scholarly journals Expression and hypoxia-responsiveness of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 in mammary gland malignant cell lines.

2005 ◽  
Vol 52 (4) ◽  
pp. 881-888 ◽  
Author(s):  
Oleksandr H Minchenko ◽  
Iryna L Opentanova ◽  
Tsutomu Ogura ◽  
Dmytro O Minchenko ◽  
Sergiy V Komisarenko ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Cancer Cells ◽  
Cell Lines ◽  
Specific Inhibitor ◽  
T47d Cell ◽  
Malignant Cell ◽  
Malignant Cells ◽  
Protein Levels ◽  
Mammary Gland Cancer

Recently, we have shown that PFKFB4 gene which encodes the testis isoenzyme of PFKFB is also expressed in the prostate and hepatoma cancer cell lines. Here we have studied expression and hypoxic regulation of the testis isoenzyme of PFKFB4 in several malignant cell lines from a female organ--the mammary gland. Our studies clearly demonstrated that PFKFB4 mRNA is also expressed in mammary gland malignant cells (MCF-7 and T47D cell lines) in normoxic conditions and that hypoxia strongly induces it expression. To better understand the mechanism of hypoxic regulation of PFKFB4 gene expression, we used dimethyloxalylglycine, a specific inhibitor of HIF-1alpha hydroxylase enzymes, which strongly increases HIF-1alpha levels and mimics the effect of hypoxia. It was observed that PFKFB4 expression in the MCF7 and T47D cell lines was highly responsive to dimethyloxalylglycine, suggesting that the hypoxia responsiveness of PFKFB4 gene in these cell lines is regulated by HIF-1 proteins. Moreover, desferrioxamine and cobalt chloride, which mimic the effect of hypoxia by chelating or substituting for iron, had a similar stimulatory effect on the expression of PFKFB mRNA. In other mammary gland malignant cell lines (BT549, MDA-MB-468, and SKBR-3) hypoxia and hypoxia mimics also induced PFKFB4 mRNA, but to variable degrees. The hypoxic induction of PFKFB4 mRNA was equivalent to the expression of PFKFB3, Glut1, and VEGF, which are known HIF-1-dependent genes. Hypoxia and dimethyloxalylglycine increased the PFKFB4 protein levels in all cell lines studied except MDA-MB-468. Through site-specific mutagenesis in the 5'-flanking region of PFKFB4 gene the hypoxia response could be limited. Thus, this study provides evidence that PFKFB4 gene is also expressed in mammary gland cancer cells and strongly responds to hypoxia via an HIF-1alpha dependent mechanism. Moreover, the PFKFB4 and PFKFB3 gene expression in mammary gland cancer cells has also a significant role in the Warburg effect which is found in all malignant cells.

The development of a computational machine learning tool to decipher malignant cell gene expression from complex tumor tissue.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e15050-e15050
Author(s):  
Maksim Chelushkin ◽  
Valentina Beliaeva ◽  
Aleksandr Zaitsev ◽  
Boris Shpak ◽  
Krystle Nomie ◽  
...  
Keyword(s):  
Gene Expression ◽  
Correlation Coefficient ◽  
Cell Lines ◽  
Cancer Cell ◽  
Tumor Tissue ◽  
Malignant Cell ◽  
Cancer Cell Lines ◽  
Malignant Cells ◽  
Cell Expression

e15050 Background: Complex tumor tissue is composed of malignant cells and diverse tumor microenvironment (TME) cellular populations. Depending on the cancer type, the percentage of malignant cells present in tumor tissue varies, with percentages sometimes below 10%. TME cellular transcripts may comprise the majority of the total transcripts in a tumor, potentially resulting in biases during biomarker development and for clinical decision-making. However, TME gene expression can be subtracted from total tumor gene expression, resulting in only malignant cell expression. Methods: A computational tool was developed for the “subtraction” of TME-specific gene expression from total gene expression in an array of solid tumors, producing in silico “purified'' malignant cell gene expression. To extract the malignant cell RNA expression values, a machine learning model was trained on an artificial transcriptome dataset created from different solid tumor cancer cell lines with the addition of various TME cellular proportions. The artificial transcriptomes, both training and test, were composed of 7,114 samples of purified TME cell types and 3,143 cancer cell lines. The final model relied on the following three major parameters: 1) RNA percentages of deconvolved TME cell types; 2) the weighted sum of the average expression of a malignant cell target gene produced by different TME cell populations where the RNA percentages (weights in the weighted sum) of the TME cell populations were predicted by deconvolution; and 3) a set of genes expressed predominantly in the TME. To experimentally validate the computational model, different proportions of COLO829 (cutaneous melanoma), MCF-7 (invasive ductal carcinoma), and K562 (chronic myeloid leukemia) cell lines were mixed in vitro with PBMCs, creating controlled representations of tumor tissue, and RNA was extracted and sequenced. Gene expression was quantified and analyzed with the computational model, with comparisons to pure cancer cell line expression. Results: The expression of at least 120 clinically relevant biomarkers was reconstructed by applying the model to artificial transcriptomes in which the percentage of malignant cells varied from 10% to 90%. The concordance correlation coefficient between pure cancer cell lines and the extracted malignant cell expression increased on average from 0.75 to 0.9 compared to unprocessed data (e.g., PTEN from 0.2 to 0.88, RB1 from 0.57 to 0.89, ERBB2 from 0.83 to 0.99). In vitro validation showed that the tool improved the concordance correlation coefficient and mean absolute error (MAE) for many tumor biomarkers. For example, the PTEN correlation coefficient increased by 0.33 and its MAE was reduced 3-fold. Conclusions: This novel computational tool can aid in treatment decision-making based on malignant cell expression, promoting the use of gene expression for personalized therapeutics.

scholarly journals The anticancer agent PB-100, selectively active on malignant cells, inhibits multiplication of sixteen malignant cell lines, even multidrug resistant

2000 ◽  
Vol 23 (1) ◽  
pp. 29-33 ◽  
Author(s):  
Mirko Beljanski
Keyword(s):  
Cancer Cells ◽  
Tumor Cells ◽  
Cell Lines ◽  
Plant Extract ◽  
Normal Cell ◽  
Anticancer Agent ◽  
Malignant Cell ◽  
Multidrug Resistant ◽  
Cell Multiplication ◽  
Malignant Cells

The plant-derived anticancer agent PB-100 selectively destroys cancer cells, even when multidrug resistant; yet, it does not inhibit normal (non-malignant) cell multiplication. Testing of PB-100 on sixteen malignant cell lines, several multidrug resistant, as well as on five normal cell lines, confirmed our previous results. Flavopereirine and dihydroflavopereirine, the active principles of PB-100, were chemically synthesized and displayed the same selectivity for tumor cells as the purified plant extract, being active at even lower concentrations.

scholarly journals Activating Hippo Pathway via Rassf1 by Ursolic Acid Suppresses the Tumorigenesis of Gastric Cancer

2019 ◽  
Vol 20 (19) ◽  
pp. 4709 ◽  
Author(s):  
Seong-Hun Kim ◽  
Hua Jin ◽  
Ruo Yu Meng ◽  
Da-Yeah Kim ◽  
Yu Chuan Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cancer Cells ◽  
Ursolic Acid ◽  
Hippo Pathway ◽  
Dependent Manner ◽  
Gastric Cancer Cells ◽  
Protein Levels ◽  
Tumor Tissues ◽  
The Hippo Pathway

The Hippo pathway is often dysregulated in many carcinomas, which results in various stages of tumor progression. Ursolic acid (UA), a natural compound that exists in many herbal plants, is known to obstruct cancer progression and exerts anti-carcinogenic effect on a number of human cancers. In this study, we aimed to examine the biological mechanisms of action of UA through the Hippo pathway in gastric cancer cells. MTT assay showed a decreased viability of gastric cancer cells after treatment with UA. Following treatment with UA, colony numbers and the sizes of gastric cancer cells were significantly diminished and apoptosis was observed in SNU484 and SNU638 cells. The invasion and migration rates of gastric cancer cells were suppressed by UA in a dose-dependent manner. To further determine the gene expression patterns that are related to the effects of UA, a microarray analysis was performed. Gene ontology analysis revealed that several genes, such as the Hippo pathway upstream target gene, ras association domain family (RASSF1), and its downstream target genes (MST1, MST2, and LATS1) were significantly upregulated by UA, while the expression of YAP1 gene, together with oncogenes (FOXM1, KRAS, and BATF), were significantly decreased. Similar to the gene expression profiling results, the protein levels of RASSF1, MST1, MST2, LATS1, and p-YAP were increased, whereas those of CTGF were decreased by UA in gastric cancer cells. The p-YAP expression induced in gastric cancer cells by UA was reversed with RASSF1 silencing. In addition, the protein levels in the Hippo pathway were increased in the UA-treated xenograft tumor tissues as compared with that in the control tumor tissues; thus, UA significantly inhibited the tumorigenesis of gastric cancer in vivo in xenograft animals. Collectively, UA diminishes the proliferation and metastasis of gastric cancer via the regulation of Hippo pathway through Rassf1, which suggests that UA can be used as a potential chemopreventive and therapeutic agent for gastric cancer.

Activation of Plasminogen Activator Inhibitor-1 Synthesis by Phorbol Esters in Human Promyelocyte HL-60

1999 ◽  
Vol 81 (03) ◽  
pp. 415-422 ◽  
Author(s):  
Sophie Lopez ◽  
Franck Peiretti ◽  
Pierre Morange ◽  
Amale Laouar ◽  
Chantal Fossat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Protein Kinase ◽  
Plasminogen Activator ◽  
Specific Inhibitor ◽  
Plasminogen Activator Inhibitor ◽  
Transduction Pathway ◽  
Protein Levels ◽  
Activator Inhibitor ◽  
Pai 1

SummaryHL-60 cells treated by PMA develop the monocyte adherent pheno-type and synthesize plasminogen activator inhibitor type-1 (PAI-1). We focused our study on the identification of the PMA-activated protein kinase C (PKC) isoform and its downstream transduction pathway activating PAI-1 synthesis. Acquisition of the monocytic phenotype was evidenced by cell adherence (90-95%) and a sharp increase of CD 36 and receptor for urokinase plasminogen activator (uPAR) surface expression. Ro 31-8220, a specific inhibitor of PKC, prevented PMA-induced PAI-1 synthesis (mRNA and protein levels) and cell adhesion. To identify the PKC isoform, we took advantage of the HL-525 cell line, an HL-60 cell variant deficient in PKCβ gene expression. This defect prevents PMA to induce the differentiation process. HL-525 stimulated by PMA did not synthesize PAI-1 nor become adherent. However, in HL-525 cells either pretreated by retinoic acid that reinduces PKCβ gene expression or transfected with PKCβ cDNA, PMA significantly activated PAI-1 synthesis and adhesion of cells. Immunoblotting of active Mitogen Activated Protein Kinase (MAPK) p42/p44 in HL-60 cells showed a preferential and sustained activation of the p42 isoform by PMA over the p44 isoform. Ro 31-8220 significantly attenuated this activation. PD 098059 and U0126, both highly specific MEK inhibitors, efficiently prevented PMA-induced PAI-1 synthesis (mRNA and protein levels) and cell adhesion whereas SB203580, a specific inhibitor of stress-activated MAPK p38, did not. Results obtained from HL-60 and HL-525 cells indicate that the PMA-activated transduction pathway of uPAR expression involves a PKC isoform other than PKCβ.In conclusion, we propose that the pathway PKCβ-MEK-MAPK p42 is a potential linear route for PAI-1 synthesis leading to morphological changes and adherence linked to PMA-induced differentiation in HL-60 cells.

scholarly journals Pervasive promoter hypermethylation of silenced TERT alleles in human cancers

2020 ◽  
Vol 43 (5) ◽  
pp. 847-861 ◽  
Author(s):  
David Esopi ◽  
Mindy Kim Graham ◽  
Jacqueline A. Brosnan-Cashman ◽  
Jennifer Meyers ◽  
Ajay Vaghasia ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Transcriptional Repression ◽  
Cpg Island ◽  
Promoter Hypermethylation ◽  
Fine Tuning ◽  
Open Chromatin ◽  
Promoter Mutations

Abstract Background In cancers, maintenance of telomeres often occurs through activation of the catalytic subunit of telomerase, encoded by TERT. Yet, most cancers show only modest levels of TERT gene expression, even in the context of activating hotspot promoter mutations (C228T and C250T). The role of epigenetic mechanisms, including DNA methylation, in regulating TERT gene expression in cancer cells is as yet not fully understood. Methods Here, we have carried out the most comprehensive characterization to date of TERT promoter methylation using ultra-deep bisulfite sequencing spanning the CpG island surrounding the core TERT promoter in 96 different human cell lines, including primary, immortalized and cancer cell types, as well as in control and reference samples. Results In general, we observed that immortalized and cancer cell lines were hypermethylated in a region upstream of the recurrent C228T and C250T TERT promoter mutations, while non-malignant primary cells were comparatively hypomethylated in this region. However, at the allele-level, we generally found that hypermethylation of promoter sequences in cancer cells is associated with repressed expression, and the remaining unmethylated alleles marked with open chromatin are largely responsible for the observed TERT expression in cancer cells. Conclusions Our findings suggest that hypermethylation of the TERT promoter alleles signals transcriptional repression of those alleles, leading to attenuation of TERT activation in cancer cells. This type of fine tuning of TERT expression may account for the modest activation of TERT expression in most cancers.

scholarly journals The Effect of Compound Sophora on Fluorouracil and Oxaliplatin Resistance in Colorectal Cancer Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
WeiHua Yin ◽  
GuPing Zhong ◽  
HuiZhen Fan ◽  
HongMei Xia
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Cell Lines ◽  
Sw480 Cell ◽  
Gastric Cancer Cells ◽  
Glycoprotein P ◽  
Chemotherapy Drugs ◽  
Protein Levels ◽  
Enhanced Expression

Fluorouracil (5-FU) and oxaliplatin (L-OHP) are the most commonly used chemotherapy drugs for colorectal cancer, though resistance is common. Compound Sophora injection is a traditional Chinese medicine that can protect the liver against oxidation, improve immunity, and enhance sensitivity to chemotherapy; it may have an effect of reversing resistance in 5-FU- and L-OHP-resistant gastric cancer cells (5-FU/SW480 and L-OHP/SW480, respectively). A concentration gradient experiment was performed to identify a nontoxic dose of compound Sophora injection. 5-FU/SW480 and L-OHP/SW480 cells were treated with the nontoxic dose of compound radix Sophorae injection for 48 h, and changes in drug resistance to 5-FU and L-OHP were detected. Alterations in apoptosis and the cell cycle were assessed, as were the mRNA and protein levels of permeability glycoprotein (P-gp), annexin A1 (ANXA1), and ATP-binding cassette superfamily G member 2 (ABCG2). Flow cytometry showed a reduction in the number of cells in the G1 phase and an increase of cells in the S phase (P<0.05). mRNA and protein expression of P-gp and ABCG2 was significantly higher in 5-FU/SW480 and L-OHP/SW480 cell lines, and ANXA1 expression decreased significantly (P<0.05). Compound Sophora injection can reverse the drug resistance of 5-FU/SW480 and L-OHP/SW480 cell lines to 5-FU and L-OHP, respectively, possibly through a mechanism involving reduced expression of P-gp and ABCG2 but enhanced expression of ANXA1, which is the basis for the identification of clinical drug resistance in colorectal cancer.

scholarly journals Trastuzumab in combination with AT-101 induces cytotoxicity and apoptosis in Her2 positive breast cancer cells

2020 ◽  
Vol 16 (3) ◽  
pp. 4485-4495
Author(s):  
Gulcan Bulut ◽  
Harika Atmaca ◽  
Burcak Karaca
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Her2 Positive ◽  
Protein Levels ◽  
Her2 Positive Breast Cancer ◽  
Synergistic Cytotoxicity ◽  
Positive Breast Cancer

Aim: AT-101 is a polyphenolic compound with potent anti-apoptotic effects in various cancers. In this study, the possible synergistic cytotoxic and apoptotic effect of trastuzumab/AT-101 combination was investigated in HER2-positive breast cancer cell lines. Materials & methods: SKBR-3, MDA-MB-453 and MCF-10A cell lines were treated with a trastuzumab/AT-101 combination. Synergistic cytotoxicity and apoptosis effects were shown and then PI3K and Akt protein levels were studied. Result: The trastuzumab/AT-101 combination induced synergistic cytotoxicity and apoptosis in both breast cancer cells but not in MCF-10A cells. Combination treatment induced cytotoxicity via inhibiting PI3K/AKT but not the MAPK/ERK pathway. Conclusion: The trastuzumab/AT-101 combination may be a good candidate for patients with trastuzumab-resistant Her2-positive breast cancer and inhibition of the PI3K/AKT pathway may be one of the underlying mechanisms.

scholarly journals GEDS: A Gene Expression Display Server for mRNAs, miRNAs and Proteins

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 675 ◽  
Author(s):  
Xia ◽  
Liu ◽  
Zhang ◽  
Guo
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Gene Expression Data ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Cancer Cell Line ◽  
Tissue Expression ◽  
The Cancer Genome Atlas ◽  
Expression Data ◽  
Protein Levels

High-throughput technologies generate a tremendous amount of expression data on mRNA, miRNA and protein levels. Mining and visualizing the large amount of expression data requires sophisticated computational skills. An easy to use and user-friendly web-server for the visualization of gene expression profiles could greatly facilitate data exploration and hypothesis generation for biologists. Here, we curated and normalized the gene expression data on mRNA, miRNA and protein levels in 23315, 9009 and 9244 samples, respectively, from 40 tissues (The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GETx)) and 1594 cell lines (Cancer Cell Line Encyclopedia (CCLE) and MD Anderson Cell Lines Project (MCLP)). Then, we constructed the Gene Expression Display Server (GEDS), a web-based tool for quantification, comparison and visualization of gene expression data. GEDS integrates multiscale expression data and provides multiple types of figures and tables to satisfy several kinds of user requirements. The comprehensive expression profiles plotted in the one-stop GEDS platform greatly facilitate experimental biologists utilizing big data for better experimental design and analysis. GEDS is freely available on http://bioinfo.life.hust.edu.cn/web/GEDS/.

scholarly journals Sulforaphane modulates telomerase activity via epigenetic regulation in prostate cancer cell lines

2016 ◽  
Vol 94 (1) ◽  
pp. 71-81 ◽  
Author(s):  
Ata Abbas ◽  
J. Adam Hall ◽  
William L. Patterson ◽  
Emily Ho ◽  
Anna Hsu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Prostate Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Prostate Cancer Cell ◽  
Histone H3 ◽  
Htert Promoter ◽  
Prostate Cancer Cells ◽  
Inhibitor Activity ◽  
Prostate Cancer Cell Lines

Epidemiologic studies have revealed that diets rich in sulforaphane (SFN), an isothiocyanate present in cruciferous vegetables, are associated with a marked decrease in prostate cancer incidence. The chemo-preventive role of SFN is associated with its histone de-acetylase inhibitor activity. However, the effect of SFN on chromatin composition and dynamic folding, especially in relation to HDAC inhibitor activity, remains poorly understood. In this study, we found that SFN can inhibit the expression and activity of human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase, in 2 prostate cancer cell lines. This decrease in gene expression is correlated with SFN-induced changes in chromatin structure and composition. The SFN-mediated changes in levels of histone post-translational modifications, more specifically acetylation of histone H3 lysine 18 and di-methylation of histone H3 lysine 4, 2 modifications linked with high risk of prostate cancer recurrence, were associated with regulatory elements within the hTERT promoter region. Chromatin condensation may also play a role in SFN-mediated hTERT repression, since expression and recruitment of MeCP2, a known chromatin compactor, were altered in SFN treated prostate cancer cells. Chromatin immuno-precipitation (ChIP) of MeCP2 showed enrichment over regions of the hTERT promoter with increased nucleosome density. These combined results strongly support a role for SFN in the mediation of epigenetic events leading to the repression of hTERT in prostate cancer cells. This ability of SFN to modify chromatin composition and structure associated with target gene expression provides a new model by which dietary phytochemicals may exert their chemoprevention activity.

Pleiotrophin Is Highly Produced by Myeloma and Breast Cancer and Transdifferentiates Human Monocytes into Endothelial Cells That Are Incorporated into Tumoral Blood Vessels.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1269-1269
Author(s):  
Haiming Chen ◽  
Richard A. Campbell ◽  
Mingjie Li ◽  
Melinda S. Gordon ◽  
Dror Shalitin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Bone Marrow ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Blood Vessels ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Human Monocytes ◽  
Endothelial Gene Expression

Abstract We have previously shown that multiple myeloma (MM) patients express pleiotrophin (PTN) and it is found at high levels in MM serum as well as PTN is a key factor in the transdifferentiation of monocytes into endothelial cells. We determined the level of PTN expression in myeloma and breast cancer and determined whether PTN produced by these tumor cells could induce endothelial cell expression in human monocytes. Both myeloma and breast cancer cells produced high levels of PTN and secreted this growth factor into the culture medium whereas normal bone marrow showed no expression of this protein. Next, MM cell lines, human bone marrow (BM) from MM patients or control subjects or breast cancer cells were cultured with CD14+ PBMCs using transwell culture plates coated with collagen I. CD14+ monocytes exposed to cells from MM cell lines or fresh BM or breast cancer cells showed expression of endothelial genes (Flk-1, Tie-2, CD144, and vWF) and lost expression of monocyte genes (c-fms). Induction of endothelial gene expression was blocked with an anti-PTN antibody. In contrast, CD14+ cells exposed to normal bone marrow as well as cell lines lacking PTN expression did not show endothelial gene expression. We determined whether human monocytes could be incorporated in vivo as vascular endothelium within human tumors that express PTN. Human myeloma LAGλ-1 cells which highly express and secrete PTN were mixed with THP1 monocytes transduced with the green fluorescent protein (GFP) gene and injected subcutaneously into SCID mice. Mice were sacrificed 6 weeks later and tumor was fixed and frozen sections. MM cells or THP1 monocytes alone did not demonstrate the presence of GFP+ blood vessels. Notably, GFP+ THP1 cells were found in blood vessels within the PTN-expressing LAGλ-1 tumor in animals injected with both cells together. When GFP+h2Kd- blood vessels were stained for anti-human and anti-mouse CD31, 60% of the endothelial cells stained positive for human CD31 and the remaining cells stained positive for mouse CD31 whereas none of these cells stained positive for both mouse and human markers. These results show that the blood vessels containing GFP+ cells do not result from fused cells. In addition, an anti-PTN antibody but not control IgG antibody blocks the incorporation of GFP+ cells into the vasculature of the LAGλ-1 tumors. Staining of serial sections with anti-Tie-2 and CD31 antibodies showed a similar distribution pattern. We further examined endothelial gene expression in these in vivo-generated samples using RT-PCR. The results showed that the THP1 monocytes or LAGλ-1 tumor cells alone did not express endothelial genes whereas THP1 monocytes mixed with PTN-expressing LAGλ-1 showed endothelial gene expression. This endothelial gene expression was blocked by anti-PTN antibody. These data show that hematologic and solid tumors through expression of PTN support new blood vessel formation by the transdifferentiation of monocytes into endothelial cells and provide a new potential target for inhibiting blood vessel formation in solid and liquid tumors.

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