CYP2W1 (Cytochrome P450 Family 2 Subfamily W Member 1)

This study provides the first comprehensive semi-quantitative proteomic map of CYP450 isoforms across multiple cancer models. The findings reveal metabolic heterogeneity and identify clinically relevant targets, offering a foundation for future functional studies and personalized therapeutic strategies.

Therefore, inhibition of the expression and activity of these orphan CYPs might be more useful in cancer treatment than in prophylaxis. This review summarizes current knowledge of orphan CYPs in breast tissue and their possible application in drug targeting or prognosis assessment.

In summary, we describe a third subtype of PLAG family-altered pediatric CNS embryonal tumor characterized by PLAG1 gene fusion, which leads to upregulation of PLAG1 and downstream genes. We therefore propose to rename ET, PLAGL to ET, PLAG (CNS embryonal tumor with PLAG family gene alteration) together with a specification of the respective subtype.

Furthermore, the placement of a hydrogen bond acceptor on either side of the azole ring differentiated those binding with high and low affinity. These physiochemical features and their relative arrangement within the CYP2W1 active site may inform the development of more selective duocarmycin prodrugs.

Furthermore, CYP2W1 expression was significantly associated with higher histological grade, advanced tumor stage, and a trend toward reduced overall survival (p = 0.082). These findings indicate that CYP2W1 is aberrantly expressed in a subset of pediatric STSs, contributing to tumor aggressiveness and highlighting its potential as a novel therapeutic target for these challenging malignancies.

Moreover, knockdown of circPHKB sensitized liver cancer cells to sorafenib in vivo. The findings reveal a novel circPHKB/miR-1234-3p/CYP2W1 pathway that decreases the sensitivity of liver cancer cells to sorafenib, suggesting that circPHKB and the axis may serve as promising targets to improve the therapeutic efficacy of sorafenib against liver cancer.

The CYP2W1 gene expression was strongly reduced by cell-free supernatants derived from LGG culture, with or without hesperidin. This suggests that the suppression may be due to bacterial byproducts rather than hesperidin. Therefore, the CYP2W1 gene in the case of deregulation of these metabolites may cause CYP2W1-related colon cancer cell proliferation.

Our results suggest that specific genes may be related to increased neuropsychological consequences.

Consistent with the findings in our study, low expression of RRM1, CYP2W1 and SOAT1 was associated with worse DFS with antitumor therapy. The results of the work indicate the need to assess the levels of immunoreactivity of these markers in patients with ACC before starting treatment with mitotane in order to predict the efficiency of therapy.

In summary, we describe a new type of biologically distinct CNS tumor characterized by PLAGL1/2 amplification that occurs predominantly in infants and toddlers (PLAGL2) or adolescents (PLAGL1) which we consider best classified as a CNS embryonal tumor and which is associated with intermediate survival. The cell of origin and optimal treatment strategies remain to be defined.

No associations with survival were observed in the METABRIC cohort. CYP2S1 and CYP2W1 are associated with patient survival in breast cancer and may be important prognostic biomarkers.