PLIN2 (Perilipin)

These findings demonstrate that EMT status modulates differential lipid handling and stress adaptation in colon cancer cells, linking mesenchymal transition to enhanced LDs biogenesis and survival under lipotoxic conditions. Data are available via ProteomeXchange with identifier PXD071641.

These show different patterns and variants, and have different nomenclature depending on the histological diversity/embryological development of the organ in which they are localized. We also noticed that adenoid cystic carcinoma and basaloid carcinoma have similar histology and are transitional to each other in many organs, necessitating a common nomenclature.

Ocular sebaceous neoplasms showed a relatively high rate of MMR deficiency. Lobular/papillary sebaceous adenomas and atypical neoplasms were frequently MMR-deficient and may carry implications for MTS, whereas organoid-pattern sebaceomas were typically MMR-proficient and showed no clinical evidence of MTS. Moreover, atypical sebaceous neoplasms, which are intermediate-grade and MMR deficiency-associated, may be classified separately from sebaceomas.

Collectively, these findings suggest that MYC expression in SebCA is responsive to FASN inhibition. Pharmacologic targeting of FASN reveals a metabolic vulnerability that may serve as a target for future therapeutic development.

On the translational front, HIF-2α inhibitors (such as belzutifan), strategies that suppress or oxidize lipids to trigger ferroptosis, and interventions targeting glutamine and one-carbon metabolism show promise when rationally combined with ICIs, TKIs, or anti-angiogenic therapies. We propose a stratified decision framework anchored in DCCD state, lipid-droplet/PLIN2 phenotype, ferroptosis sensitivity, and HIF activity, and discuss the emerging roles of radiopathomics (e.g., CT HU-PLIN2 coupling) and circulating metabolic fingerprints in companion diagnostics. Looking toward clinical deployment, advancing standardization within MSI/IBSI and FAIR data principles-and launching biomarker-enriched, prospective multicenter trials-will be essential to demonstrate the real-world value of precision metabolic oncology in the personalized treatment of ccRCC.

The ICVs are immunoreactive for adipophilin and are therefore considered to represent lipid vacuoles. Identifying tumor cells with ICVs in cytology specimens and immunocytochemistry for CK7, CK20, CD5, p40, CDX2, MUC2, KIT, adipophilin, and CEA may be useful for diagnosis.

While not definitive, this evidence may potentially support the transcriptomic and splicing findings. SRPK1 inhibition may remodel the cervical cancer transcriptome in an HPV-linked manner, with SiHa cells exhibiting changes consistent with suppression of oncogenic signaling, whereas C33A cells adapt through translational and metabolic reprogramming.

Foamy cell change is a distinctive cytoplasmic alteration in STIC and HGSC. The presence of this histologic feature should prompt immunohistochemical studies to confirm serous differentiation.

Standardized reporting is crucial for accurate diagnosis, management and prognosis. Improving compliance with core data reporting will enhance the quality of pathological information, which in turn enhances clinical decision making.

In addition, TRPS1 exhibited higher AUC values than GATA3 and adipophilin in differentiating primary and recurrent SCs, although the difference was not significant. Collectively, our findings indicate that the TRPS1/GATA3/adipophilin-based model demonstrated excellent discriminatory efficacy for eyelid malignancies (Kappa = 0.784, micro-average F1 = 0.882, AUC-ROC = 0.964 [95%CI:0.934-0.994]), achieving clinical-grade performance.

This study provides proof-of-concept supporting a nanoparticle-based agent as a LD homeostasis-targeted therapeutic to treat MASLD and related metabolic diseases.

Mechanistically, the hypoxic tumor microenvironment facilitates crosstalk between tumor cells and adipocytes, increasing triglyceride supply from adipocytes. This, in turn, promotes lipid droplet-mitochondria contact in HNSCC cells through PLIN2-CPT1A binding, counteracting cisplatin-induced ROS elevation and contributing to chemoresistance.