Advances in targeted therapy for triple-negative breast cancer / 中国肿瘤临床

Triple negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that is characterized by the lack of estro-gen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER-2), thereby making it difficult to treat. Owing to the aggressive clinical behavior of TNBC and the lack of recognized molecular targets for therapy, patients with TNBC have shown poorer outcomes than those with other subtypes of breast cancer. Chemotherapy is the primary established systemic treatment for TNBC. However, various novel therapeutic targets have come into focus with the advances in molecular characterization of TNBC. In recent years, several targeted drugs have undergone clinical trials and have shown certain curative effects with relatively mild adverse reactions. The Food and Drug Administration has approved some of these drugs. In the current review, we have summa-rized the advances in the targeted therapy of TNBC.

Targeting DNA damage response pathway: recent progress of PARP inhibitors in cancer therapy / 中国药理学通报

Genomic instability is one of the most pervasive characteristics of cancer cells,and DNA damage response (DDR) pathway plays a crucial role in genomic stability.The DDR pathway is a complex signaling network,which involves cell DNA repair,apoptosis and cell cycle regulation.Deficiencies in these repair pathways can result in several different genetic disorders,including cancer.Targeted therapy based on inhibiting the DDR pathway in cancers offers a novel therapy strategy for patients with tumors lacking specific DDR functions.Many small-mole-cule compounds targeting DDR pathway are typically developed for solid cancer therapy.The poly (ADP-ribose) polymerase (PARP) inhibitor is a kind of DDR inhibitors which exploits the principle of synthetic lethality to selectively kill cancer cells.This review highlights the molecular mechanisms of PARP inhibitor action,the progress of PARP inhibitors in cancer therapy,drug resistance and the challenge of PARP inhibitor in the future.

Poly(ADP-ribose)polymerase inhibitors for ovarian cancer treatment:research advances / 国际药学研究杂志

Ovarian cancer is the leading cause of death in women suffering from cancer,with a high mortality rate in gyneco?logical cancer. Poly(ADP-ribose)polymerase(PARP)inhibitors cause targeted tumor cell death in homologous recombination(HR)-deficient cancers,including breast cancer susceptibility gene(BRCA)tumors,and the mechanism is calledsynthetic lethality. At present,there are three PARP inhibitors approved by FDA for the treatment of advanced ovarian cancer with BRCA-mutation. This pa?per reviews the role of PARP inhibitors in the treatment of ovarian cancer in clinical trial,elaborates the therapeutic mechanism of PARP inhibitors,and lights the way for the development of anti-ovarian cancer drugs.

Poly(ADP-ribose)polymerase inhibitors for ovarian cancer treatment: Research advances / 国际药学研究杂志

Ovarian cancer is the leading cause of death in women suffering from cancer, with a high mortality rate in gynecological cancer. Poly(ADP-ribose)polymerase(PARP)inhibitors cause targeted tumor cell death in homologous recombination(HR)-deficient cancers, including breast cancer susceptibility gene(BRCA)tumors, and the mechanism is called “synthetic lethality”. At present, there are three PARP inhibitors approved by FDA for the treatment of advanced ovarian cancer with BRCA-mutation. This paper reviews the role of PARP inhibitors in the treatment of ovarian cancer in clinical trial, elaborates the therapeutic mechanism of PARP inhibitors, and lights the way for the development of anti-ovarian cancer drugs.

Study on 3-nminobenzamide enhancing the radiosensitivity of human esophageal carcinoma cell strain in vitro / 中华放射医学与防护杂志

Objective To evaluate the ability of 3-AB to sensitize the human esophageal carcinoma cell strain (CaEs-17) to radiation in v/tro and its mechanisms. Methods CaEs-17 cells were treated with 3-AB at 0, 2.5, 7.5 mmol/L and given irradiation O, 3, 6, 9, 12 Gy. 3-AB concentration in each group was made dose-survival curve using multi-target single-hit maiths model by clonogenie assay. MTT assay was performed to observe the survival of irradiated cells.comet assay and metaphase chromosome analysis were used to measure the DNA damage degree and chromosome aberration of CaEs-17 cell after 3-AB treatment and irradiation. Results Cell survival experiments showed SER of 1.21, 1.52 for 2.5 mmol/L, 7.5 mmol/L 3-AB respectively using multi-target single-hit maths model. The survival fraction of irradiated CaEs-17 cell was decreased after 3-AB treatment. DNA damage and the chromatid breakage number of irradiated CaEs-17 cells were increased after 3-AB treatment. Conclusions 3-AB, a PARP inhibitor, can enhance the radiosensitivity of human esophageal carcinoma cell strain (CaEs-17). DNA damage repair inhibition by 3-AB might be one of the mechanisms.