A blocking mAb to human SIRPα significantly enhanced the inhibitory effect of rituximab on the growth of tumors formed by Burkitt's lymphoma Raji cells in immunodeficient mice engineered to express human SIRPα.The survival of tumor-bearing mice treated with both the mAb and rituximab was also markedly prolonged in comparison with that of those treated with either Ab alone. Our results thus suggest that the combination of Abs to human SIRPα with therapeutic Abs specific for tumor antigens warrants further investigation for potential application to cancer immunotherapy.

The interactions between ovarian cancer cells and macrophages promoted macrophage recruitment dependent on increased periostin production.

We designed two novel lipopeptides as anti-tumor immunoadjuvants that can coat tumor cell surfaces. Tumor cells coated with these engineered lipopeptides (called bacteria-mimicking tumor cells) promoted DC phagocytosis and antigen cross-presentation via TLR2 and induced the strong anti-tumor effect.

HiPorfin (HPD)-induced SDT killed tumor cells, promoted calreticulin expression on the cell surface and provoked immune responses. Meanwhile, we observed functional antitumor vaccination and the abscopal effect as a result of SDT in H22 tumor-bearing mice. Furthermore, this strategy conferred an immunological memory, which could protect against tumor recurrence after elimination of the initial tumor.

In A549 and H1299 cells, overexpression of malat1 increased SP1 stability. In turn, SP1 transcriptionally regulated malat1, thus forming a positive feedback loop and promoted SP1 target gene expression, which was involved in malignant transformation and carcinogenesis.

SLP-2 inhabits the apoptosis by the activation of MEK/ERK signaling pathway and the suppression of the mitochondrial apoptosis pathway in human cervical cancer cells and the expression of SLP-2 is up-regulated under stress of high cisplatin concentrations.

LKB1 is negatively correlated with Snail at protein level in pancreatic cancer (PC). Loss of LKB1 promotes PC's metastasis via elevating Snail protein in AMPK-independent pathway. LKB1 enhances E3 ligase FBXL14 to interact with Snail protein, leading to increasing ubiquitin-mediated Snail degradation Metformin inhibits metastasis through LKB1-mediated Snail ubiquitination in PC cells.

miR-491-5p is remarkably downregulated in gastric cancer. Restoration of miR-491-5p could effectively inhibited tumor growth and metastasis. We discovered that miR-491-5p directly targeted SNAIL and indirectly inhibited FGFR4, resulted in suppressed EMT and tumor metastasis.

Decreased expression of miR-708-3p was correlated with metastasis in breast cancer. Overexpression of miR-708-3p inhibits breast cancer cell metastasis and enhances chemosensitivity of breast cancer cells by inhibiting EMT.

This study is the first to demonstrated that PRMT9 is an oncogene that plays an important role in HCC invasion and metastasis through EMT by regulating Snail expression via activation of the PI3K/Akt/GSK-3β/Snail signalling pathway. Thus, PRMT9 may serve as a candidate prognostic biomarker and a potential therapeutic target.

LncRNA RP11-552M11.4 correlates with worse prognosis, and promotes cell proliferation, migration, invasion, and inhibits cell apoptosis by down-regulating BRCA2 in epithelial ovarian cancer cells.

The authors provide new insights into the role of periostin in lung fibrosis and metastatic colonization. Inhibition of periostin implies a rational therapeutic concept for targeting the premetastatic niche which promotes lung metastasis.

The extremely potent miR-143#12 enabled us to well understand K-Ras signaling networks and shut them down by combination treatment with this miRNA and EGFR inhibitor in K-Ras-driven colon cancer cell lines.

Metabolic stress is one of the mechanisms that leads to elevated Pim1 expression in CRC, and Pim1 upregulation ensures CRC growth in response to metabolic stress by facilitating the Warburg effect in a compensatory way.

C57BL/6 mouse transplantable C57BL/6 mouse gastric cancer cell lines were established. These cell lines would be useful for analysis of the molecular function of trans-gene or knockout in a C57BL/6 mouse background, and gastric cancer immune therapy. Identification of the efficacy of FGFR4 blockade is a pertinent example of how these mouse cancer lines can be used for analyzing the effectiveness of cancer therapy.

This is the first report in which afatinib-resistant cell lines were experimentally established using HER2-altered NSCLC cell lines, and their resistance mechanisms were thoroughly investigated. As a result, the afatinib-resistant NSCLC cell lines displayed various resistant mechanisms such as MET amplification, loss of HER2 amplification, and epithelial to mesenchymal transition or cancer stem cell-like features, with specific sensitivity to various drugs such as MET-tyrosine kinase inhibitor crizotinib.

This study demonstrated that the scFvs from dynamic screening by ribosome display in a natural state could result in high-affinity evolution to recognize the microspheres. The scFvs could effectively inhibit the microspheres’ collective growth and invasion through targets that might be CD44⁺/CD24⁺. When combined with chemotherapy, the scFvs exhibited enhancement of their high-affinity efficiency in inhibiting the proliferation and invasion of microspheres in vitro and in vivo.

A single transposon vector efficiently induced malignant glioma. Co-transduction of two transposon vectors spontaneously generated intratumoral heterogeneity.

TNF-α acts as a regulator of increased prostate cancer cell migration via upregulation of CCR7. Targeting TNF-α and ultimately the CCL21/CCR7 axis my be a novel therapeutic strategy in prostate cancer.

PLGF enhanced the migration, invasion and tumorsphere formation of GBC cells through inducing miR-19a expression by upregulating c-MYC. Thus, PLGF may be a promising molecular therapeutic target for GBC.

Vaccination-induced immune response could improve prognosis of HLA-A* 2402-positive patients and immune responses that occur shortly after initiating therapy could be used to predict the therapeutic effect. In addition, an HLA-A status double-blind biologically randomized study, what we call “HLA key open method”, could have some limitations due to potential cross-reactivity of the peptides to other serotypes.

Bortezomib plus dexamethasone showed better 1-year progression-free survival than thalidomide plus dexamethasone in patients with relapsed or refractory multiple myeloma.

Kaplan-Meier curves of (a) local control and (b) overall survival following re-irradiation

The absence of grade 3/4 neutropenia during cabazitaxel therapy was significantly associated with shorter overall survival.

In this retrospective study, we analyzed the predictive value ot the expression of IDO1 on tumor tissue of renal cell carcinoma patients undergoing checkpoint inhibition. A signifcanty correlation between the overexpression of IDO1 in tumor endothelial cells and response to nivolumab therapy could be found for the first time.

This article reports the first study of taselisib administration in Japanese patients with solid tumors or hormone receptor (HR)-positive advanced or recurrent breast cancer. In this phase I, multicenter study, taselisib was well tolerated, with no dose-limiting toxicities or deaths reported. All patients who achieved partial response were positive for PIK3CA gene mutations.

A phase II trial of postoperative adjuvant chemotherapy with paclitaxel and nedaplatin for cervical cancer was conducted. The 2-year RFS and OS were 79.0% and 93.5%, respectively. Treatment was effective and feasible, and phase III trials are warranted.

We firstly evaluated the efficacy and toxicity of anti-EGFR therapy concurrently with induction chemotherapy in advanced nasopharyngeal carcinoma. We found that additional anti-EGFR could prolong survival outcomes.

Tumor uptake of 18F-FBPA was well correlated with that of BPA. Thefore, 18F-FBPA PET would be a powerful tool to estimate 10B concentration in tumors and predict the therapeutic effects of BNCT.

Simvastatin significantly suppressed tumor angiogenesis promoted by HIF-1α-induced pro-angiogenic factors in 4T1 tumor cells. Further inhibition of AMPK phosphorylation by compound C almost completely abrogated simvastatin-induced anti-angiogenesis, which was accompanied by the reduction of protein levels of HIF-1α and its downstream pro-angiogenic factors.

The present study demonstrated that fluorescence contrast-enhanced imaging following intravenously administered indocyanine green (ICG), a fluorescent contrast agent, can be applied to the detection of colon tumors in a mouse colitis-associated colon cancer model. The tumor tissue preference of ICG in the present model can be attributed to the enhanced vascular leakage of ICG involving inflammatory mediators, such as COX-2 and iNOS, in conjunction with increased tumor vascularity.

Triple-negative breast cancer (TNBC) is the most intractable subgroup as, so far, there are no effective targeted drugs. Studies indicated that TNBC has shown high sensitivity to c-Src inhibitor in vitro but is of limited benefit in clinical tests. Our study showed that vimentin is a crucial molecule to affect the therapeutic effects of the c-Src inhibitor in TNBC, and it provides an important rationale for the clinic to precisely select TNBC patients who would benefit from c-Src inhibitor treatment.

The anti-metastatic effect of α-mangostin extracted from mangosteen pericarp was enhanced by conjugation with lauric acid to form synthetic α-mangostin dilaurate, which markedly suppressed wide-spectrum organ metastasis in a mouse model of mammary cancer.

We analyzed targeted blood metabolites quantitatively by gas chromatography/tandem mass spectrometry in a nested case-control study including 170 pancreatic cancer cases and 340 matched controls. We found that some metabolites are useful for early detection of pancreatic cancer but are not associated with the risk of pancreatic cancer.

Angioimmunoblastic T-cell lymphoma (AITL) is a distinct subtype of nodal peripheral T-cell lymphoma (PTCL). Somatic RHOA mutations, (most frequently c.G50T, p.G17V RHOA mutation) are a genetic hallmark of AITL. Our results showed that a combination of NGS, ddPCR and PNA-LNA clamp methods increased the detection rate of RHOA mutations at the p.G17 position.

A new methodology for quantification of DNA methylation based on high-performance liquid chromatography has been developed using an anion-exchange column. Examination of tissue specimens indicated that this can be a powerful tool for DNA methylation diagnostics in a clinical setting.

This is the first study using the proteomics technique to find a diagnostic marker for metastatic NSCLC. It provides an objective basis for the early diagnosis, early treatment and prognosis of metastatic NSCLC, and provides a key point for the diagnosis of other cancerous solid tumors. It also provides a new idea for non-invasive biomarkers for other metastatic cancers, and the clinical application of exosomes will have better prospects.

Our study revealed that EBV infection promotes the production of CCL5, which increases VEGF expression and NPC angiogenesis by interacting with the PI3K/AKT and HIF-1α pathways.

Dead tumor cells are delivered to draining lymph nodes via lymphatic vessel. CD169+ macrophages in the regional lymph nodes capture dead tumor cells and present the tumor antigen to CD8+ T cells. The activated CD8+ T cells travel to the bladder tumor and suppress their proliferation.