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Hybrid aluminum dialkylphosphinates were synthesized from mixed diethyl-, ethylisobutyl-, and diisobutylphosphinates and Al3+ in water. The XRD, DSC, and TGA results of these Al phosphinates established that phosphinate ligands are randomly distributed in the species. The thermal and thermoxidative stabilities of the hybrid phosphinates were easily adjustable by varying the ratio of phosphinate ligands, a desirable feature for efficient flame retardants. The hybrid aluminum dialkylphosphinates with a relatively low ratio of diethylphosphinate demonstrated higher efficiency than Al diethylphosphinate and Al diisobutylphosphinate in flame-retarding polyamide 66. Detailed investigations on the thermal and thermoxidative stabilities of Al dialkylphosphinates and the morphologies of char obtained in UL-94 tests revealed that timely vaporization of degradation products of hybrid dialkylphosphinates at a temperature which closely matches the degradation temperature of polyamides and their ability to promote char formation of polyamides are two key factors which contribute to the excellent performance of hybrid aluminum dialkylphosphinates. [ABSTRACT FROM AUTHOR]

In this work, an organophosphorus flame retardant (BHD) was synthesized using 4‐formylphenylboronic acid and 1,6‐hexanediamine; a charring‐coupling agent containing epoxy (DE) was synthesized using daidzein and epichlorohydrin. The BHD and DE were reacted and coated on the surface of aluminum diethylphosphinate (ADP) and the product is identified as BD‐ADP. PA6 with 12 wt% BD‐ADP achieves a UL‐94 V‐0 rating and a limiting oxygen index (LOI) value of 30.0 vol%. Substitute 1.0 wt% DE for BD‐ADP, PA6‐1.0E not only achieves a UL‐94 V‐0 rating, but also goes out before dripping. The time to ignition of PA6‐1.0E is 19 s longer than that of PA6. The flame‐retardant mode is the combination of the gas‐phase effect of ADP and the condensed‐phase effect of DE. In addition, the tensile strength and impact strength of PA6‐1.0E are 103.9 MPa and 6.6 kJ/m2 which are 35.6% and 43.5% more than that of PA6‐12A. Both BD coating and DE contribute to a strong interfacial adhesion between ADP and PA6 which improves the mechanical properties. The DE plays a key role in the flame retardancy and mechanical properties of PA6 blends. [ABSTRACT FROM AUTHOR]

DDX46, a member of DEAD‐box (DDX) proteins, is associated with various cancers, while its involvement in the pathogenesis of breast cancer hasn't been reported so far. The study demonstrated the overexpression of DDX46 in human breast cancer cells and tissue samples, and correlated with high histological grade and lymph node metastasis. Downregulation of DDX46 in the breast cancer cell lines inhibited their proliferation and invasiveness in vitro. Furthermore, the growth of MDA‐MB‐231 xenografts was suppressed in nude mice by DDX46 knockingdown. Taken together, our findings suggest that DDX46 is an oncogenic factor in human breast cancer, and a potential therapeutic target. [ABSTRACT FROM AUTHOR]

T‐cell‐based immunotherapy and immune checkpoint blockade have been successfully used to treat several human solid cancers. The present study attempted to investigate the feasibility and efficacy of the antitumor effect of adoptive cell therapy along with programmed cell death protein 1 (PD‐1) inhibitor on triple‐negative breast cancer (TNBC). Tumor infiltration lymphocytes (TILs) from TNBC mouse tumor tissues were isolated and expanded, and TILs for adoptive cell therapy (TILs‐ACT) were applied in combination with a PD‐1 inhibitor to the TNBC mouse model. The pre‐ and post‐therapy antitumor efficacy, cytokine secretion, and pathological changes were assessed both in vitro and in vivo. We found that TILs exhibited higher IFN‐γ and TNF‐α secretion than conventional T cells. The TILs‐ACT combined with PD‐1 inhibitor promoted active T‐cell infiltration into the tumor tissue and exerted a strong antitumor effect in an in vivo model. Additionally, the strategy could downregulate the expression of inhibitory marker PD‐1 on TILs. In conclusion, PD‐1 blockade regulated T‐cell exhaustion that synergized with adoptive TIL transfer immunotherapy, leading to eradication of established TNBC tumors. These findings might be useful in developing a feasible and effective therapeutic approach for TNBC. [ABSTRACT FROM AUTHOR]

Abstract Objective To measure clusterin expression in pancreatic cancer tissues and cell lines and to evaluate whether clusterin confers resistance to gmcitabine in pancreatic cancer cells. Methods Immunohistochemistry for clusterin was performed on 50 primary pancreatic cancer tissues and 25 matched backgrounds, and clusterin expression in 5 pancreatic cancer cell lines was quantified by Western blot and PT-PCR. The correlation between clusterin expression level and gmcitabine IC50 in pancreatic cancer cell lines was evaluated. The effect of an antisense oligonucleotide (ASO) against clusterin(OGX-011) on gmcitabine resistance was evaluated by MTT assays. Xenograft model was used to demonstrate tumor growth. Results Pancreatic cancer tissues expressed significantly higher levels of clusterin than did normal pancreatic tissues (P < 0.01). Clusterin expression levels were correlated with gmcitabine resistance in pancreatic cancer cell lines, and OGX-011 significantly decreased BxPc-3 cells resistance to gmcitabine (P < 0.01). In vivo systemic administration of AS clusterin and gmcitabine significantly decreased the s.c. BxPC-3 tumor volume compared with mismatch control ODN plus gmcitabine. Conclusion Our finding that clusterin expression was significantly higher in pancreatic cancer than in normal pancreatic tissues suggests that clusterin may confer gmcitabine resistance in pancreatic cancer cells.