In vivo experiments confirmed that ATM knockout (ATM KO) or treatment with small-molecule ATM inhibitor KU55933 markedly inhibited osteoclastogenesis of SK-BR-3 cells and the progression of breast cancer bone metastasis. Our results underscore the pivotal role of ATM in regulating NFκB-CCL2 expression and promoting the progression of breast cancer bone metastasis.

Moreover, our analysis identified six subtype-specific drugs, such as KU_55933 and Cyclophosphamide, that were more sensitive to PS1. In conclusion, this study successfully constructed and evaluated a pathway-based molecular subtype and classification model for HCC, thoroughly investigated the biological and multi-omics differences between subtypes. Additionally, the identification of three telomere-associated biomarkers offers guidance and a theoretical basis for personalized treatment and clinical use of drugs for HCC patients.

Here, we studied three approved PARPi, niraparib, olaparib, and rucaparib in three ovarian cancer cell lines and their cisplatin-resistant sublines. Notably, cisplatin resistance was not directly correlated with PARPi resistance, and ATM and ATR inhibitors can increase PARPi activity against cisplatin-sensitive and -resistant ovarian cancer cells. Moreover, we demonstrated for the first time that cell adhesion-mediated resistance can contribute to PARPi resistance, which can also be alleviated by ATR and ATM.

A total of 135 drugs differed in sensitivity between HRG and LRG, including KU.55933...Expression analysis showed that CTSK was significantly downregulated in the BLCA group, while MTERF3, SRC, and CSNK2B were significantly upregulated. In conclusion, CTSK, MTERF3, SRC, and CSNK2B laid the foundation for targeted therapy in the treatment of BLCA.

P2, N=63, Active, not recruiting, EMD Serono Research & Development Institute, Inc. | Recruiting --> Active, not recruiting | N=130 --> 63

Inhibitors such as KU-55933, KU-60019, and AZD1390 have shown the potential to sensitize cancer cells to radiotherapy by impairing DNA repair, thereby enhancing treatment efficacy...Currently, none have gained approval from the FDA or EMA, but six candidates, AZD1390, AZD0156, ZN-B-2262, SYH2051, WSD0628 and M3541 are in clinical trials, often as adjuncts to radiotherapy or in combination with PARP inhibitors. Their safety and effectiveness, however, are still under investigation. This review synthesizes ATM's dual roles and the therapeutic promise of targeting ATM in cancer radiotherapy.

AMA demonstrates significant antitumor activity against NPC by inducing apoptosis, causing cell cycle arrest, and inhibiting HRR. These findings suggest AMA as a promising therapeutic or adjuvant agent for NPC.

We used AZD0156, an ATM inhibitor, and VE-822, an ATR inhibitor, in combination with normo-fractionated RT to treat two HPV-positive and two HPV-negative HNSCC cell lines. In co-culture with NK cells, an upregulation of activation markers on NK cells was observed, particularly after contact with RT + ATMi-treated HPV-negative HNSCC cells. We conclude that ATM inhibitor-related induction of senescence in HNSCC cells shapes the tumor micro-environment in way that NK cell phenotype is changed.

P1, N=94, Recruiting, Mayo Clinic | N=67 --> 94

P=N/A, N=25, Active, not recruiting, Fujian Cancer Hospital

P2, N=130, Recruiting, EMD Serono Research & Development Institute, Inc. | N=60 --> 130

P1/2, N=138, Not yet recruiting, Sun Yat-sen University Cancer Center, Fujian Provincial Cancer Hospital; CSPC Megalith Biopharmaceutical Co., Ltd..