scholarly journals Annexin A2 Expression in the Aerogenous Spread of Pulmonary Invasive Mucinous Adenocarcinoma with Gastric Lineage

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Kazumori Arai ◽  
Tomohiro Iwasaki ◽  
Chinatsu Tsuchiya ◽  
Akihiro Sonoda
Keyword(s):  
Subcellular Localization ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Mucinous Adenocarcinoma ◽  
Immunohistochemical Analysis ◽  
Annexin A2 ◽  
Alveolar Wall ◽  
Biomarker Pattern ◽  
Invasive Mucinous Adenocarcinoma

Spread through air spaces (STAS) is a unique form of lung cancer progression associated with a worse prognosis. However, the mechanisms underlying STAS and the associated proteins remain unclear. Annexin A2 (ANX A2), which is a membrane-binding protein involved in cell adhesion, is known to promote cancer invasion. In this report, we describe the immunohistochemical analysis of ANX A2 expression in an invasive mucinous adenocarcinoma (IMAC) resected from a 63-year-old man in whom the tumor cells had detached from the alveolar wall and exhibited STAS. At the detachment site, we observed cytoplasmic ANX A2 positivity on the basal side and in the exfoliative gap, as well as reduced collagen IV positivity expression. This biomarker pattern suggested an IMAC with gastric lineage. We hypothesize that ANX A2 is secreted from the basal sides of tumor cells and induces tumor cell detachment by degrading the basement membrane. A further comparison of this case with an IMAC with nongastric lineage suggested the following probabilities: (1) ANX A2 likely contributes to STAS in a manner that is dependent on its subcellular localization. (2) Both the subcellular localization of ANX A2 and the detachment site depend on tumor cell characteristics, including the biomarker immunophenotype.

scholarly journals Annexin A2 Expression in Aerogenous Metastasis of Pulmonary Invasive Mucinous Adenocarcinoma: A Case Report including Immunohistochemical Analysis

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Kazumori Arai ◽  
Masahide Hirose
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Mucinous Adenocarcinoma ◽  
Single Layer ◽  
Annexin A2 ◽  
Alveolar Epithelial Cells ◽  
Alveolar Wall ◽  
Cell Aggregates ◽  
Invasive Mucinous Adenocarcinoma ◽  
Cell Cell

Aerogenous metastasis (AM) is a form of lung cancer that spreads in a unique fashion, but its mechanisms are still unclear. Annexin A2 (ANX A2), a membrane-binding protein, promotes cancer invasion and is involved in cell adhesion and polarity. The relationship between ANX A2 and cancers with poor stromal invasion capacity has not been studied. We immunohistochemically analyzed ANX A2 expression in AM observed in a patient with pulmonary invasive mucinous adenocarcinoma. In the primary site, ANX A2 immunopositivity on the cell-cell borders weakened as tumor cells projected and separated into alveolar spaces. In AM, tumor cell aggregates with ANX A2 immunopositivity near the surface and within the cytoplasm attached to alveolar epithelial cells, then engulfed them and formed a protrusion. As tumor cell aggregates adhered to the alveolar wall and formed a single layer, cytoplasmic ANX A2-positive products accumulated in the lateral sides of the tumor cells and exhibited distinct membranous positivity. These results indicated that ANX A2 near the tumor cell surface was related to alveolar wall attachment. Furthermore, the translocation of cytoplasmic ANX A2 to cell-cell borders changed cell morphology, adhesion, and polarity restoration.

Prognostic impact of mucin spread, tumor cell spread, and invasive size in invasive mucinous adenocarcinoma of the lung

Lung Cancer ◽  
2020 ◽  
Vol 146 ◽  
pp. 50-57
Author(s):  
Tomohito Saito ◽  
Koji Tsuta ◽  
Osamu Honda ◽  
Mitsuaki Ishida ◽  
Ryosuke Yamaka ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Mucinous Adenocarcinoma ◽  
Prognostic Impact ◽  
Adenocarcinoma Of The Lung ◽  
Invasive Mucinous Adenocarcinoma ◽  
Cell Spread

scholarly journals Cell-free DNA promotes malignant transformation in non-tumor cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Aline Gomes de Souza ◽  
Victor Alexandre F. Bastos ◽  
Patricia Tieme Fujimura ◽  
Izabella Cristina C. Ferreira ◽  
Letícia Ferro Leal ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Malignant Transformation ◽  
Cancer Progression ◽  
Biological Fluids ◽  
Cellular Migration ◽  
Cell Phenotype ◽  
Cell Free Dna ◽  
Prostate Cell ◽  
Free Dna

AbstractCell-free DNA is present in different biological fluids and when released by tumor cells may contribute to pro-tumor events such as malignant transformation of cells adjacent to the tumor and metastasis. Thus, this study analyzed the effect of tumor cell-free DNA, isolated from the blood of prostate cancer patients, on non-tumor prostate cell lines (RWPE-1 and PNT-2). To achieve this, we performed cell-free DNA quantification and characterization assays, evaluation of gene and miRNA expression profiling focused on cancer progression and EMT, and metabolomics by mass spectrometry and cellular migration. The results showed that tumor-free cell DNA was able to alter the gene expression of MMP9 and CD44, alter the expression profile of nine miRNAs, and increased the tryptophan consumption and cell migration rates in non-tumor cells. Therefore, tumor cell-free DNA was capable of altering the receptor cell phenotype, triggering events related to malignant transformation in these cells, and can thus be considered a potential target for cancer diagnosis and therapy.

A Review of Enrichment Methods for Circulating Tumor Cells: from Single Modality to Hybrid Modality

The Analyst ◽  
2021 ◽  
Author(s):  
Yi Zhang ◽  
Yifu Li ◽  
Zhongchao Tan
Keyword(s):  
Early Diagnosis ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Treatment Efficacy ◽  
Circulating Tumor Cell ◽  
Early Diagnosis Of Cancer ◽  
Diagnosis Of Cancer ◽  
Single Modality ◽  
Enrichment Methods

Circulating tumor cell (CTC) analysis as a liquid biopsy can be used for early diagnosis of cancer, evaluate cancer progression, and assess treatment efficacy. Enrichment of CTC from patient blood...

scholarly journals The Fate of Fusions

Cells ◽  
2018 ◽  
Vol 8 (1) ◽  
pp. 13 ◽  
Author(s):  
Gary Clawson
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Fusion ◽  
Cancer Progression ◽  
Genetic Instability ◽  
Cell Heterogeneity ◽  
Metastatic Dissemination ◽  
Tumor Cell Heterogeneity ◽  
Long Time

The concept of leukocyte-tumor cell fusion as a significant driver of cancer progression has been around a long time, and has garnered growing support over the last several years. The underlying idea seems quite simple and attractive: Fusion of tumor cells (with their inherent genetic instability) with leukocytes, particularly macrophages, could produce hybrids with high invasive capabilities, greatly facilitating their metastatic dissemination, while potentially accelerating tumor cell heterogeneity. While there are a number of attractive features with this story on the surface, the various studies seem to leave us with a conundrum, namely, what is the fate of such fusions?

scholarly journals Exosomes and Their Role in Cancer Progression

2021 ◽  
Vol 11 ◽  
Author(s):  
Yang Liu ◽  
Ke Shi ◽  
Yong Chen ◽  
Xianrui Wu ◽  
Zheng Chen ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Extracellular Vesicles ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Immune Escape ◽  
Research Progress ◽  
Chemotherapeutic Drugs ◽  
Other Substances

Exosomes from extracellular vesicles can activate or inhibit various signaling pathways by transporting proteins, lipids, nucleic acids and other substances to recipient cells. In addition, exosomes are considered to be involved in the development and progression of tumors from different tissue sources in numerous ways, including remodeling of the tumor microenvironment, promoting angiogenesis, metastasis, and invasion, and regulating the immune escape of tumor cells. However, the precise molecular mechanisms by which exosomes participate in these different processes remains unclear. In this review, we describe the research progress of tumor cell-derived exosomes in cancer progression. We also discuss the prospects of the application of exosomes combined with nanoengineered chemotherapeutic drugs in the treatment of cancer.

scholarly journals Resolvins suppress tumor growth and enhance cancer therapy

2017 ◽  
Vol 215 (1) ◽  
pp. 115-140 ◽  
Author(s):  
Megan L. Sulciner ◽  
Charles N. Serhan ◽  
Molly M. Gilligan ◽  
Dayna K. Mudge ◽  
Jaimie Chang ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Tumor Burden ◽  
Cell Debris ◽  
Resolvin D1 ◽  
Multiple Tumor ◽  
Macrophage Phagocytosis

Cancer therapy reduces tumor burden by killing tumor cells, yet it simultaneously creates tumor cell debris that may stimulate inflammation and tumor growth. Thus, conventional cancer therapy is inherently a double-edged sword. In this study, we show that tumor cells killed by chemotherapy or targeted therapy (“tumor cell debris”) stimulate primary tumor growth when coinjected with a subthreshold (nontumorigenic) inoculum of tumor cells by triggering macrophage proinflammatory cytokine release after phosphatidylserine exposure. Debris-stimulated tumors were inhibited by antiinflammatory and proresolving lipid autacoids, namely resolvin D1 (RvD1), RvD2, or RvE1. These mediators specifically inhibit debris-stimulated cancer progression by enhancing clearance of debris via macrophage phagocytosis in multiple tumor types. Resolvins counterregulate the release of cytokines/chemokines, including TNFα, IL-6, IL-8, CCL4, and CCL5, by human macrophages stimulated with cell debris. These results demonstrate that enhancing endogenous clearance of tumor cell debris is a new therapeutic target that may complement cytotoxic cancer therapies.

Interaction of Human Tumor Cells with Human Platelets and the Coagulation System

1983 ◽  
Vol 50 (03) ◽  
pp. 726-730 ◽  
Author(s):  
Hamid Al-Mondhiry ◽  
Virginia McGarvey ◽  
Kim Leitzel
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Lines ◽  
Human Tumor ◽  
Human Platelets ◽  
Factor Vii ◽  
Coagulation System ◽  
Breast Adenocarcinoma ◽  
Activate Factor ◽  
Tumor Cell Lines

SummaryThis paper reports studies on the interaction between human platelets, the plasma coagulation system, and two human tumor cell lines grown in tissue culture: Melanoma and breast adenocarcinoma. The interaction was monitored through the use of 125I- labelled fibrinogen, which measures both thrombin activity generated by cell-plasma interaction and fibrin/fibrinogen binding to platelets and tumor cells. Each tumor cell line activates both the platelets and the coagulation system simultaneously resulting in the generation of thrombin or thrombin-like activity. The melanoma cells activate the coagulation system through “the extrinsic pathway” with a tissue factor-like effect on factor VII, but the breast tumor seems to activate factor X directly. Both tumor cell lines activate platelets to “make available” a platelet- derived procoagulant material necessary for the conversion of prothrombin to thrombin. The tumor-derived procoagulant activity and the platelet aggregating potential of cells do not seem to be inter-related, and they are not specific to malignant cells.

Anticancer Activity of Diosgenin and its Semi-synthetic Derivatives: Role in Autophagy Mediated Cell Death and Induction of Apoptosis

2021 ◽  
Vol 21 ◽  
Author(s):  
Nivedita Bhardwaj ◽  
Nancy Tripathi ◽  
Bharat Goel ◽  
Shreyans K. Jain
Keyword(s):  
Cell Death ◽  
Cancer Treatment ◽  
Anticancer Activity ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Rational Approach ◽  
Potential Candidate ◽  
Potential Implication ◽  
Apoptosis Protein ◽  
Synthetic Derivatives

: During cancer progression, the unrestricted proliferation of cells is supported by the impaired cell death response provoked by certain oncogenes. Both autophagy and apoptosis are the signaling pathways of cell death, which are targeted for cancer treatment. Defects in apoptosis result in reduced cell death and ultimately tumor progression. The tumor cells lacking apoptosis phenomena are killed by ROS- mediated autophagy. The autophagic programmed cell death requires apoptosis protein for inhibiting tumor growth; thus, the interconnection between these two pathways determines the fate of a cell. The cross-regulation of autophagy and apoptosis is an important aspect to modulate autophagy, apoptosis and to sensibilise apoptosis-resistant tumor cells under metabolic stress and might be a rational approach for drug designing strategy for the treatment of cancer. Numerous proteins involved in autophagy have been investigated as the druggable target for anticancer therapy. Several compounds of natural origin have been reported, to control autophagy activity through the PI3K/Akt/mTOR key pathway. Diosgenin, a steroidal sapogenin has emerged as a potential candidate for cancer treatment. It induces ROS-mediated autophagy, inhibits PI3K/Akt/mTOR pathway, and produces cytotoxicity selectively in cancer cells. This review aims to focus on optimal strategies using diosgenin to induce apoptosis by modulating the pathways involved in autophagy regulation and its potential implication in the treatment of various cancer. The discussion has been extended to the medicinal chemistry of semi-synthetic derivatives of diosgenin exhibiting anticancer activity.

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