and co-existing high-risk mutations, underscoring the importance of early molecular profiling and consideration of allogeneic hematopoietic stem cell transplantation in cases with poor risk features.

Our findings suggest that NOTCH3 ITDs represent a novel oncogenic mechanism in pericytic tumour pathogenesis, likely driving constitutive activation of the NOTCH signalling pathway. Given the potential therapeutic relevance, particularly in aggressive or life-threatening cases with CNS involvement, our findings highlight the importance of extensive molecular profiling. Targeted therapy with NOTCH inhibitors may represent a promising strategy in the management of aggressive cases of ITD-driven pericytic tumours.

We sequenced genomic DNA from patients (n = 20) with a known or suspected TK gene fusion and identified rearrangements in 18 cases, including all cases with a known TK fusion, typical and atypical BCR::ABL1 rearrangements, an 843Kb deletion causing a FIP1L1::PDGFRA fusion, novel AGAP2::PDGFRB and NFIA::PDGFRB fusions, and a complex CCDC88C::PDGFRB rearrangement with multiple translocation events. The approach was fast (<72 h/sample from DNA to result), flexible with minimal hands-on laboratory time, and provided accurate, patient-specific characterisation of genomic breakpoints.

This study established a genetic-transcriptional regulatory framework for sintilimab-induced thyroid irAEs and identified a candidate gene set with biomarker potential. Our findings highlighted the central role of complement-driven mechanisms, providing a foundation for precision risk prediction and targeted intervention strategies that preserve antitumor efficacy while mitigating autoimmune toxicity.

Their aggressive clinical behavior, combined with unique histopathological and genetic features, underscores the need for molecular testing to ensure accurate diagnosis. Tyrosine kinase inhibitors such as imatinib may hold therapeutic promise, but further research is needed to optimize treatment strategies.

The immune-related gene PDGFRB demonstrated significant prognostic value in GC and may serve as a potential biomarker for immune response modulation. Our findings highlight its association with tumor progression and tumor microenvironment characteristics, supporting its role in GC prognosis evaluation.