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Background: The incidence of spindle cell/pleomorphic lipomas ranges from 2.2% to 47.2%. Its diagnosis is impeded by its diverse histological features, including adipocytes and myxo-collagenous stroma. Accordingly, we aimed to reexamine oral adipocytic tumors, focusing on RB1-deficient tumors, to reveal the diversity of oral spindle cell lipomas.
Methods: We selected 30 cases of spindle cell/pleomorphic lipomas and their mimics from 111 oral adipocytic tumors. Subsequently, we performed analysis using immunohistochemistry for CD34 and RB protein (pRB) and RB1 fluorescence in situ hybridization (FISH) in limited cases.
Results: Among the included cases, 16 were CD34-positive with pRB and/or the RB1 loss. Among them, 15 were spindle cell lipomas (SCLs) with 27% of them being confirmed through FISH in cases where pRB status was mosaic. These included five low-fat SPLs (including one low-fat pleomorphic lipoma), four conventional SCLs, three fibrous SCLs, two myxoid, and one fat-rich SCL. The remaining case was an atypical spindle cell lipomatous tumor. Only prominent spindle cell and myxoid changes showed significant differences between SCL and fibrous lipoma. Two cases, initially identified as spindle cell lipomas, were reclassified as fibrolipoma and lipoma.
Conclusion: Oral spindle cell/pleomorphic lipomas frequently exhibit prominent collagenous stroma, which results in low-fat and fibrous variants that require careful differentiation from fibrous lipomas or non-adipocytic tumors. Given the diverse histological findings, meticulous diagnosis of rare spindle cell lipoma variants and other lipomas in daily surgical pathology is essential. Specifically, it should apply CD34 and retinoblastoma protein immunohistochemistry, as well as RB1 FISH when necessary.
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http://dx.doi.org/10.1111/jop.70007 | DOI Listing |
Injections have been linked to feline sarcomas (feline injection-site sarcoma; FISS) and cutaneous lymphomas (cutaneous lymphoma at injection site; CLIS). Both tumors often exhibit lymphoplasmacytic inflammation ascribed to injected immunogenic material. CLIS is hypothesized to emerge from transformation and clonal expansion of lymphoid cells following persistent immune stimulation with feline leukemia virus (FeLV) reactivation and transformation.
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September 2025
Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna BioCenter (VBC), Dr. Bohr-Gasse 3, 1030 Vienna, Austria. Electronic address:
PIWI-clade Argonaute proteins and their associated PIWI-interacting RNAs (piRNAs) are essential guardians of genome integrity, silencing transposable elements through distinct nuclear and cytoplasmic pathways. Nuclear PIWI proteins direct heterochromatin formation at transposon loci, while cytoplasmic PIWIs cleave transposon transcripts to initiate piRNA amplification. Both processes rely on target RNA recognition by PIWI-piRNA complexes, yet how this leads to effector recruitment is unclear.
View Article and Find Full Text PDFMol Cell
September 2025
Department of Integrative Structural and Computational Biology, Scripps Research, La Jolla, CA, USA. Electronic address:
In animal germ cells, PIWI proteins use piRNAs to detect active selfish genetic elements. Base-pairing to a piRNA defines transposon recognition, but how this interaction triggers a defensive response remains unclear. Here, we identify a transposon recognition complex composed of the silkworm proteins Siwi, GTSF1, and Maelstrom.
View Article and Find Full Text PDFFront Oncol
August 2025
Department of Pathology, West China Hospital, Sichuan University, Chengdu, China.
In this study, we retrospectively analyzed the clinicopathological features of a case of hepatic infantile hemangioma (HIH) that malignantly transformed into hemangiosarcoma. HIH, a congenital disease, is the most common benign tumor of the liver in children, and its malignant transformation into hepatic angiosarcoma (HAS) is rare. HIH expresses markers of vascular origin and specifically expresses glucose transporter protein isoform 1.
View Article and Find Full Text PDFIn most solid tumors, hypoxia constitutes a defining microenvironmental feature that reprograms malignant cells into a highly metastatic state by driving cellular plasticity and exacerbating chromosomal instability (CIN). However, the mechanisms by which cancer cells concurrently co-opt these elements of hypoxic adaptation to promote metastasis remains poorly understood. Here, we report that hypoxia promotes metastasis by suppressing the JmjC-containing histone lysine demethylase Kdm8.
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