PDGFB (Platelet Derived Growth Factor Subunit B)

Both cases showed classic DFSP morphology and diffuse CD34 expression. These findings expand the molecular landscape of DFSP and illustrate convergent mechanisms of PDGFR-β activation achieved through diverse yet functionally equivalent genomic rearrangements.

The aim of this case report is to introduce the reader to dermatofibrosarcoma protuberans (DFSP). In addition to the general characteristics of this rare skin tumor with possible metastatic potential, we also describe an atypical genetic finding that made our patient's case unique.

Following recurrence and metastasis, the patient was treated with imatinib mesylate and radiotherapy, resulting in a sustained major partial response. This report presents a rare case of aggressive sacroiliac spindle cell sarcoma with COL1A1::PDGFB fusion, expands the clinicopathologic spectrum of DFSP and its variants, and underscores the importance of molecular studies for definitive diagnosis, as well as the potential for targeted therapies in managing complex sarcoma cases.

This macrophage-tumor crosstalk was validated by single-cell transcriptomics, genetic perturbation, and coculture experiments. Collectively, our findings define a macrophage-derived PDGFB-PDGFRB axis that drives CRC liver metastasis and highlight a potential therapeutic target for overcoming metastatic progression and immune resistance.

SRSF2 mutations promoted DNR resistance through multiple mechanisms, and targeted combination therapy with PDGFB pathway inhibitors may represent a novel strategy to improve therapeutic outcomes in patients with mutations.

This study establishes the first migrasome-based prognostic model for LUAD, demonstrating both independent survival prediction capability and clinical utility for identifying immunotherapy beneficiaries. The MIGsig signature provides novel biological insights into migrasome-mediated tumor-immune interactions and represents a promising tool for precision oncology applications in LUAD management.

Careful dermatological surveillance is warranted in this patient population. Any new or abnormal skin lesions should prompt early referral, histopathological assessment, and tailored surgical management, preferably with Mohs' micrographic surgery or wide local excision.

These defects sensitized cells to radiation and decreased clonogenic survival after ionizing radiation and PARP inhibition. Ppm1d mutations confer intermediate suppression of the p53 pathway, consistent with the clinical features of PPM1D -mutant DMGs and are associated with radiosensitivity and PARP inhibitor vulnerability.

This case highlights the diagnostic challenges posed by the indolent presentation of DFSP and the importance of early treatment with WLE. Awareness about this rare entity is essential to prevent misdiagnosis and delayed treatment.

Additionally, the transcription factor myocyte enhancer factor 2 C (MEF2C) was found to bind to the promoters of PDGFA, PDGFB, ANGPT1, and ANGPT2, initiating their transcription. Knockdown of MEF2C inhibited the pro-angiogenic activity of MCAM+ myCAFs both in vitro and in vivo MCAM+ myCAFs promote the transcription of pro-angiogenic factors through MEF2C, thereby enhancing angiogenesis and promoting tumor growth in solid-type ACC.

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.

The FKBP9-IGF2BP1 axis may serve as both a biomarker and a therapeutic target to guide the development of new treatment strategies. Further studies are warranted to validate these results in larger patient cohorts and to assess the clinical feasibility of targeting this pathway.