HMGA2 (High mobility group AT-hook 2)

Furthermore, flow cytometry and colony formation assays revealed that PCZ attenuates and reduces the apoptotic/necrotic effects of ATO. In conclusion, PCZ synergistically and effectively reduces the adverse cytotoxic effects of ATO in lung cancer cells, providing a promising new therapeutic strategy for lung cancer treatment.

The patient remains disease-free at 4 months. This case expands the molecular spectrum of ELMS and, concomitantly, broadens the emerging morphologic spectrum of RAD51B-rearranged uterine sarcomas, underscoring the diagnostic value of fusion testing in unusual uterine mesenchymal neoplasms.

Importantly, this study is the first to reveal the inhibitory role of let-7b-3p in LUAD through the HMGA2-LIN28A axis in regulating the Wnt/TGF-β signaling pathway and EMT. These findings highlight the originality of this work and underscore the potential clinical translational value of targeting let-7b-3p or the HMGA2-LIN28A axis as novel therapeutic strategies for LUAD.

RNA sequencing and RT-PCR of the two lipomas showed the presence of the HMGA2::CIBAR1-DT chimera. The HMGA2::CIBAR1-DT fusion, identified here for the first time, is a recurrent transcript in lipomas.

Our results indicate a role of HMGA2 in the EC, because its inhibition reduces cell malignant characteristics, and may represent a viable therapeutic target to improve the prognosis of CisR TGCTs.

This study revealed uterine leiomyoma subtypes to have distinct chromosomal aberration landscapes. Our large sample collection, detailed subclassification and extensive expression data integration enabled the identification of rare aberrations and subtype-specificity not previously feasible. Further research is implicated in studying the recurrently aberrant regions to identify the specific targets. This study shows, once again, the benefits for accurate subtype information in leiomyoma research and provides a new framework for further studies - towards comprehensive knowledge on the tumorigenesis and potential subtype-specific diagnostic and therapeutic strategies.

In summary, we describe herein the genetic landscape of PDST, demonstrate correlation of genetic features with high-grade versus low-grade histology, and identify TP53 among key oncogenic drivers of HGPDST, including in Li-Fraumeni Syndrome. The genetics of HGPDST overlap with borderline or malignant PT, consistent with their classification as PT variants that arise through a MED12-independent pathway.

RNA sequencing revealed HMGA2 fusions in 8 of the 12 tumors tested. Intra-articular and juxta-articular lipomas of the knee, particularly the herniated intra-articular subset, are likely under-recognized and can be a source of diagnostic concern because of peculiar histology and unawareness of the relationship with the joint.

These results demonstrate the feasibility of AI/ML-based RISH quantification and suggest that elevated wild-type HMGA2 expression may represent a biomarker linked to prostate cancer aggressiveness and racial disparities. These findings highlight the importance of interdisciplinary collaboration and equitable computational tools in advancing biomarker discovery and addressing cancer health inequities.

To our knowledge, this is the first report of an HMGA2::PLCZ1 rearrangement, expanding the molecular spectrum of uterine smooth muscle tumors. This case also emphasizes the biological link between HMGA2 activation and cyclin D1 overexpression, providing new insights into the molecular mechanisms underlying uterine smooth muscle tumorigenesis.

OCS is the most aggressive, drug-resistant gynaecological malignancy and eribulin-based combination therapies, particularly triple combination therapies, have the potential to improve patient outcomes.