AGR2 in malignant cells regulates cell-cell communication by coordinating cytokine-chemokine signaling and immune infiltration. AGR2 could affect tumor immune microenvironment and thus promoted the progression of breast cancer.

The stimulation of BW5147.3 cells expressing objective TCRs with a single dose of antigenic peptides and analysis combining the expression of CD69, CD137, and PD1 allows us to select highly responsive T cell receptors.

1. Programmed death ligand 1 regulates cancer stem cells in hepatocellular carcinoma.
2. Programmed death ligand 1 regulates liver cancer cell migration, invasion, and epithelial–mesenchymal transition.
3. Programmed death ligand 1 regulates epithelial–mesenchymal transition and cancer stem cells through serum and glucocorticoid kinase 2/β-catenin signaling.

Our study found that MED27 was highly expressed in breast cancer, especially in triple-negative breast cancer, and promoted breast cancer cell metastasis and stemness maintenance by targeting KLF4 both in vitro and in vivo. Mechanistically, MED27 transcriptionally activated KLF4 in breast cancer cells by binding to its promoter region. MED27 silencing sensitized breast cancer cells to epirubicin therapy and the high expression of MED27 and KLF4 alone or together were positively correlated with the differentiation status of cancer cells and predicted poor prognosis of breast cancer patients.

In the present study, we evaluated the potential mechanism(s) of STAT3-induced 5-fluorouracil (5-Fu) resistance in colorectal cancer (CRC). Our results show that STAT3 regulates 5-Fu resistance in CRC by promoting Mcl-1–dependent cytoprotective autophagy. Our results provide a novel role of STAT3 and may offer a new approach for the management of CRC 5-Fu resistance.

High SLC3A2 expression in lung adenocarcinoma (LUAD) patients were associated with tumor-associated macrophages and poor prognosis. SLC3A2 in LUAD cells was essential for macrophage M2 polarization. SLC3A2 regulated metabolic properties in LUAD cells. SLC3A2-mediated arachidonic acid secretion promoted macrophage M2 polarization.

ALKBH5 regulated PKM2 by modifying circNRIP1 via competing for sponge actions of miR-541-5p and miR-3064-5p, thereby affecting the glycolytic functions of PTC cells

The present study investigated the status of KRAS/PIK3CA driver mutations in normal endometrial glands as well as spheroids derived from single glands. High mutation allele frequency of PIK3CA mutation in a single gland as well as frequent PIK3CA mutation in stem cell-rich spheroids that originated from a single gland suggest the role of PIK3CA mutation in stem cell propagation.

The main novel finding of this study was that miR-324-3p expression was markedly reduced in OS and miR-324-3p regulated OS growth via targeting PGAM1-mediated aerobic glycolysis. Thus, targeting the miR-324-3p/PGAM1 axis is a promising OS treatment strategy.

In this study, we showed for the first time that the increase of exosomes secreted by gastric cancer (GC) cells caused by Fusobacterium nucleatum (Fn) infection can promote the progression of GC. Mechanistically, our results suggested that Fn infection induced the elevation of exosomal HOTTIP and promoted the proliferation, migration, and invasion of uninfected GC cells through the microRNA-885-3p/EphB2/PI3K/AKT pathway.

In this study, we applied an in vivo CRISPR screen targeting recurrence-related genes. Furthermore, we systematically identified RhoV as a key modulator of breast tumor migration.

Hepatocellular carcinoma (HCC) is one of the most lethal and fastest growing malignancies worldwide. The authors aimed to investigate the differences between patients with HCC based on tumor molecular classification and provide targeted therapeutic options for them. The authors elucidated the cooperation between certain driver genes that leads to different transcriptomic and proteomic profiles, reflecting the intertumor complexity observed in HCC patients and screened out targeted inhibitors of sorafenib-resistant tumors with different molecular classifications.

Genetic and pharmacological inhibition of TIP60 attenuates tumorigenesis in non-small cell lung cancer, implicating that targeting TIP60 could be a novel approach for lung cancer treatment.

Our study found that Fusobacterium nucleatum (Fn) was enriched in early-stage esophageal cancer (EEC) tissues, and the abundance of Fn was associated with the progression of esophageal cancer. We demonstrated that Fn led to tumor progression in vitro and in vivo by inducing IL-32/PRTN3 expression and thereby activating the PI3K/AKT pathway. Our study shows that Fn may be a target for early screening markers and treatment of esophageal squamous cell carcinoma (ESCC) and provides further insight into the pathogenesis of esophageal cancer.

Our results revealed the TGF-β-STAT3/Smad3-PLEK2-PPM1B signaling cascade in TGF-β-induced breast cancer cell migration and invasion. These findings suggest that PLEK2/PPM1B may represent novel targets for breast cancer metastasis intervention.

TRIM36 can promote the occurrence of ferroptosis and finally inhibit the NED of PCa (prostate cancer) cells by inhibiting the ferroptosis-related gene glutathione peroxidase 4 through hexokinase 2 in the ubiquitin glycolysis pathway. This mechanism has great potential to design new strategies to retard NEPC and may help prostate cancer researchers to find potential therapeutic targets for treating NEPC.

This study aimed to examine the effects of the inhibition of sclerostin, an inhibitor of the canonical Wnt pathway, on the development of bone metastases of breast cancer using mouse models. Treatment with an anti-sclerostin antibody significantly increased the bone metastases of MDA-MB-231 cells, which are highly responsive to canonical Wnt ligands. In contrast, bone metastases of other breast cancer cells, 4T1 and E0771/Bone, with low responsiveness or nonresponsiveness to canonical Wnt ligands were not affected by the antibody.

Colorectal cancer tissues have high PKCδ expression. Colorectal cancer cells with wild-type p53 show that the inhibition/CRISPR-mediated knockout of PKCδ leads to p21 upregulation.PKCδ phosphorylates and targets p21 for proteosomal degradation.The increase in p21 levels promotes senescence and leads to a decrease in tumor growth.

We provided a novel concept that CD69 is strongly expressed in epithelial, nonhematological ovarian clear cell carcinoma (CCC) cells. CD69 protein induced in response to fatty acid and oxygen starvation is responsible for fibronectin-driven epithelial–mesenchymal transition, potentially contributing to the poor prognosis of CCC patients.

We found that conditioned medium (CM) of mesenchymal stem cells (MSCs) greatly inhibited in vitro and in vivo tumor growth and angiogenesis, and that insulin-like growth factor binding protein-4 (IGFBP-4) in the MSC-CM was critically involved in the inhibitory effects. This is the first report on the antitumor effects of MSC-CM, of which IGFBP-4 in the CM was shown to play important roles. Thus, cell-free therapy using the MSC-CM could be a safer and promising alternative for even cancer patients.

Ovarian cancers with HR-associated gene mutations show platinum sensitivity, leading to better outcomes. In particular, advanced-stage clear cell carcinoma harboring HR-associated gene mutations demonstrated longer PFS and OS.

This retrospective observational study examined data claims for patients with lung cancer in Japan between June 1, 2019, and March 31, 2020. During this period, the use of single biomarker testing decreased over time while the use of the Oncomine Dx target test (ODxTT), a next-generation sequencing–based multiplex biomarker panel test, gradually increased. These results indicate that biomarker testing frequency has changed the clinical practice in Japan, leading to improvements in time to treatment.

The prospective, single-arm, phase II trial was conducted at multiple institutions for NPC patients who experienced relapse after radical therapy. We found PLDR-IMRT combined with systematic therapy can effectively treat patients with locoregionally recurrent nasopharyngeal carcinoma and causes fewer adverse events than the rates expected with IMRT.

In this manuscript, we developed a rapid genotyping system using a real-time PCR device (GeneSoC), which could detect MYD88 L265P within 15 min. We could detect MYD88 L265P in 8 PCNSL cases during surgery. The MYD88 L265P mutation could also be detected using cell-free DNA derived from the cerebrospinal fluid of two PCNSL cases.

Uncommon EGFR mutation contained heterogeneous subtypes with limited data. We identified significantly worse efficacy of first-generation EGFR-TKIs than afatinib in L861Q; for the frequent application of first-generation TKIs in the real world, this result deserves attention. For resistance mechanisms, the low incidence of T790M, but a high frequency of c-MET amplification, in uncommon mutations differed from common mutations, especially when afatinib was applied. Our results complement the limited available data on uncommon mutations and provide valuable insights.

Of 1954 patients treated with alectinib, 221 were identified from the Japan Medical Data Vision database as receiving lorlatinib; 70% received lorlatinib as a second-line therapy and 30% received lorlatinib as a third- or later-line therapy. The median duration of treatment for all lorlatinib-treated patients was 161 days. This real-world observational study supports data suggesting the effectiveness of lorlatinib after alectinib failure in Japanese patients with ALK-positive non-small-cell lung cancer.

Neoadjuvant chemoimmunotherapy for non–small-cell lung cancer (NSCLC) has achieved an excellent pathological response. The dynamic changes in the tumor immune microenvironment are closely related to the efficacy of neoadjuvant immunotherapy in NSCLC patients. Some special gene alterations, such as ATR kinase, are associated with immune infiltrations and better pathological response using neoadjuvant immunotherapy treatment.

Multiorgan comprehensive epigenomic analysis identified ELF3 as a super-enhancer–associated transcription factor and revealed its oncogenic properties in neuroendocrine carcinoma.

We observed upregulation of the expression of stemness-related and cell-cycle-related genes in recurrent GBM cells. Further, we observed that recurrent GBM tissues showed a decreased proportion of microglia, consistent with previous reports, and that vascular endothelial growth factor A expression and the blood–brain barrier permeability were high, and the O⁶-methylguanine DNA methyltransferase-related signaling pathway was activated in recurrent GBM. Our results provide new insights into treatment strategies for recurrent glioblastomas.

Both C–X–C motif chemokine ligands 9 and 10 (CXCL9 and CXCL10) stained strongly in Epstein–Barr (EBV)-positive pyothorax-associated lymphoma (PAL) but were negative or faintly positive in EBV-negative diffuse large B-cell lymphoma, not otherwise specified (DLBCL, NOS). Double staining for CD20 and CXCL9/CXCL10 demonstrated that most CD20-positive PAL cells expressed CXCL9 and CXCL10. This study shows that the chemokines produced by PAL cells can attract cytotoxic lymphocytes via CXCR3.

We aimed to investigate potential roles of LRRC75A-AS1 delivered by M2 macrophage exosomes in inducing epithelial to mesenchymal transition (EMT) and cervical cancer progression.

miR-152-3p regulates cisplatin resistance in lung cancer by inhibiting autophagy. miR-152-3p suppresses autophagy-mediated cisplatin resistance via NCAM1. NCAM1 targets ERK1/2 to enhance autophagy-mediated cisplatin resistance.

The first report to elucidate the actual pre-analytical laboratory procedures of main Southeast Asian oncology hospitals. An external quality assessment program may improve factors associated with tumor FFPE specimen quality.

We investigated the role of bone marrow adipocytes on cancer cells, by focusing on an invasive front that reflects the direct effects of stromal cells on caner. Bone marrow adipocytes provide a favorable tumor microenvironment for cancer invasion and therapeutic resistance of bone metastasized cancers through cancer-associated fibroblast induction and immune evasion, providing a potential target for the treatment of bone metastasis.