SLC34A2 (Solute carrier family 34 member 2)

These findings indicate patient-specific patterns of tumor evolution in LUAD, with one case showing a progressive AT2-to-tumor transition and another driven by ROS1 fusion-mediated oncogenic signaling. Together, they highlight how transcriptional and epigenetic programs diverge across tumor contexts, contributing to inter-patient heterogeneity in LUAD.

Integrating single-cell and bulk transcriptomes links malignant epithelial state programs to prognosis, yields a practical eight-gene risk model validated in multiple LUAD cohorts, and nominates FAM189A2 as a putative tumor suppressor and potential biomarker in lung cancer. These findings suggest testable strategies for risk stratification and therapy selection that warrant prospective evaluation.

By targeting these transporters with small molecule inhibitors, it may be possible to disrupt essential metabolic pathways in cancer cells, thereby enhancing treatment efficacy and improving patient outcomes. This research establishes a foundation for the development of SLC-targeted therapies in precision oncology, aiming to improve survival rates for patients with OV.

The patient was discharged uneventfully and has not shown any obvious recurrence or metastasis during the 2-month follow-up. Improved prognosis of postoperative incisional metastasis of lung cancer is observed after timely comprehensive treatment.

Currently, mirvetuximab soravtansine and tisotumab vedotin have been approved by the Food and Drug Administration for the treatment of folate receptor-alpha-positive, platinum-resistant ovarian cancer and recurrent cervical cancer, respectively, exhibiting promising objective response rates and manageable toxicity profiles in pivotal clinical trials...Additionally, multiple investigational ADCs, such as upifitamab rilsodotin (targeting NaPi2b), trastuzumab deruxtecan (targeting HER2), and sacituzumab govitecan (targeting trophoblast cell surface antigen 2), have demonstrated preliminary efficacy in ongoing clinical trials, offering new therapeutic opportunities for gynecologic malignancies. This review comprehensively summarizes the current clinical applications and research progress of ADCs in gynecologic cancers, including key clinical trials, therapeutic efficacy, safety profiles, and associated challenges. Furthermore, we discuss future optimization strategies, including the identification of novel targets, rational combination therapies, and molecular design improvements to advance ADC-based precision treatment in gynecologic oncology.

Repeated-dose toxicological assessment in rats indicates that TUB-040 is well-tolerated, with no evidence of lung toxicity or thrombocytopenia. Taken together, TUB-040 is designed to enable long-lasting, durable tumor responses and to optimize both efficacy and tolerability, supporting the advancement of TUB-040 into clinical trials.

In summary, our current research revealed a novel SLC34A2/LRRK2/TTF-1/SELENBP1 axis and its involvement in inhibiting the malignant characteristics of LUAD cells for the first time, which made contribution to further exploring the clinical application of SLC34A2. Furthermore, it also might offer novel insights into understanding how AT2 cells undergo malignant transformation into LUAD cells in the future.

However, challenges like antigen heterogeneity, off-target toxicity, and resistance mechanisms remain. This review highlights the current ADCs used in the clinic for the treatment of ovarian cancer, their challenges, and the future potential of ADC-based therapies in overcoming resistance and improving patient outcomes.

Mineral disturbance in vitro using calcium or phosphate treatment induced deposition of calcium phosphate in a spermatogonial cell line and this effect was fully rescued by the mineralization inhibitor pyrophosphate. In conclusion, testicular microcalcifications arise secondary to local alterations in mineral homeostasis, which in combination with impaired Sertoli cell function and reduced levels of mineralization inhibitors due to high alkaline phosphatase activity in GCNIS and TGCTs facilitate osteogenic-like differentiation of testicular cells and deposition of hydroxyapatite.

L3 (28/1) monoclonal antibodies specific to the MX35 epitope failed to recognize the mutant NaPi2bp.T330M variant compared to the wild-type of the NaPi2b in both Western blot and confocal microscopy experiments. The obtained data may serve as a basis for predicting the efficacy of monoclonal antibody-based targeted therapy binding to the MX35 epitope of NaPi2b in the treatment of oncological diseases.

The five identified AAMRGs in LUAD were validated and appropriately utilized to construct a risk assessment model that could potentially act as prognostic biomarkers for LUAD patients.

Finally, we found that potential drugs such as Cisplatin can benefit high-risk LUAD patients. In-vitro experiments demonstrated that silencing of Angiopoietin-like 4 (ANGPTL4), Gap Junction Protein Beta 3 (GJB3), Family with sequence similarity 83-member A (FAM83A), and Anillin (ANLN) reduced the number of invasive cells and the wound healing rate, while silencing of solute carrier family 34 member 2 (SLC34A2) had the opposite effect. This study, collectively speaking, developed a prognosis model with senescence signature genes to facilitate the diagnosis and treatment of LUAD.