Inhibition of mouse breast adenocarcinoma growth by ablation with intratumoral alpha-irradiation combined with inhibitors of immunosuppression and CpG
In this study, we investigated the anti-tumor potency of a treatment strategy, which combines DaRT tumor ablation with two approaches for the enhancement of anti-tumor reactivity: (1) neutralization of immunosuppressive cells such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) and (2) boost the immune response by the immunoadjuvant CpG. Mice bearing DA3 mammary adenocarcinoma with metastases were treated with DaRT wires in combination with a MDSC inhibitor (sildenafil), Treg inhibitor (cyclophosphamide at low dose), and the immunostimulant, CpG. Combination of all four therapies led to a complete rejection of primary tumors (in 3 out of 20 tumor-bearing mice) and to the elimination of lung metastases. The treatment with DaRT and Treg or MDSC inhibitors (without CpG) also resulted in a significant reduction in tumor size, reduced the lung metastatic burden, and extended survival compared to the corresponding controls. We suggest that the therapy with DaRT combined with the inhibition of immunosuppressive cells and CpG reinforced both local and systemic anti-tumor immune responses and displayed a significant anti-tumor effect in tumor-bearing mice.
ConclusionThe iodine quantification parameters derived from enhanced DE-CT during the VP may be useful for distinguishing lung squamous cell carcinoma from adenocarcinoma.
Clinical significance and prospective molecular mechanism of C‑C motif chemokine receptors in patients with early‑stage pancreatic ductal adenocarcinoma after pancreaticoduodenectomy. Oncol Rep. 2019 Aug 13;: Authors: Zhou X, Liao X, Wang X, Huang K, Yang C, Yu T, Liu J, Han C, Zhu G, Su H, Qin W, Han Q, Liu Z, Huang J, Gong Y, Ye X, Peng T Abstract The present study aimed to determine the clinical significance and potential molecular mechanisms of C‑C motif chemokine receptor (CCR) genes in patients with early‑stage pancreatic ductal adenocarcinoma (PDAC). The transcriptomic, survival and clin...
EMX2 is epigenetically silenced and suppresses epithelial‑mesenchymal transition in human esophageal adenocarcinoma. Oncol Rep. 2019 Aug 20;: Authors: Wang L, Jin J, Zhou Y, Tian Z, He B, Huang Y, Ding F Abstract Esophageal adenocarcinoma (EAC) is an aggressive and challenging disease to treat, with an overall five‑year survival rate of
ConclusionOligometastatic PC represents nowadays a setting of particular interest in which local ablative therapies play a decisive role. In the present study, we recognized the importance of DFI, together with NCCN class risk, to predict the risk of new metastases after SBRT in oligometastatic PC.
ConclusionDifferentially expressed in tumors, PLA2G4A, PRKCB, PIK3R1, KDR, PLA2G1B and PTGS2 are potential therapeutic targets of Yupingfengsan in the treatment of LAD, and MAPK, VEGF and ErbB signaling pathways are involved.
Condition: Gastric Cancer Interventions: Drug: Sintilimab; Drug: Oxaliplatin; Drug: Capecitabine Sponsor: First Affiliated Hospital of Zhejiang University Not yet recruiting
Contributors : W Zhang ; J Wang ; B Chiu ; L Hou ; Z Zhang ; C ZengSeries Type : Methylation profiling by arrayOrganism : Homo sapiensGenome wide DNA hydroxymethylation profiling of tumor and adjacent tissue samples in pancreatic cancer. The Illumina Infinium MethylationEPIC BeadChip was used to obtain DNA hydroxymethylation profiles across approximately 850,000 CpGs in paired tumor and tumor adjacent tissues in 17 adult patients with primary pancreatic adenocarcionoma .
Conclusions: This study supports the use of NGS as the first-line test for genomic profiling of patients with advanced lung adenocarcinoma.
This study examined whether cancer-associated fibroblasts (CAFs), a major component of a tumor microenvironment, promote cancer cell regrowth after chemotherapy. First, we treated human lung adenocarcinoma cell line A549 and CAFs from four patients with cisplatin. Cisplatin treatment inhibited the viable cell number of A549 cells and induced epithelial –mesenchymal transition. After cisplatin was removed, A549 cells continued to manifest the mesenchymal phenotype and proliferated 2.2-fold in 4 days (regrowth of A549 cells). Cisplatin treatment inhibited the viable cell number of CAFs from four patients also. The...
CONCLUSIONUsing 3D-MDCT, we could accurately divide A4 + 5 and safely perform the surgery.