Gynecologic cancers remain a major global health burden for women. Their management has evolved toward a gynecologic oncologist‐led multimodal paradigm. While these approaches have improved outcomes, critical limitations persist, including challenges in decision‐making during surgical procedures and suboptimal efficacy coupled with frequent resistance and substantial toxicities during medical management. Recent high‐quality clinical trials have helped refine these areas. In early‐stage cervical cancer, sentinel lymph node biopsy has emerged as a safe and effective alternative to systematic lymphadenectomy, preserving oncologic outcomes while minimizing morbidity. In advanced ovarian cancer, primary debulking surgery has been established as superior to neoadjuvant chemotherapy followed by interval debulking surgery in fit patients treated at experienced centers. Meanwhile, immunotherapy demonstrates promise through strategic combinations, including dual checkpoint inhibition and triplet regimens incorporating chemotherapy and anti‐angiogenic agents. Antibody‐drug conjugates (ADCs) directed against folate receptor alpha (FRα) and tissue factor (TF) have shown durable responses in biomarker‐selected populations. By critically synthesizing these advances, this review seeks to delineate the clinical utility of emerging therapies, highlight knowledge gaps, and inform evidence‐based decision‐making for clinicians and researchers.

T cell activity is fundamental to effective immunotherapies and sustained tumor control. Recent studies have demonstrated that the therapeutic potential of T cells is notably affected by DNA damage dynamics. Notably, DNA damage within T cells is both a predictive biomarker for therapeutic responses and a druggable vulnerability whose modulation enhances the anti-tumor efficacy of immunotherapies and targeted treatments. This review is aimed at assessing current understanding of the origins of DNA damage in T cells, its consequences, and therapeutic implications within the tumor microenvironment and during anticancer treatment. By elucidating the mechanisms through which DNA damage dictates T cell fate and function, we highlight its dual role as a biomarker and a therapeutic target. Our goal is to accelerate the optimization of immunotherapeutic regimens and the development of combinatorial approaches leveraging a dynamically regulated immune microenvironment by integrating T cell-intrinsic DNA damage response into patient stratification and trial design, together with rational optimization of genotoxic therapies and immunotherapy, to enable a durable response while minimizing immune toxicity.