ABT-737

ABT-737 exerts potent antitumor effects through the induction of PANoptosis in hepatocellular carcinoma, providing a promising therapeutic strategy for HCC treatment.

EGCG has been shown to possess antitumor properties in breast cancer cells. Moreover, EGCG has the potential to enhance the apoptotic effects of ABT-737 by suppressing the expression of Mcl-1.

SRT-1720 induces oxidative stress and apoptosis in leukemic lymphocytes through SIRT1-independent pathway(s). In contrast, it enhances antioxidant defense in normal lymphocytes through a SIRT1-dependent pathway. These findings highlight the potential of SRT-1720 as an adjuvant to chemotherapy in T-ALL, particularly in drug combinations demonstrating strong synergism, which may allow dose reduction and decreased toxicity.

In conclusion, curcumin demonstrates anti-tumor activity in human breast cancer cells by inhibiting colony formation, cell migration, and cell survival. Furthermore, curcumin can augment the apoptotic effect of ABT-737 by suppressing the expression of Mcl-1.

Furthermore, Drug sensitivity profiling linked ELFN1 to ABT-737 susceptibility and benzaldehyde resistance through molecular docking. In CRC cells, ELFN1 knockdown significantly inhibited tumor proliferation, migration, and motility. The expression level of ELFN1 may provide insights into tumor development and progression in multiple cancers, including CRC, highlighting its potential utility as an effective prognostic biomarkers and immunotherapeutic targets.

Triple-Negative Breast Cancer can develop resistance to gemcitabine and overcoming this resistance is critical for effective treatment. In silico analysis using GEPIA revealed a relation between hENT1 with Mcl-1 and Bcl2. These findings reveal ABT-737 and NVP-BEZ235 attenuate MDA-MB-231GEMR cell line and show potential implication on reversing resistance in TNBC for further studies.

Small-molecule inhibitors such as ABT-737 and Navitoclax, kinase inhibitors targeting NF-κB (Nuclear Factor kappa-light-chain-enhancer of Activated B Cells) and JAK/STAT (Janus Kinase/Signal Transducer and Activator of Transcription) pathways, and natural compounds including fucoxanthin, peridinin, and thymoquinone have demonstrated the ability to overcome apoptosis resistance in preclinical models. Recent strategies combining MCL-1 inhibitors with antiretroviral therapy or immune checkpoint blockade further highlight the translational potential of targeting BCL-2 pathways. Collectively, the evidence positions the BCL-2 family as a critical determinant of deltaretroviral persistence and leukemogenesis, and as a promising therapeutic axis for the development of novel treatments for HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) and BLV-associated leukosis.

Transcriptomic profiling indicated lactylation-associated immunosuppression (e.g., downregulated CXCL9/10-CXCR3 axis, enrichment of T cell exhaustion markers) and heightened in silico-predicted sensitivity to BCL-2/FGFR inhibitors (ABT-737/AZD4547) in high-risk patients. Collectively, integrated analyses uncovered lactate/lactylation-associated heterogeneity in AML. Our machine learning-based prognostic model predicts survival, therapeutic response, and drug sensitivity, suggesting a potential strategy for precision therapeutics in AML.

In vivo, 23 demonstrated anticancer efficacy comparable to that of the BKM120/JQ1 combination treatment in a KYSE450 xenograft mouse model. Significantly, the senolytic agent ABT737 enhanced the efficacy of compound 23 through the selective clearance of senescent cancer cells. Collectively, this work establishes 23 as a promising PI3K/BRD4 dual-targeting lead and supports senescence induction combined with senolytics as a novel strategy for esophageal cancer treatment.

For this purpose, we combined this drug with the BH3 mimetics ABT-199 and ABT-737, which inhibit anti-apoptotic members of the Bcl-2 family, and with the PDK1 inhibitor dichloroacetate (DCA), respectively. Mechanistically, the expression of Bcl-2-family proteins was explored, exhibiting increases in pro-apoptotic, but also in anti-apoptotic, proteins upon ibrutinib treatment and a relative increase in the amount of the pro-apoptotic protein PUMA after treatment with DCA. Our data provides new insights into combined therapies with ibrutinib for CLL, which further expands our knowledge and the potential of this drug for cancer treatment.

This systematic review demonstrates that inhibition of Bcl-2 family anti-apoptotic proteins can potentiate the efficacy of standard treatments for prostate cancer. These findings provide a compelling rationale for further research into targeted combination therapies to overcome therapeutic resistance in PCa.

We have constructed an angiogenesis-related gene prognostic signature that enriches the prognostic assessment system for AML and provides novel therapeutic directions for this disease.