肿瘤特异新抗原对T细胞的反应性能够推动内源性和治疗诱导的抗肿瘤免疫。然而，大多数肿瘤特异新抗原对每个患者来说是独特的（私有），并且针对它们需要个性化的治疗。较小的一部分新抗原包括跨越肿瘤驱动基因和肿瘤抑制基因的突变热点、易位或基因融合以及源于病毒致癌蛋白的表位。这些抗原很可能在患者间共享（公有），在肿瘤内统一表达，并且对癌细胞的生存和适应性至关重要。尽管这些公有新抗原中仅有有限数量的天然免疫原性，最近的研究表明它们在临床上具有实用价值。在本综述中，我们重点介绍了利用经过改造的T细胞目标突变型KRAS、突变型p53以及源于致癌病毒的表位的努力。我们还讨论了在固体肿瘤背景下实现更有效的T细胞疗法时面临的挑战和策略。

T cell reactivity to tumor-specific neoantigens can drive endogenous and therapeutically induced antitumor immunity. However, most tumor-specific neoantigens are unique to each patient (private) and targeting them requires personalized therapy. A smaller subset of neoantigens includes epitopes that span recurrent mutation hotspots, translocations, or gene fusions in oncogenic drivers and tumor suppressors, as well as epitopes that arise from viral oncogenic proteins. Such antigens are likely to be shared across patients (public), uniformly expressed within a tumor, and required for cancer cell survival and fitness. Although a limited number of these public neoantigens are naturally immunogenic, recent studies affirm their clinical utility. In this review, we highlight efforts to target mutant KRAS, mutant p53, and epitopes derived from oncogenic viruses using T cells engineered with off-the-shelf T cell receptors. We also discuss the challenges and strategies to achieving more effective T cell therapies, particularly in the context of solid tumors.