PDGFRB (Platelet Derived Growth Factor Receptor Beta)

Integrating our results with published datasets of AFX and PDS mutation profiles we observed a divergent distribution of alterations in genes signalling through angiogenic pathway (KDR, PDGFRB), DNA damage response (ATR), cellular migration/metastasis (DDR2, CDH1). These differences do not reach statistical significance, and histopathological evaluation remains the diagnostic gold standard, however, they offer valuable insights into the pathogenesis of these tumours.

Eleven genes differentially expressed (p≤0.05) in AAA lesions vs. normal aortas were not reported previously: upregulated: COL6A3, COL15A1, ICAM2, APOD, CIB and SERPINB6; downregulated: GJA1, SCNN1B, NPR1, ACTN1 and PLN. Remaining results confirmed previous reports regarding 21 genes differentially expressed in AAA. qRT-PCR results were in general in agreement with microarray results.

The patient achieved complete remission following the standard 7 + 3 induction chemotherapy regimen for AML with gemtuzumab ozogamicin. This case illustrates the diagnostic challenges posed by concomitant class-defining alterations in hematologic neoplasms and underscores the importance of integrated genomic assessment.

P2/3, N=87, Recruiting, Universita Degli Studi Di Milano Bicocca | Not yet recruiting --> Recruiting

Furthermore, we developed a prognostic risk model that incorporated DDR2, DPYSL3, MFAP5, PDGFRB, and SPOCD1, allowing accurate prediction of patient outcomes based on immunological status. In conclusion, this study highlights that HSPB6 overexpression can restrain the proliferation of BC cells and inhibit EMT, underscoring its potential as a diagnostic marker and therapeutic target in BC.

Furthermore, PDGFRB expression by Fib-like T cells in the affected skin is likely to influence disease severity by regulating TcMT. Additionally, we observe the manifestation of the fibrotic phenotype of T cells in single-cell data from the stromal vascular fraction (SVF) of CRL patients, suggesting that TcMT may be a pathological feature and potential therapeutic target of CRL and providing deep insights into disease pathophysiology.

In conclusion, our data support a role for VAP1 in driving fibroblast activation and cardiac fibrosis. Therefore, targeting VAP1 can be considered as a reasonable approach for the intervention of heart failure.

© 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland

Wistar rats (n = 45; male) were assigned to Control, DEN (200 mg/kg, i.p.), or AFB1 (2 mg/kg, i.p.) groups, each further divided into saline, Ampicillin (50 mg/kg; p.o), or Ciprofloxacin (12.5 mg/kg; p.o) treatments over 21 days-14 days of antibiotics followed by 7 days of AFB1 or DEN co-treatment. Antibiotic misuse may intensify the neurotoxic effects of AFB1 and DEN by increasing oxido-inflammatory responses and neuronal damage, leading to memory impairment and heightened anxiety-like behaviours. Addressing antibiotic misuse and promoting gut microbiota could improve brain health.

No phenotypes present in the original Pdgfrb+/P583R mice were reverted to normal after Stat1 deletion. Therefore, the P583R mouse model mirrored KOGS phenotypes and increased activation of multiple PDGFRb signaling mediators; in this context, STAT1 activity opposes PDGFRb-driven overgrowth and fibrosis.

Two-sample MR showsthat higher PDGFRB expression is associated with lower pancreatic cancer risk (IVW OR ≈0.92), primarily mediated by cg11042320 methylation (~98%), with findings robust to heterogeneity and pleiotropy tests. Together with single-cell evidence, these data prioritize PDGFRB and its epigenetic regulation as actionable targets and ensure functional and multi-ancestry validation.