
Clinical Nutrition, Год журнала: 2024, Номер 43(11), С. 137 - 152
Опубликована: Окт. 1, 2024
Язык: Английский
Clinical Nutrition, Год журнала: 2024, Номер 43(11), С. 137 - 152
Опубликована: Окт. 1, 2024
Язык: Английский
Cancers, Год журнала: 2025, Номер 17(7), С. 1110 - 1110
Опубликована: Март 26, 2025
Small-cell lung cancer (SCLC) is a highly aggressive malignancy characterized by rapid proliferation, early metastasis, and frequent recurrence, which contribute to poor prognosis. SCLC defined the near-universal inactivation of key tumor suppressor genes, notably TP53 RB1, play central roles in its pathogenesis resistance therapy. The p53 family proteins, including p53, p63, p73, essential maintaining cellular homeostasis suppression. mutations are almost ubiquitous SCLC, leading dysregulated apoptosis cell cycle control. Moreover, p73 shows potential as compensatory mechanism for loss, while p63 has minimal role this type. In review, we explore molecular functional interplay emphasizing members' distinct yet interconnected suppression, immune modulation, therapy resistance. We highlight emerging therapeutic strategies targeting these pathways, reactivating mutant exploiting synthetic lethality, addressing evasion mechanisms. Furthermore, review underscores urgent need novel, isoform-specific interventions enhance treatment efficacy improve patient outcomes challenging disease.
Язык: Английский
Процитировано
0Clinical Nutrition, Год журнала: 2024, Номер 43(11), С. 137 - 152
Опубликована: Окт. 1, 2024
Язык: Английский
Процитировано
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