Ovarian Serous Adenocarcinoma

Nevertheless, the case underscores the importance of comprehensive germline testing and highlights potential, yet underexplored, genetic interactions that may influence ovarian cancer risk. To our knowledge, this represents the first reported case of HGSOC in a patient harboring both variants, offering a hypothesis‑generating observation for future investigation.

P1, N=104, Completed, Royal Marsden NHS Foundation Trust | Active, not recruiting --> Completed | Trial completion date: Jun 2025 --> Oct 2025 | Trial primary completion date: Jun 2025 --> Oct 2025

The following ten drugs received FDA approval in 2025 - avutometinib (inhibiting MEK1/2 in serous ovarian carcinomas), defactinib (blocking FAK in low grade serous ovarian carcinomas), delgocitinib (antagonizing the JAK family in hand eczema), mirdametinib (inhibiting MEK1/2 in type I neurofibromatosis), remibrutinib (blocking BTK in chronic spontaneous urticaria), rilzabrutinib (antagonizing BTK in chronic immune thrombocytopenia), sunvozertinib (blocking mutant exon 21 insertion EGFR NSCLC), taletrectinib (inhibiting mutant ROS1 in NSCLC), vimseltinib (blocking CSF1R in tenosynovial giant cell tumors), and zongertinib (antagonizing mutant HER2 in NSCLC). This article summarizes the physicochemical properties of all 94 FDA-approved small molecule protein kinase inhibitors including the molecular weight, number of hydrogen bond donors/acceptors, ligand efficiency, lipophilic efficiency, polar surface area, and solubility. A total of 45 of the 94 FDA-approved drugs have a least one Lipinski rule of five violation.

Our findings provide new insights into the metabolic and immunological mechanisms underlying SOC, and highlight potential targets for therapeutic interventions.

Ovarian cancer stem cell markers (ZIP-4 and ALDH1A1) can be considered potential prognostic markers in ovarian cancer patients. Moreover, ZIP-4 and ALDH1A1 expressions are related to resistance to platinum-based chemotherapy, which leads to ovarian serous carcinoma progression. Clinical implications suggest that future therapeutic regimens targeting ZIP-4 and ALDH1A1 may help overcome platinum-based chemotherapy resistance and improve patients outcomes.

P2, N=104, Not yet recruiting, Qinglei Gao

The oral drug combination was well tolerated with no dose-limiting toxicity or need for dose reduction over the 4 year period. The Avutometinib and Defactinib combination may represent a new standard treatment option for platinum-resistant and AI-resistant/recurrent LGSOC who have failed other MEKi.

This case underscores the diagnostic challenges of MLA, particularly its ability to masquerade as low-grade or high-grade serous carcinoma on morphology, including cytology, frozen, and permanent sections. We compare the cytologic, histologic, immunophenotypic, and molecular features of MLA and serous carcinoma, highlighting the importance of thorough evaluation to avoid the pitfall of morphology-only diagnosis.

P=N/A, N=1330, Completed, Abramson Cancer Center at Penn Medicine | Enrolling by invitation --> Completed | N=3000 --> 1330

Moreover, SOD2 expression correlated with signatures related to pro-tumorigenic neutrophil and T-regulatory cell populations. Our data suggest SOD2 positively regulates pro-metastatic pathways, and those identified in MCAs more closely reflect gene expression profiles associated with SOD2 expression in patient tumors.

Moreover, HDGF re-expression counteracted the suppressive effects of MAZ knockdown on HGSOC cell malignant behaviors, HUVEC tube formation, M2 macrophage polarization, and the growth of xenograft tumors. In conclusion, our study unveils the MAZ/HDGF axis as a novel SE-mediated oncogenic pathway in HGSOC, providing previously unrecognized insights into SE-driven oncogenesis and highlighting potential targets for HGSOC treatment.

IGF2BP3 knock down, and chemical blockade of de novo cholesterol biosynthesis, both alone or in combination, achieved attenuated disease progression, in vivo. Effectively, our study links RNA modifications with metabolic reprogramming in the HGSC mesenchymal subtype through delineation of a m6A-IGF2BP3-cholesterol biosynthesis axis-mediated regulation of tumor cell stemness and aggression.