The use of chimeric antigen receptor (CAR) in natural killer (NK) cells for cancer therapy is gaining momentum, marking a significant shift in cancer treatment. This review aims to explore the potential of CAR-NK cell therapy in cancer immunotherapy, providing a fresh perspective. It discusses the innovative approaches in CAR-NK cell design and engineering, particularly targeting refractory or recurrent cancers. By comparing CAR-NK cells with traditional therapies, the review highlights their unique ability to tackle tumor heterogeneity and immune system suppression. Additionally, it explains how novel cytokines and receptors can enhance CAR-NK cell efficacy, specificity, and functionality. This review underscores the advantages of CAR-NK cells, including reduced toxicity, lower cost, and broader accessibility compared to CAR-T cells, along with their potential in treating both blood cancers and solid tumors.

ObjectiveThe study aimed to identify distinct molecular subtypes of endometrial cancer (EC) by immunohistochemistry and to analyze their pathological characteristics, independent prognostic factors, and patient survival outcomes for potential clinical applications.Method576 patients with preoperative EC confined to the uterus were divided into three subgroups based on the immunohistochemical detection method: MMR-deficiency (MMRd), P53 wild type (P53wt) and P53 abnormal (P53abn). These subgroups were retrospectively analyzed, and their pathological characteristics, prognostic factors and survival outcomes were compared.ResultsWe identified 401 (69.6%), 123 (21.4%), and 52 (9%) cases of P53wt, MMRd, and P53abn subgroups, respectively. A significant difference was observed in the median age of onset, tumor stage, high-grade tumor differentiation, non-endometrioid carcinoma, myometrial invasion, lymphovascular invasion, the incidence of lymph node metastasis postoperative, and expression of ER and PR receptors among the three groups. Pathological type, lymphovascular invasion, ER and PR expression were identified as independent prognostic factors for disease-free survival (DFS). Additionally, pathological type, lymphovascular invasion, myometrial invasion, and PR expression were recognized as independent prognostic factors for overall survival (OS) in the study cohort. However, the survival outcome for P53abn was the worst, with lymphovascular invasion identified as an independent prognostic factor for DFS. Lymph node status, FIGO stage, and ER expression were identified as independent prognostic factors for OS.ConclusionThe study concludes that immunohistochemical detection-based subtyping of EC holds clinical practicality and can be employed to explore both pathological and clinical prognoses for EC patients.

Cervical cancer is a significant global health concern, with a substantial portion of cases attributed to human papillomavirus (HPV) infection. Recent advancements in molecular profiling have identified distinct subtypes of cervical cancer based on their genomic alterations. One such subgroup is neurotrophic tropomyosin receptor kinase (NTRK) fusion‑positive cervical cancers, characterized by gene fusions involving the NTRK genes. Although both NTRK fusion genes and HPV infections are independently recognized as significant risk factors in cervical cancer, their interplay and mutual effects on cancer progression are not yet fully understood. The present review is the first of its kind to explore the potential interplay between NTRK fusion genes and HPV infections. It surveys in detail how their combined effect can influence the signaling pathways during cervical cancer development and progression. Moreover, the present study discussed the clinical features, histopathological examinations, treatment procedures and follow‑up outcomes of NTRK‑fusion gene‑positive cervical cancer. The present review may help in the understanding of the management and treatment of such rare, lethal and resistant cervical cancers.

Cervical cancer, a prevalent gynecological malignancy, is primarily associated with human papillomavirus (HPV) infection. However, some cases display distinct molecular alterations beyond HPV, significantly impacting the tumor immune microenvironment (TIME) and posing therapeutic challenges. Among these molecular changes, NTRK gene fusions have emerged as critical drivers of tumor progression, invasiveness, and poor prognosis. This review highlights the role of NTRK fusions in cervical cancer oncogenesis, examining their effects on cellular signaling pathways and their interplay with HPV status in shaping TIME. The relationship between HPV infection and NTRK fusions is explored, revealing their combined influence on disease progression. Additionally, the potential of NTRK‐targeted therapies in precision oncology is discussed, emphasizing their promise as treatment options for cervical cancer. By addressing the molecular, immune, and clinical complexities of cervical cancer, this review provides valuable insights into advancing research and therapeutic strategies.