DHANYA K. NAMBIAR¹, DEEPALI MISHRA², RANA P. SINGH^2,3,*

Oncology Research, Vol.31, No.4, pp. 405-421, 2023, DOI:10.32604/or.2023.028310

Abstract Ionizing radiation is frequently used to treat solid tumors, as it causes DNA damage and kill cancer cells. However, damaged DNA is repaired involving poly-(ADP-ribose) polymerase-1 (PARP-1) causing resistance to radiation therapy. Thus, PARP-1 represents an important target in multiple cancer types, including prostate cancer. PARP is a nuclear enzyme essential for single-strand DNA breaks repair. Inhibiting PARP-1 is lethal in a wide range of cancer cells that lack the homologous recombination repair (HR) pathway. This article provides a concise and simplified overview of the development of PARP inhibitors in the laboratory and their clinical applications. We focused on the… More > Graphic Abstract

Qiuyun Luo^*†1, Wentao Pan^*†‡1, Suna Zhou^*†1, Guangfeng Wang^‡, Hanjie Yi^*§, Lin Zhang^*¶, Xianglei Yan^*†, Luping Yuan^*†, Zhenyi Liu^#, Jing Wang^**, Haibo Chen^#, MiaoZhen Qiu^*††, DaJun Yang^*†‡, Jian Sun^*‡‡

Oncology Research, Vol.28, No.4, pp. 331-344, 2020, DOI:10.3727/096504020X15825405463920

Abstract Despite therapeutic advances, the effective treatment for relapsed or refractory diffuse large B-cell lymphoma (DLBCL) remains a major clinical challenge. Evasion of apoptosis through upregulating antiapoptotic B-cell lymphoma-2 (BCL-2) family members and p53 inactivation, and abnormal activation of B-cell receptor signaling pathway are two important pathogenic factors for DLBCL. In this study, our aim is to explore a rational combination of BCL-2 inhibitor plus Bruton’s tyrosine kinase (BTK) blockade or p53 activation for treating DLBCL with the above characteristics. We demonstrated that a novel BCL-2 selective inhibitor APG-2575 effectively suppressed DLBCL with BCL-2 high expression via activating the mitochondrial apoptosis… More >