Introduction to Tumor Cells

What is/are Tumor Cells?

Tumor Cells - Here, we show that epigenetic silencing of NDRG4 modulates integrin signaling by assembling β1-integrins into large punctate clusters at the leading edge of tumor cells to promote an “adhesive switch,” decreasing cell adhesion to fibronectin and increasing cell adhesion and migration towards vitronectin, an important component of human lymph nodes. ^[1] Circulating tumor cells (CTCs) and cell-free DNA (cfDNA) were evaluated in 89 previously treated NSCLC patients receiving nivolumab. ^[2] iRGD (CRGDK/RGPD/EC) is a kind of tumor-penetrating peptide which can contribute CNs to increasing cancer vascular and tissue permeability in a αv integrin and neuropilin1(expressing at the surface of tumor blood vessel endothelial cells and tumor cells)–dependent manner. ^[3] Correlation of BRD4 binding and drug-mediated displacement at RNA Pol II pause sites with gene expression revealed a differential behavior of sensitive and resistant tumor cells to I-BET and identified a BRD4 signature at promoters of sensitive coding and non-coding genes. ^[4] Complex 1 containing alanine inhibited the cell viability of A549 and K562 tumor cells by inducing apoptosis, as evidenced by an increased number of Annexin V-positive cells and the induction of DNA damage and cell cycle arrest. ^[5] Together we substantiate the identification of novel lead molecules, which may provide a new treatment to overcome selectivity issues and enhance the radiosensitivity of tumor cells, opening a conceptually novel strategy of CDK-targeting for different cancer types. ^[6] Its overexpression is one of the main reasons for the multidrug resistance (MDR) of tumor cells. ^[7] We found multiple correlations between parameters characterizing the immune profiles of tumor cells and TILs in both baseline and on-treatment samples. ^[8] Our first-in-class NKp30xBCMA NK cells engager, CTX-4419, binds to BCMA on MM cells and to NKp30 and CD16A (FcγRIIIA) on NK cells, specifically redirecting NK cells towards tumor cells expressing BCMA. ^[9] However, these methods are unable to eradicate tumor cells completely, and easily lead to the recurrence and progression of tumor. ^[10] Background: Tumor budding is defined as small cluster of tumor cells located at the invasive edge of tumor and was assumed to be linked with epithelial-mesenchymal transition (EMT), which is an early event in metastasis. ^[11] The combination analysis of UHPLC-QTOF/MS and DESI-MSI revealed that the different molecular species of TGs were associated with tumor distribution and were useful for characterizing the progression of tumor cells and discovering prospective biomarkers. ^[12] PD-L1 and PD-L2 are important targets for immune checkpoint blockade, but how tumor cells achieve their expression remains to be addressed. ^[13] In vitro, activities against B16-F10 (mouse melanoma), HepG2 (human hepatocellular carcinoma), HL-60 (human promyelocytic leukemia) and K562 (human chronic myelocytic leukemia) and non-tumor cells: PBMC (human peripheral blood mononuclear cells activated with concanavalin A - human lymphoblast) were carried out. ^[14] Immunohistochemical staing showed complete loss of SMARCA4 in tumor cells. ^[15] Additionally, cytotoxicity experiments showed that the Cur/FA-AmCS-TPP nanoparticles had good targeting ability for tumor cells. ^[16] The motion of circulating tumor cells (CTCs) in microcirculatory system is one of the critical steps during cancer metastasis. ^[17] Besides their direct activity against tumor cells, monoclonal antibodies and tyrosine kinase inhibitors (TKIs) also influence the antitumoral activity of immune cells, which has important implications for the design of immunotherapies. ^[18] VPS9D1-AS1/MEF2D and miR-4739 were inversely correlated in tumor cells. ^[19] Conversely, the knocking down of GOLPH3 in GOLPH3-overexpressing tumor cells reduces tumorigenic features, such as cell proliferation and cell migration and invasion. ^[20] In this enhancement, the edges of the tumor cells and its dead cells are magnified efficiently. ^[21] Poorly functional tumor vessels inefficiently deliver chemotherapy to tumor cells; vessel hyper-permeability promotes chemotherapy delivery primarily to a tumor’s periphery. ^[22] However, only a small fraction of cell-free DNA (cfDNA) fragments originate from tumor cells, requiring an ultra-sensitive method to detect MSI status from cfDNA. ^[23] 4); hence, NCs became cationic in the tumor area, what facilitates their internalization into tumor cells. ^[24] Meanwhile, the in vitro cytotoxicity assays indicated that these nanoparticles coencapsulated with PTX and Ce6 showed a combined cell-killing effect toward MDA-MB-231 tumor cells, exhibiting great potential for drug delivery systems that realize the synergistic chemo-photodynamic therapy for cancer treatment. ^[25] Ascitic ovarian cancer developed in 100 % of the animals injected with the tumor cells. ^[26] Expression of matrix metalloproteinase 9 (MMP9) in the tumor cells is related to tumor invasion and metastasis. ^[27] In particular, we performed the 3D imaging of human breast adenocarcinoma MCF-7 cells, opening the way for the full characterization of circulating tumor cells (CTCs) in the new paradigm of liquid biopsy. ^[28] Autologous tumor cells (ATCs) could be unbiased stimulators in activating and enriching tumor-reactive T cells. ^[29] As an example, platelets promote invasive properties of tumor cells by induction of epithelial to mesenchymal transition (EMT). ^[30] Superparamagnetic iron oxide nanoparticles were shown to exhibit a high performance as X-ray dosage enhancer in tumor cells. ^[31] To this end, the expression of CD8+ and FoxP3+ T cells, CD20+ B cells, PD-1+ and PD-L1+ immune cells and PD-L1+ tumor cells was evaluated by immunohistochemistry on tissue microarrays with paired transurethral resection (TURB) specimens, cystectomy specimens and lymph node metastases from 145 patients, 65 of whom had received NAC. ^[32] The dissemination of tumor cells into bone is thought to be an early event, often occurring before clinical detection of the primary tumor. ^[33] Although the detection of circulating tumor cells (CTCs) should be crucial for future personalized medicine, no efficient and flexible methods have been established. ^[34] While originally shown to be produced in the liver, recent studies show localized complement production in numerous cell types including immune cells and tumor cells. ^[35] Surprisingly, even though Smc3 D733A turned out to be the immune-dominant neoepitope in CT26 tumor bearing mice, neither T cells specific for this neoepitope nor their T cell receptors (TCRs) were able to recognize or lyse tumor cells. ^[36] In that context, STIC CTC (NCT01710605) was set up as a strategy trial to test whether circulating tumor cells (CTC) count could help customize the choice between 1st line HT or CT. ^[37] The primary objective of our study is to determine whether primary tumor tissue and cultured tumor cells in 2D and 3D tissue culture systems have the same methylation signature for PAX5, TMPRSS2, and SBDS. ^[38] Numerous studies have shown that non-coding RNAs play crucial roles in the development and progression of various tumor cells. ^[39] Recent advances in understanding the molecular genetic mechanisms of oncogenesis and anti-cancer immune responses open new opportunities for the development of novel effective therapeutic strategies against cancer diseases; the strategies that would be more specific to tumor cells and less toxic to the host. ^[40] Vasculogenic mimicry (VM) formed by tumor cells plays a vital role in the progress of tumor, because it provides nutrition for tumor cells and takes away the metabolites. ^[41] In this study, we aim to explore the values of serum dickkopf-1 (DKK1) and circulating tumor cells (CTCs) in predicting the efficacy and prognosis of transcatheter arterial chemoembolization (TACE) treatment on patients with hepatocellular carcinoma (HCC). ^[42] Pediatric solid tumors have long been known to shed tumor cells, DNA, RNA, and proteins into the blood. ^[43] Therefore, the extensive reprogramming of gene expression that occurs in tumor cells might create a hurdle for viral propagation. ^[44] Elevated expression of enhancer of zeste homolog 2 (EZH2) histone methyltransferase, a core member of the polycomb repressive complex 2 (PRC2), results in cancer progression through histone methylation‐driven tumor cells dedifferentiation. ^[45] It has been established that tumor cells are more resistant to the hypoxia cue than non-malignant cells and can remain viable in hypoxia. ^[46] Moreover, the structure of the NETs makes it able to catch the circulating tumor cells, which could lead to metastasis. ^[47] In a recent proteomic screen, we identified that the PKMT SETD6 methylates PLK1—a key regulator of mitosis and highly expressed in tumor cells. ^[48] Adjuvant treatment was given to 79% of patients with macrometastasis (MAC), 77% with MIC, and 11% with isolated tumor cells (ITC). ^[49] M8891 inhibited growth of primary endothelial cells as well as patient-derived tumor cells and demonstrated antiangiogenic and antitumoral activity in mouse models. ^[50]