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1

Deniz, Özdemir. "KAN0438757: A NOVEL PFKFB3 INHIBITOR THAT INDUCES PROGRAMMED CELL DEATH AND SUPPRESSES CELL MIGRATION IN NON-SMALL CELL LUNG CARCINOMA CELLS." Biotechnologia Acta 16, no. 5 (October 31, 2023): 34–44. http://dx.doi.org/10.15407/biotech16.05.034.

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Aim. PFKFB3 is glycolytic activators that is overexpressed in human lung cancer and plays a crucial role in multiple cellular functions including programmed cell death. Despite the many small molecules described as PFKFB3 inhibitors, some of them have shown disappointing results in vitro and in vivo. On the other hand KAN0438757, selective and potent, small molecule inhibitor has been developed. However, the effects of KAN0438757, in non-small cell lung carcinoma cells remain unknown. Herein, we sought to decipher the effect of KAN0438757 on proliferation, migration, DNA damage, and programmed cell death in non-small cell lung carcinoma cells. Methods. The effects of KAN0438757 on cell viability, proliferation, DNA damage, migration, apoptosis, and autophagy in in non-small cell lung carcinoma cells was tested by WST-1, real-time cell analysis, comet assay, wound-healing migration test, and MMP/JC-1 and AO/ER dual staining assays as well as western blot analysis. Results. Our results revealed that KAN0438757 significantly suppressed the viability and proliferation of A549 and H1299 cells and inhibited migration of A549 cells. More importantly, KAN0438757 caused DNA damage and triggered apoptosis and this was accompanied by the up-regulation of cleaved PARP in A549 cells. Furthermore, treatment with KAN0438757 resulted in increased LC3 II and Beclin1, which indicated that KAN0438757 stimulated autophagy. Conclusions. Overall, targeting PFKFB3 with KAN0438757 may be a promising effective treatment approach, requiring further in vitro and in vivo evaluation of KAN0438757 as a therapy in non-small cell lung carcinoma cells.
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Ahmed Elkammar, Hala. "Effect of human bone marrow derived mesenchymal stem cells on squamous cell carcinoma cell line." International Journal of Academic Research 6, no. 1 (January 30, 2014): 110–16. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.14.

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3

Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.
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4

Fujimoto, Naohiro, Bin Han, Masayoshi Nomura, and Tetsuro Matsumoto. "WS1-1-1 Nitrogen-Containing Bisphosphonates Inhibit the Growth of Renal Cell Carcinoma Cells(Renal Cell Cancer)." Japanese Journal of Urology 99, no. 2 (2008): 142. http://dx.doi.org/10.5980/jpnjurol.99.142_1.

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5

Ohshima, Kôichi, Junji Suzumiya, and Masahiro Kikuchi. "T cell rich B cell lymphoma." Journal of the Japan Society of the Reticuloendothelial System 36, no. 5-6 (1996): 391–93. http://dx.doi.org/10.3960/jslrt1961.36.391.

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6

Gaddikeri1, Kavitha, and Deepak D. Bhorgonde2. "Assessment of role of mast cells in oral squamous cell carcinoma." Asian Pacific Journal of Health Sciences 3, Supplimentary 2016 (December 31, 2016): 63–66. http://dx.doi.org/10.21276/apjhs.2016.3.4s.9.

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7

Abramova, V. A., A. Kali, N. Abdolla, O. Yu Yurikova, Yu V. Perfilyeva, Ye O. Ostapchuk, R. T. Tleulieva, S. K. Madenova, and N. N. Belyaev. "Influence of tumor cells on natural killer cell phenotype and cytotoxicity." International Journal of Biology and Chemistry 8, no. 1 (2015): 9–14. http://dx.doi.org/10.26577/2218-7979-2015-8-1-9-14.

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8

CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.
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9

YAMAMOTO, Takamitsu. "C207 DEVELOPMENT OF FUEL CELLS POWERED RAILWAY VEHICLE(Fuel Cell-1)." Proceedings of the International Conference on Power Engineering (ICOPE) 2009.2 (2009): _2–213_—_2–218_. http://dx.doi.org/10.1299/jsmeicope.2009.2._2-213_.

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10

Nagayama, Kazuaki. "OS18-1 Nuclear-cytoskeletal Interactions in Vascular Smooth Muscle Cells : Possible Roles in the Regulation of Cell Differentiation(Cell and Tissue mechanics 1,OS18 Cell and tissue mechanics,BIOMECHANICS)." Abstracts of ATEM : International Conference on Advanced Technology in Experimental Mechanics : Asian Conference on Experimental Mechanics 2015.14 (2015): 235. http://dx.doi.org/10.1299/jsmeatem.2015.14.235.

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11

Arai, Masataka, Shota Hori, Satoshi Miyamoto, Kazuhiro Nakashima, Toshihiro Sera, and Susumu Kudo. "OS18-5 Mechanical Stimulus Effects Diacylglycerol Distribution in Vascular Endothelial Cells(Cell and Tissue mechanics 2,OS18 Cell and tissue mechanics,BIOMECHANICS)." Abstracts of ATEM : International Conference on Advanced Technology in Experimental Mechanics : Asian Conference on Experimental Mechanics 2015.14 (2015): 239. http://dx.doi.org/10.1299/jsmeatem.2015.14.239.

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12

J, Otsuka. "A Theoretical Study on the Cell Differentiation Forming Stem Cells in Higher Animals." Physical Science & Biophysics Journal 5, no. 2 (2021): 1–10. http://dx.doi.org/10.23880/psbj-16000191.

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The recent genome sequencing of multicellular diploid eukaryotes reveals an enlarged repertoire of protein genes for signal transmission but it is still difficult to elucidate the network of signal transmission to drive the life cycle of such an eukaryote only from biochemical and genetic studies. In the present paper, a theoretical study is carried out for the cell differentiation, the formation of stem cells and the growth from a child to the adult in the higher animal. With the intercellular and intracellular signal transmission in mind, the cell differentiation is theoretically derived from the process by the transition of proliferated cells from proliferation mode to differentiation mode and by both the long-range interaction between distinctive types of cells and the short-range interaction between the same types of cells. As the hierarchy of cell differentiation is advanced, the original types of self-reproducible cells are replaced by the self-reproducible cells returned from the cells differentiated already. The latter type of self-reproducible cells are marked with the signal specific to the preceding differentiation and become the stem cells for the next stage of cell differentiation. This situation is realized under the condition that the differentiation of cells occurs immediately after their proliferation in the development. The presence of stem cells in the respective lineages of differentiated cells strongly suggests another signal transmission for the growth of a child to a definite size of adult that the proliferation of stem cells in one lineage is activated by the signal from the differentiated cells in the other lineage(s) and is suppressed by the signal from the differentiated cells in its own lineage. This style of signal transmission also explains the metamorphosis and maturation of germ cells in higher animals.
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13

M. Baghdadi, Houry. "Effect of stem cells on genetic mutations and proliferation in squamous cell carcinoma." International Journal of Academic Research 6, no. 1 (January 30, 2014): 192–97. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.25.

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14

Ogushi, Fumiko, and Hiroshi Kori. "3P277 Dependence of cell differentiation ratio on cell-cell interaction and noise(24. Mathematical biology,Poster)." Seibutsu Butsuri 53, supplement1-2 (2013): S257. http://dx.doi.org/10.2142/biophys.53.s257_6.

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15

Bernstein, Matthew N., Zhongjie Ma, Michael Gleicher, and Colin N. Dewey. "CellO: comprehensive and hierarchical cell type classification of human cells with the Cell Ontology." iScience 24, no. 1 (January 2021): 101913. http://dx.doi.org/10.1016/j.isci.2020.101913.

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16

Sugawara, Michiko, Keisuke Ao, Yoshihisa Shimizu, Kazuo Yamazuchi, Hao Liu, and Jun Nakanshi. "OS18-4 Analysis of Nuclear-Centrosomal Axis in HeLa Cells Using a Photoactivatable Substrate(Cell and Tissue mechanics 2,OS18 Cell and tissue mechanics,BIOMECHANICS)." Abstracts of ATEM : International Conference on Advanced Technology in Experimental Mechanics : Asian Conference on Experimental Mechanics 2015.14 (2015): 238. http://dx.doi.org/10.1299/jsmeatem.2015.14.238.

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17

Rimpo, Kenji, Yumiko Kagawa, and Tetsushi Yamagami. "T-cell-rich B-cell lymphoma in a dog." Journal of Japan Veterinary Cancer Society 4, no. 1 (2013): 1–5. http://dx.doi.org/10.12951/jvcs.2012-001.

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18

Hananeh, W., R. Al Rukibat, and M. Daradka. "Primary splenic diffuse large B-cell lymphoma with multinucleated giant cells in a horse." Veterinární Medicína 66, No. 2 (February 2, 2021): 76–79. http://dx.doi.org/10.17221/61/2020-vetmed.

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A diagnosis of a diffuse splenic large B-cell lymphoma with multinucleated giant cells in a 5-year-old mare was made based upon the clinical, pathological, and immunohistochemical findings. The enormous primary splenic mass weighed 51.75 kg. To the best of our knowledge, this is the biggest reported splenic mass and the first case of an equine diffuse large B-cell lymphoma with multinucleated giant cells.
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19

FUKAGAWA, Shuji, Yuichi YOSHIDA, Kazunori URABE, Tetsuya KOGA, Masutaka FURUE, Aiko SUMINOE, and Akinobu MATSUZAKI. "Langerhans Cell Histiocytosis." Nishi Nihon Hifuka 65, no. 3 (2003): 211–12. http://dx.doi.org/10.2336/nishinihonhifu.65.211.

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20

INOUE, Hiroko, Chikage MITOMA, Yumi YASUKOCHI, Hiroshi UCHI, and Masutaka FURUE. "Basosquamous Cell Carcinoma." Nishi Nihon Hifuka 78, no. 6 (2016): 581–82. http://dx.doi.org/10.2336/nishinihonhifu.78.581.

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21

Beigh, Aamir Nazir, and Er Prabhjot Kaur. "Inter-Cell Interference." International Journal of Trend in Scientific Research and Development Volume-2, Issue-6 (October 31, 2018): 43–46. http://dx.doi.org/10.31142/ijtsrd18406.

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22

Wang, Junfeng, Shukei Sugita, Kazuaki Nagayama, and Takeo Matsumoto. "OS18-3 Spatiotemporal Dynamics of Actin during Adhesion Process of MC3T3-E1 Cells to Substrate(Cell and Tissue mechanics 1,OS18 Cell and tissue mechanics,BIOMECHANICS)." Abstracts of ATEM : International Conference on Advanced Technology in Experimental Mechanics : Asian Conference on Experimental Mechanics 2015.14 (2015): 237. http://dx.doi.org/10.1299/jsmeatem.2015.14.237.

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23

Eusebi, Fabrizio, Francesca Grassi, Guiseppe Fratamico, Susanna Dolci, Marco Conti, and Mario Stefanini. "Cell-to-cell communication in cultured Sertoli cells." Pfl�gers Archiv European Journal of Physiology 404, no. 4 (August 1985): 382–84. http://dx.doi.org/10.1007/bf00585353.

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24

Kumazaki, Taisei, Chinatsu Yonekawa, and Tomomi Tsubouchi. "Microscopic Analysis of Cell Fate Alteration Induced by Cell Fusion." Cellular Reprogramming 25, no. 5 (October 1, 2023): 251–59. http://dx.doi.org/10.1089/cell.2023.0073.

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25

Mohapatra, Manisha, and Yerraguntala Subramanya Sarma. "T-Cell/ Histiocyte-Rich Large B-Cell Lymphoma of Posterior Mediastinum." Annals of Pathology and Laboratory Medicine 6, no. 6 (June 24, 2019): C63–66. http://dx.doi.org/10.21276/apalm.2389.

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26

Chinnikatti, Shravana kumar, Soumya shravan, H. N. Asikur Rahaman, and Shraavya Shraavya. "New Treatments for Synovial Cell Sarcoma with Genetically Modified T-Cell?" Cancer Research and Cellular Therapeutics 6, no. 3 (May 16, 2022): 01–02. http://dx.doi.org/10.31579/2640-1053/113.

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Synovial cell sarcoma is rare but very aggressive tumour if not treated early, due to the painless nature of this tumour patients normally come in late and advances stage, can occur in bones, muscle cells, cartilages, ligaments and de-novo from pleuripotent stem cells from asnywhere in the body but most commonly arm, leg, or foot, and near joints such as the wrist or ankle and possibly from any joints in the body, even from soft tissues of lung and abdomen, the other name for this tumour is called malignant synovioma.The 5 year survival after the effective primary treatment is 30-75% and the survival rate is less than 5% if the tumour recurred within 1 year of primary treatment and that’s why new treatments are explored continuously. Due to late recognition and diagnosis of this rare tumour leads to many problems in treatment and in disease course. This tumour can occur at any age but is most common in growing periods like teen agers and adolescents. This tumour can spread to any organ in the body but most commonly distant metastases occur in lungs. Synovial sarcomas actually a misnomer as previously thought, now with advances in cell structure advances, These tumours can occur not only from synovial cells but from any cell of bone, muscle, tendon, ligaments and cartilage forming cells and supporting cells. These tumours occur with equal propensity in both men and women of younger age. If diagnosed early and treated early with surgery alone patients can be cured completely without any morbidity and mortality
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27

Ateş, İhsan, Ozan Yazıcı, Hale Ateş, Doğan Yazılıtaş, Ayşe Naz Özcan, Yetkin Ağaçkıran, and Nurullah Zengin. "Squamous Cell Cancer of The Lung with Synchronous Renal Cell Carcinoma." Turkish Thoracic Journal 17, no. 3 (September 10, 2016): 125–27. http://dx.doi.org/10.5578/ttj.30510.

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28

PANGESTY, Azizah intan, Takaaki ARAHIRA, and Mitsugu TODO. "1F42 Characterization of Osteochondral Cell Sheets of Human Mesenchymal Stem Cell." Proceedings of the Bioengineering Conference Annual Meeting of BED/JSME 2015.27 (2015): 253–54. http://dx.doi.org/10.1299/jsmebio.2015.27.253.

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29

E. Ghazy, Shaimaa, Ehab S. Abdel-Hamid, Amira M. Ali, Aly F. Mohamed, and Houry M. Baghdadi. "Paclitaxel effect on head and neck squamous cell carcinoma cell line." International Journal of Academic Research 6, no. 1 (January 30, 2014): 94–99. http://dx.doi.org/10.7813/2075-4124.2014/6-1/a.12.

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30

Negash, Sewite, Hwai-Shi Wang, Chun Gao, Dolena Ledee, and Peggy Zelenka. "Cdk5 regulates cell-matrix and cell-cell adhesion in lens epithelial cells." Journal of Cell Science 115, no. 10 (May 15, 2002): 2109–17. http://dx.doi.org/10.1242/jcs.115.10.2109.

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Cdk5 is a member of the cyclin-dependent kinase family, which is expressed predominantly in terminally differentiated neurons. Lower levels of Cdk5 are also found in a wide variety of cell types, including the lens. Although Cdk5 has been shown to play an important role in neuronal migration and neurite outgrowth, its function in non-neuronal cells is not known. Therefore, this study was undertaken to explore the role of Cdk5 in the lens. Results showed that, within the adult mouse lens, Cdk5 was localized to the cytoplasm,especially along the lateral membranes of differentiating primary fiber cells,which suggests a role in cell-cell adhesion. Staining at the tips of elongating fiber cells was also particularly strong, suggesting a role in cell-matrix adhesion. To examine the possible role of Cdk5 in lens epithelial cell adhesion, we stably transfected N/N1003A rabbit lens epithelial cells with cDNAs for Cdk5 or a dominant-negative mutation, Cdk5-T33. Attachment to a fibronectin matrix, as measured with substrate-coated cell adhesion strips,was increased by Cdk5 overexpression, while an equivalent overexpression of Cdk5-T33 had no effect. Cdk5 also increased the rate of cell attachment and spreading as measured by electric cell-substrate impedance sensing (ECIS). In addition, Cdk5 overexpression decreased cell-cell adhesion as measured by a cell aggregation assay. These findings suggest that Cdk5 plays a role in regulating both cell-matrix and cell-cell interactions in the lens.
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Aoshiba, K., S. I. Rennard, and J. R. Spurzem. "Cell-matrix and cell-cell interactions modulate apoptosis of bronchial epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 1 (January 1, 1997): L28—L37. http://dx.doi.org/10.1152/ajplung.1997.272.1.l28.

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Apoptosis is an important process maintaining cell number and tissue structure. To determine whether cell-extracellular matrix (ECM) and cell-cell interactions modulate apoptosis in bronchial epithelium, we cultured human bronchial epithelial cells in different conditions and evaluated the cells for apoptosis. We found that plating cells in conditions that prevent cell-ECM adhesion induced apoptosis. Plating cells on type I collagen, fibronectin, and biosynthesized matrix prevented apoptosis, due at least in part to integrin-mediated adhesion. When cells were cultured at high density but under conditions preventing cell-substratum adhesion, aggregation occurred. Apoptosis was inversely correlated with aggregation. Cell-cell adhesion in these conditions was mediated at least partly by integrins containing alpha v. Cell aggregation was not associated with activation of a signaling pathway that is usually activated by cell-ECM adhesion, phosphorylation of focal adhesion kinase, but was associated with Bcl-2 protein expression, consistent with the concept that Bcl-2 protects against apoptosis. We conclude that both cell-ECM and cell-cell interactions, likely mediated in part by integrins, modulate apoptosis in bronchial epithelium.
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Brooks, Robert F., and Robert Shields. "Cell growth, cell division and cell size homeostasis in Swiss 3T3 cells." Experimental Cell Research 156, no. 1 (January 1985): 1–6. http://dx.doi.org/10.1016/0014-4827(85)90255-1.

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33

MILLER, ANDREW S., DEBORAH M. COTTAM, and MARTIN J. MILNER. "CELL–CELL AND CELL–SUBSTRATE ADHESION IN CULTURED DROSOPHILA IMAGINAL DISC CELLS." In Vitro Cellular & Developmental Biology - Animal 36, no. 3 (2000): 180. http://dx.doi.org/10.1290/1071-2690(2000)036<0180:ccacsa>2.0.co;2.

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34

MILLER, ANDREW S., DEBORAH M. COTTAM, and MARTIN J. MILNER. "CELL–CELL AND CELL–SUBSTRATE ADHESION IN CULTURED DROSOPHILA IMAGINAL DISC CELLS." In Vitro Cellular and Developmental Biology--Animal 36, no. 3 (March 2000): 180–87. http://dx.doi.org/10.1290/1071-2690(2000)036<0180:ccacsa>2.3.co;2.

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35

Kalkan, Fatih, and Mehmet Özler. "DELTA-9 TETRAHYDROCANNABINOID AND GEMSITABIN COMBINATION ON NON-SMALL CELL (SQUAMOUS CELL, SK-MES-1) LUNG CANCER CELL LINE." Era's Journal of Medical Research 10, no. 01 (June 2023): 1–12. http://dx.doi.org/10.24041/ejmr2023.1.

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Squamous cell carcinoma falls within the category of non-small cell lung cancers, presenting a considerable challenge in terms of treatment management. There has been growing interest in the potential anti-cancer properties of Delta-9 tetrahydrocannabinol. Gemcitabine, a nucleoside analog, has shown effectiveness against diverse cancer types. This study aimed to assess the combined efficacy of Delta-9 tetrahydrocannabinol and Gemcitabine in treating cancer. The squamous lung cancer cell line required for our study was provided by the stem cell unit. The doses were determined as 5µm/L and 10µm/L for Delta-9 tetrahydrocannabinol, 20 and 40 µm/Lfor Gemcitabine by performing a literature review. In our study, CellViabilityAnalysis by MTT, Xcelligence Real-Time Cell Analysis, Annexin V Apoptosis Flow Cytometry Analysis, Total Oxidant, Antioxidant Status, and Caspase-3 Detection Analysis was performed. Upon evaluating the rates of apoptotic cell death, it was observed that the THC 5 and THC 10 treatment groups exhibited a 30% and 60% increase, respectively, compared to the alcohol group. A significant difference in cytotoxic effect, as determined by MTT, was found between the control group and the Gemsitabin 20, Delta-9 Tetrahydrocannabinol 5µm/L, and Gemsitabin 20+Delta-9 Tetrahydrocannabinol 5µm/L groups (p<0.001). There was a statistically significant difference between the groups regarding TOS (p<0.001). All experimental groups exhibited a higher level of caspase 3 activations, in comparison to the control group. We observed a significant cytotoxic effect of Gemcitabine on squamous cell lung cancer cells. Delta-9 tetrahydrocannabinol, when used alone, exhibited a relatively low cytotoxic effect. However, no significant difference was observed in the groups where Delta-9 tetrahydrocannabinolwas combined with Gemcitabine.
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OSAWA, Kumiko, Tomoaki AOKI, Reiko WATANABE, Michihide TOKUHIRA, Keiko ABE, Eiichi ARAI, Masahiro KIZAKI, and Jun-ichi TAMARU. "A case report of diffuse large B-cell lymphoma, spindle cell variant." Journal of the Japanese Society of Clinical Cytology 55, no. 4 (2016): 239–44. http://dx.doi.org/10.5795/jjscc.55.239.

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37

Huang, Bin, Yi Jun Huang, Zhi Jun Yao, Xu Chen, Sheng Jie Guo, Xiao Peng Mao, Dao Hu Wang, Jun Xing Chen, and Shao Peng Qiu. "Cancer Stem Cell-Like Side Population Cells in Clear Cell Renal Cell Carcinoma Cell Line 769P." PLoS ONE 8, no. 7 (July 11, 2013): e68293. http://dx.doi.org/10.1371/journal.pone.0068293.

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38

Jacobs, Evan S., Thaddeus C. George, Sukhwinder Singh, Richard Wnek, Paul Fischer, Shila K. Nordone, Gregg A. Dean, and Patricia Fitzgerald-Bocarsly. "Plasmacytoid dendritic cell interaction with HIV-infected T cells: Live cell nibbling vs cell–cell fusion." Cytokine 48, no. 1-2 (October 2009): 66–67. http://dx.doi.org/10.1016/j.cyto.2009.07.214.

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MAS, Bezerra, Ferreira LAM, Kawasaki-Oyama RS, Nascimento MCA, Cuzziol CI, Castanhole-Nunes MMU, Pavarino EC, Maniglia JM, and Goloni-Bertollo EM. "Effectiveness of Hypoxia-Induced Accumulation of Cancer Stem Cells in Head and Neck Squamous Cell Carcinoma." Cancer Medicine Journal 3, S1 (November 30, 2020): 13–23. http://dx.doi.org/10.46619/cmj.2020.3.s1-1003.

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INTRODUCTION: The small number of cancer stem cells, which correspond to only 0.01% - 0.1% of total tumor cells, has been the biggest obstacle in understanding their biology and role in the origin and maintenance of tumors, their metastatic and recurrence potentials, and resistance to radio-chemotherapy. Therefore, promoting its accumulation will enable further studies and future advances in the diagnosis and treatment of head and neck cancer squamous cell carcinoma. OBJECTIVE: To induce cancer stem cell accumulation in primary cell cultures of head and neck squamous cell carcinoma using a hypoxia chamber. METHODS: Head and neck squamous cell carcinoma samples were cultured and subjected to hypoxia. Oxygen deprivation aimed to induce cancer stem cell accumulation. RESULTS: Immediately after hypoxia, the percentage of O2-deprived cancer stem cells increased 2-fold as compared to control. Surprisingly, new phenotyping performed 45 days after hypoxia showed a 9-fold increase in cancer stem cell percentage in cells that suffered hypoxia. Hypoxic cells showed an increase in spheroid formation when compared to control cells, as well as enhanced abilities in invasion and migration. CONCLUSION: Hypoxia was efficient in cancer stem cell accumulation. As cancer stem cells are a small number of cells within the tumor, promoting their accumulation will enable further studies and future advances in the diagnosis and treatment of head and neck cancer.
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MG, Bottone. "A Brief Communication on a Cell Line of Neural Stem Cells B50 Cells Treated With a New Cisplatin - Based Drug." Journal of Embryology & Stem Cell Research 2, no. 1 (2018): 1–4. http://dx.doi.org/10.23880/jes-16000108.

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41

Manimaran, K., Arun Kumar, AvinashGandi D, and S. Sankaranarayanan. "Interaction of Human Dental Pulp Stem Cells and Ameloblastic Cell In-vitro- A Preclinical Analysis." Annals of Oral Health and Dental Research 2, no. 1 (January 17, 2018): A1–5. http://dx.doi.org/10.21276/aohdr.1831.

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Guo, Y. M., J. Gong, Y. G. Zheng, B. L. Shi, X. Y. Guo, and S. M. Yan. "Protection of bovine mammary epithelial cells from hydrogen peroxide-induced oxidative cell damage by selenium." Czech Journal of Animal Science 63, No. 3 (February 9, 2018): 94–102. http://dx.doi.org/10.17221/76/2017-cjas.

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The uncontrolled release of arachidonic acid (ARA) and its metabolism by lipoxygenase (LOX) pathway can induce and aggravate cellular oxidative stress. Selenium (Se) is an integral part of some antioxidative selenoproteins and may protect cells from oxidative damage by modulating ARA release and metabolism. The present study aimed to investigate the protective response of Se against hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative damage in bovine mammary epithelial cells (BMECs). The BMECs were incubated for 24 h in serum-free medium and then divided into four groups randomly. The cells in groups 1 and 2 were subsequently incubated for 30 h in serum-free medium containing 0 (control) and 50 nM Se (Se treatment group). The cells in groups 3 and 4 were incubated for 24 h in serum-free medium containing 0 and 50 nM Se, and then treated with 600 μM H<sub>2</sub>O<sub>2</sub> for 6 h (H<sub>2</sub>O<sub>2</sub> damage group and Se prevention group). The results showed that Se attenuated the H<sub>2</sub>O<sub>2</sub>-induced production of reactive oxygen species and the decrease of antioxidative enzymes as glutathione peroxidase (GPX), thioredoxin reductase (TrxR), selenoprotein P (SelP), superoxide dismutase, and catalase in BMECs. The preventive effects of Se on the decrease of selenoprotein activity were demonstrated further by the increase of mRNA expression for GPX1, TrxR1, and SelP, and protein expression for GPX1 and TrxR1. Pretreatment of cells with Se inhibited the H<sub>2</sub>O<sub>2</sub>-induced increase of mRNA expressions and activities for cytosolic phospholipase A2 and 5-lipoxygenase, ARA release, and 15-hydroperoxyeicosatetraenoic acid production. Se also blocked the H<sub>2</sub>O<sub>2</sub>-induced activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase but not that of extracellular signal-regulated kinase. These results suggested that Se may protect BMECs against H<sub>2</sub>O<sub>2</sub>-induced oxidative damage by increasing selenoproteins synthesis, inhibiting MAPK pathway, and then decreasing ARA release and its metabolism by LOX pathway.
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43

Y, Elshimali. "Chimeric Antigen Receptor T-Cell Therapy (Car T-Cells) in Solid Tumors, Resistance and Success." Bioequivalence & Bioavailability International Journal 6, no. 1 (2022): 1–6. http://dx.doi.org/10.23880/beba-16000163.

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CARs are chimeric synthetic antigen receptors that can be introduced into an immune cell to retarget its cytotoxicity toward a specific tumor antigen. CAR T-cells immunotherapy demonstrated significant success in the management of hematologic malignancies. Nevertheless, limited studies are present regarding its efficacy in solid and refractory tumors. It is well known that the major concerns regarding this technique include the risk of relapse and the resistance of tumor cells, in addition to high expenses and limited affordability. Several factors play a crucial role in improving the efficacy of immunotherapy, including tumor mutation burden (TMB), microsatellite instability (MSI), loss of heterozygosity (LOH), the APOBEC Protein Family, tumor microenvironment (TMI), and epigenetics. In this minireview, we address the current and future applications of CAR T-Cells against solid tumors and their measure for factors of resistance and success.
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44

Moorthy, Rajesh Kannan, Chandhru Srinivasan, Sridharan Jayamohan, Mahesh Kumar Kannan, Siva Sankari Thirugnanam, Janaki Sankar Ganesh, and Antony Joseph Velanganni Arockiam. "Knockdown of microRNA-375 suppresses cell proliferation and promotes apoptosis in human breast cancer cells." Indian Journal of Science and Technology 14, no. 43 (November 12, 2021): 3199–209. http://dx.doi.org/10.17485/ijst/v14i43.1719.

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45

Kobayashi, Hideyuki, Tsunetaka Mizuki, Yoshiro Koda, Akihiko Wada, and Futoshi Izumi. "Cell-cell contact modulates expression of cell adhesion molecule L1 in PC12 cells." Japanese Journal of Pharmacology 55 (1991): 292. http://dx.doi.org/10.1016/s0021-5198(19)39264-9.

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46

Jossin, Yves, Minhui Lee, Olga Klezovitch, Elif Kon, Alexia Cossard, Wen-Hui Lien, Tania E. Fernandez, Jonathan A. Cooper, and Valera Vasioukhin. "Llgl1 Connects Cell Polarity with Cell-Cell Adhesion in Embryonic Neural Stem Cells." Developmental Cell 41, no. 5 (June 2017): 481–95. http://dx.doi.org/10.1016/j.devcel.2017.05.002.

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47

Kobayashi, H., T. Mizuki, A. Wada, and F. Izumi. "Cell-cell contact modulates expression of cell adhesion molecule L1 in PC12 cells." Neuroscience 49, no. 2 (July 1992): 437–41. http://dx.doi.org/10.1016/0306-4522(92)90108-e.

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48

Hegazy, Ragia M., Eman Farouk, and Taghreed G. Kharboush. "Silver Nitrate Particlesnanotoxicity using Cell Culture and Apoptosis (Genetic and Cell Study)." Indian Journal of Applied Research 4, no. 6 (October 1, 2011): 1–8. http://dx.doi.org/10.15373/2249555x/june2014/184.

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49

Zhen-Ning Wu, Zhen-Ning Wu, Hao-Sen Huang Zhen-Ning Wu, Jun-Jun Jiang Hao-Sen Huang, Zhong-Zhe Xiao Jun-Jun Jiang, and Min Huang Zhong-Zhe Xiao. "Intelligent Tumor Cell Detection Method Based on Circulating Tumor Cell (CTC) Technology." 電腦學刊 34, no. 1 (February 2023): 117–30. http://dx.doi.org/10.53106/199115992023023401009.

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<p>Cancer has become one of the greatest threats for human life. Doctors can get original images of the sick organs with the assistance of medical technology. However, manual interpretation of the original images is time consuming and labor consuming. Nowadays, the intelligent detection of tumor cell images is commonly adopted in cancer diagnosis. In this paper, we propose Imporved Selective Search (ISS) algorithm and CTCNet based on Circulating Tumor Cell (CTC) technology to improve the cancer images&rsquo; detection efficiency. CTCs can be collected by a sampling needle with EpCAM antibody which can specifically bind to tumor cells. After fluorescent staining process, images obtained from sampling needle will be processed by the ISS algorithm for candidate region preselection. All of the eligible areas are evaluated with a self-designed neural network called CTCNet, resulting in efficient recognition of circulating tumor cells. During this process, all algorithms are accelerated through the GPU and NPU hardware platform, which further improves the detection speed of the system. In the experiment, we first verify the efficiency of proposed ISS algorithm by compared with Original Selective Search (OSS), we found that the number of candidate boxes reduced from 549 to 16 and the time consuming reduced by 0.3s after adopting the ISS algorithm. In order to evaluate the performance of the proposed 7-layer CTCNet, we compared CTCNet with SVM, BP neural network, AlexNet and VGGNet by using the dataset of 12312 samples from 30 patients, among them, there were 12 patients with early cancer and 18 patients with advanced cancer. And we got the highest recognition accuracy of 97.95% on CTCNet, which even beyond the VGGNet with deeper layers. In contrast to other combinations, we detect CTC in diverse clinical CTC images, the joint application of ISS algorithm and CTCNet achieves an outstanding system performance with accuracy up to 94.03% in the whole view images. Meanwhile, because of the application of a lightweight network in different hardware acceleration platform, the detection time of the CTC image in a single view can be less than 12s.</p> <p>&nbsp;</p>
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Kim, Eun Young, Eun Ji Noh, Hyo Young Park, Min Jee Park, Eun Hyung Noh, Jun Beom Lee, Chang Jin Jeong, Dong Sun Lee, Key Zung Riu, and Se Pill Park. "Establishment of Bovine Embryonic Stem Cell Lines Using a Minimized Feeder Cell Drop." Cellular Reprogramming 14, no. 6 (December 2012): 520–29. http://dx.doi.org/10.1089/cell.2012.0038.

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