Relevant bibliographies by topics / Colony Formation Assay

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Academic literature on the topic 'Colony Formation Assay'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Colony Formation Assay"

1

Kluin-Nelemans, J. C., H. W. J. Hakvoort, S. E. Boom, E. J. E. G. Bast, and R. Willemze. "Radioresistant pseudo-colony formation in the PHA-leukocyte feeder colony assay." Leukemia Research 12, no. 11-12 (January 1988): 917–22. http://dx.doi.org/10.1016/0145-2126(88)90019-7.

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2

UETSUJI, Yasutomo, Shota FUJIMOTO, Kazuyoshi TSUCHIIYA, and Yoshiaki HIRANO. "Cytotoxicity of Piezoelectric Materials in Colony Formation Assay." Journal of the Society of Materials Science, Japan 58, no. 11 (2009): 943–47. http://dx.doi.org/10.2472/jsms.58.943.

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Horman, Shane R., Jeremy To, and Anthony P. Orth. "An HTS-Compatible 3D Colony Formation Assay to Identify Tumor-Specific Chemotherapeutics." Journal of Biomolecular Screening 18, no. 10 (August 5, 2013): 1298–308. http://dx.doi.org/10.1177/1087057113499405.

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There has been increasing interest in the development of cellular behavior models that take advantage of three-dimensional (3D) cell culture. To enable assessment of differential perturbagen impacts on cell growth in 2D and 3D, we have miniaturized and adapted for high-throughput screening (HTS) the soft agar colony formation assay, employing a laser-scanning cytometer to image and quantify multiple cell types simultaneously. The assay is HTS compatible, providing high-quality, image-based, replicable data for multiple, co-cultured cell types. As proof of concept, we subjected colorectal carcinoma colonies in 3D soft agar to a mini screen of 1528 natural product compounds. Hit compounds from the primary screen were rescreened in an HTS 3D co-culture matrix containing colon stromal cells and cancer cells. By combining tumor cells and normal, nontransformed colon epithelial cells in one primary screening assay, we were able to obtain differential IC50 data, thereby distinguishing tumor-specific compounds from general cytotoxic compounds. Moreover, we were able to identify compounds that antagonized tumor colony formation in 3D only, highlighting the importance of this assay in identifying agents that interfere with 3D tumor structural growth. This screening platform provides a fast, simple, and robust method for identification of tumor-specific agents in a biologically relevant microenvironment.
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4

Kajiwara, Yoshinori, Sonali Panchabhai, and Victor A. Levin. "A New Preclinical 3-Dimensional Agarose Colony Formation Assay." Technology in Cancer Research & Treatment 7, no. 4 (August 2008): 329–34. http://dx.doi.org/10.1177/153303460800700407.

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5

Takahashi, Ryo, Nariko Sekine, and Toshihiko Nakatake. "Influence of Monoclonal Antiplatelet Glycoprotein Antibodies on In Vitro Human Megakaryocyte Colony Formation and Proplatelet Formation." Blood 93, no. 6 (March 15, 1999): 1951–58. http://dx.doi.org/10.1182/blood.v93.6.1951.406a33_1951_1958.

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The influence of antiplatelet glycoprotein (GP) antibodies on megakaryocytopoiesis in patients with idiopathic or immune thrombocytopenic purpura (ITP) has been well studied. However, the influence of GP antibodies on proplatelet formation is poorly understood. Here we investigated whether in vitro human megakaryocyte colony formation and proplatelet formation are affected by various monoclonal antiplatelet GP antibodies (MoAb). The megakaryocyte colony formation inhibition assay was performed by methylcellulose culture with modifications, using peripheral blood nonadherent mononuclear cells. The proplatelet formation inhibition assay was performed by megakaryocytes derived from CD34+ cells, stimulated with thrombopoietin + stem cell factor, which were then incubated with antiplatelet GP MoAb for 24 or 48 hours. Anti-GP-Ib MoAb (CD42b; HIP1) slightly inhibited megakaryocyte colony formation (P < .05). and strongly inhibited proplatelet formation (after 24 hours incubation, P < .0002; after 48 hours incubation, P < .0007). Anti-GP-IIb MoAb (CD41; 5B12) inhibited only proplatelet formation (only after 24 hours incubation,P < . 03). Anti-integrin vβ3MoAb (CD51/CD61; 23C6) only slightly inhibited colony size (P < .05). However, anti-GP-IIIa MoAb (CD61; Y2/51) did not inhibit either colony formation or proplatelet formation. These results suggest that antiplatelet GP MoAbs have differing effects on in vitro megakaryocyte colony formation and proplatelet formation.
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6

Dahl, CA, and C. Lindqvist. "Effects of normal mouse serum on the IL-3-induced proliferation of bone marrow cells." Blood 73, no. 3 (February 15, 1989): 700–705. http://dx.doi.org/10.1182/blood.v73.3.700.700.

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Abstract Normal mouse serum (NMS) devoid of colony-stimulating factor (CSF) was found to enhance the interleukin 3 (IL-3)-driven colony formation of bone marrow in vitro. Inclusion of NMS in bone marrow colony-forming assays resulted in greatly increased numbers of colonies and clusters following seven days incubation; however, incubation of bone marrow with NMS before the colony-forming assay had no effect on resultant colony number. The levels of serum-enhancing activity (SEA) did not appear to vary significantly with age and in part was species restricted, in that human and guinea pig serum did not enhance mouse bone marrow colony formation. Conversely, NMS had no effect on human bone marrow colony formation. Levels of SEA were found to vary between strains, as did the degree to which bone marrow from various strains was enhanced by the serum. Serum fractionation studies indicated three active fractions with molecular weights of 800–900 Kd, 60–70 Kd, and 20- 30 Kd. The fraction at 800–900 Kd inhibited colony formation at high concentrations and enhanced colony formation on dilution, whereas the two other active fractions contained enhancing activity at all concentrations tested. These results would indicate that normal serum can play a greater role in colony-forming assays than nutritional supplements. The relationship of the SEA factors to other factors that have been reported to modulate bone marrow colony formation is discussed.
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Dahl, CA, and C. Lindqvist. "Effects of normal mouse serum on the IL-3-induced proliferation of bone marrow cells." Blood 73, no. 3 (February 15, 1989): 700–705. http://dx.doi.org/10.1182/blood.v73.3.700.bloodjournal733700.

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Normal mouse serum (NMS) devoid of colony-stimulating factor (CSF) was found to enhance the interleukin 3 (IL-3)-driven colony formation of bone marrow in vitro. Inclusion of NMS in bone marrow colony-forming assays resulted in greatly increased numbers of colonies and clusters following seven days incubation; however, incubation of bone marrow with NMS before the colony-forming assay had no effect on resultant colony number. The levels of serum-enhancing activity (SEA) did not appear to vary significantly with age and in part was species restricted, in that human and guinea pig serum did not enhance mouse bone marrow colony formation. Conversely, NMS had no effect on human bone marrow colony formation. Levels of SEA were found to vary between strains, as did the degree to which bone marrow from various strains was enhanced by the serum. Serum fractionation studies indicated three active fractions with molecular weights of 800–900 Kd, 60–70 Kd, and 20- 30 Kd. The fraction at 800–900 Kd inhibited colony formation at high concentrations and enhanced colony formation on dilution, whereas the two other active fractions contained enhancing activity at all concentrations tested. These results would indicate that normal serum can play a greater role in colony-forming assays than nutritional supplements. The relationship of the SEA factors to other factors that have been reported to modulate bone marrow colony formation is discussed.
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8

Caracciolo, D., N. Shirsat, G. G. Wong, B. Lange, S. Clark, and G. Rovera. "Recombinant human macrophage colony-stimulating factor (M-CSF) requires subliminal concentrations of granulocyte/macrophage (GM)-CSF for optimal stimulation of human macrophage colony formation in vitro." Journal of Experimental Medicine 166, no. 6 (December 1, 1987): 1851–60. http://dx.doi.org/10.1084/jem.166.6.1851.

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Human macrophage colony-stimulating factor (M-CSF or CSF-1), either in purified or in recombinant form, is able to generate macrophagic colonies in a murine bone marrow colony assay, but only stimulates small macrophagic colonies of 40-50 cells in a human bone marrow colony assay. We report here that recombinant human granulocytic/macrophage colony stimulating factor (rhGM-CSF) at concentrations in the range of picograms enhances the responsiveness of bone marrow progenitors to M-CSF activity, resulting in an increased number of macrophagic colonies of up to 300 cells. Polyclonal antiserum against M-CSF did not alter colony formation of bone marrow progenitors incubated with GM-CSF at optimal concentration (1-10 ng/ml) for these in vitro assays. Thus, GM-CSF at higher concentrations (nanogram range) can by itself, elicit macrophagic colonies, and at lower concentrations (picogram range) acts to enhance the responsiveness of these progenitors to M-CSF.
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9

Sedeeq, Mohammed, Ahmed Maklad, Nuri Gueven, and Iman Azimi. "Development of a High-throughput Agar Colony Formation Assay to Identify Drug Candidates against Medulloblastoma." Pharmaceuticals 13, no. 11 (November 5, 2020): 368. http://dx.doi.org/10.3390/ph13110368.

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Medulloblastoma (MB) is the most common malignant childhood brain cancer. High-risk MB tumours have a high incidence of metastasis and result in poor patient survival. Drug screens, commonly used to identify potential novel therapeutic agents against MB, focus on 2D cell proliferation and viability assays given that these assays are easily adaptable to high-throughput regimes. However, 2D models fail to address invasive characteristics that are crucial to MB metastasis and are thus not representative of tumour growth in vivo. In this study, we developed a 3D 384-well agar colony formation assay using MB cells of molecular subgroup 3 that is associated with the highest level of metastasis. Two fluorescence substrates, resazurin and glycyl-phenylalanyl-aminofluorocoumarin (GF-AFC) that measure cell viability via distinct mechanisms were used to assess the growth of MB cells in the agar matrix. The assay was optimised for seeding density, growth period, substrate incubation time and homogeneity of the fluorescent signals within individual wells. Our data demonstrate the feasibility to multiplex the two fluorescent substrates without detectable signal interference. This assay was validated by assessing the concentration-dependent effect of two commonly used chemotherapeutic agents clinically used for MB treatment, vincristine and lomustine. Subsequently, a panel of plasma membrane calcium channel modulators was screened for their effect on the 3D growth of D341 MB cells, which identified modulators of T-type voltage gated and ORAI calcium channels as selective growth modulators. Overall, this 3D assay provides a reproducible, time and cost-effective assay for high-throughput screening to identify potential drugs against MB.
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Pragnell, IB, EG Wright, SA Lorimore, J. Adam, M. Rosendaal, JF DeLamarter, M. Freshney, L. Eckmann, A. Sproul, and N. Wilkie. "The effect of stem cell proliferation regulators demonstrated with an in vitro assay." Blood 72, no. 1 (July 1, 1988): 196–201. http://dx.doi.org/10.1182/blood.v72.1.196.196.

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Abstract Spleen colony formation after transplantation of bone marrow cells into irradiated mice has been used as an assay for hematopoietic stem cells (CFU-S), but has serious limitations intrinsic to an in vivo assay. In this report we describe experiments using an in vitro clonogenic assay that is especially suitable for studies of stem cell regulation as defined growth factors and normal untreated bone marrow can be used. We have demonstrated that the colony-forming cells have proliferative properties in common with CFU-S and respond to specific proliferation regulators previously detected using the spleen colony assay.
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Dissertations / Theses on the topic "Colony Formation Assay"

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Chen, Yi-Ning, and 陳誼寧. "Evaluation of An In Vitro Colony Formation Assay for Chinese Herb Function and Toxicities." Thesis, 2002. http://ndltd.ncl.edu.tw/handle/78319687984614253181.

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碩士
台北醫學院
細胞及分子生物研究所
90
Abstract The highly proliferative potential colony - forming Assay (CFA) has been known as one of the most informative, reliable, and versatile short-term in vitro assay for examining stem/progenitor cell function. Chinese drugs working on hematopoietic system were usually examined by feeding mice with herb extract before or after irradiation damage of hematopoietic stem/progenitor cells (HS/PC) in bone marrow. In this study we use human cord blood HS/PC to conduct a human erythoid and myeloid colony assay (hCFA) for evaluation of Chinese herb function on blood renewing and immunity improving. Our results show that (1) the methanol extract of PG increases the size of the CFU-GM colonies significantly, and the cells are similar to the activated macrophage. (2) CSZ extract in 50% EtOH promotes cell proliferation of the CFU-GM. (3) The extract,SD, and ,SM, enhance both BFU-E and CFU-E formation. (4) The effects of chemical BJ-1, BJ-2, BJ-3, TWD-1 significantly inhibited the formation of BFU-E and CFU-E, however, TWD-1 inhibits the formation of BFU-E and CFU-E. (5) The extract, SC, at concentration 100μg/ml inhibits the all kind colony formation slightly ,but at the same concentration entirely inhibits the TF-1 cell proliferation. The above results suggest that the in vitro CFA method presented an advantage on economic and speed. In this study we concluded that changes in morphology, size, number of colony can be used to evaluate the function and toxicity of Chinese herb as well as the synthetic chemical drug candidates. Key Words: Chinese Herb Function,In Vitro Colony Formation Assay,Hematopoietic Stem Cell
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2

Katz, David. "Searching for Radiosensitizers: Development of a Novel Assay and High-throughput Screening." Thesis, 2008. http://hdl.handle.net/1807/17184.

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The colony formation assay (CFA) is the gold standard for measuring cytotoxic effects on cells. To increase efficiency, the CFA was converted to a 96-well format using an automated colony counting algorithm. The 96-well CFA was validated using ionizing radiation (IR) on the FaDu and A549 cancer cell lines. Its ability to evaluate combination therapies was investigated using cisplatin and IR. The 96-well CFA was transferred to a robotic platform for evaluation as a high-throughput screen (HTS) readout for the discovery of novel anti-cancer compounds, and radiosensitizers. Screening yielded eight putative anti-cancer hits, and five putative radiosensitizing hits. Secondary screening confirmed 6/8 anti-cancer compounds, and 0/5 radiosensitizing compounds. Thus, the 96-well CFA can be adopted as an alternative assay to the 6-well CFA in the evaluation of cytotoxicity in vitro, providing a possible readout to be utilized in HTS for discovering anti-cancer compounds, but with limited applicability in discovering radiosensitizers.
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Book chapters on the topic "Colony Formation Assay"

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Kronstein-Wiedemann, Romy, and Torsten Tonn. "Colony Formation: An Assay of Hematopoietic Progenitor Cells." In Stem Cell Mobilization, 29–40. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9574-5_3.

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2

Steinberg, Pablo. "Automated Soft Agar Colony Formation Assay for the High-Throughput Screening of Malignant Cell Transformation." In High-Throughput Screening Methods in Toxicity Testing, 309–16. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118538203.ch16.

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Corbett, Thomas H., Frederick A. Valeriote, Lisa Polin, Chiab Panchapor, Susan Pugh, Kathryn White, Nancy Lowichik, et al. "Discovery of Solid Tumor Active Agents Using a Soft-Agar-Colony-Formation Disk-Diffusion-Assay." In Cytotoxic Anticancer Drugs: Models and Concepts for Drug Discovery and Development, 35–87. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3492-1_3.

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"Lung Colony Formation Assay." In Encyclopedia of Cancer, 2115. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3436.

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Conference papers on the topic "Colony Formation Assay"

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Alley, Michael C., Mark W. Burkett, Karen M. Hite, Susan D. Mertins, John E. Niederhuber, and Robert H. Shoemaker. "Abstract 3379: Adaptation of soft agar colony formation assays to identify agents which block proliferation of putative colon cancer stem cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3379.

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Mohamed, Islam, Ahmed Moahmed, Mennatallah Abdelkader, Alaaeldin Saleh, and Ala-Eddin Al-Moustafa. "Elaeagnus Angustifolia: a Promising Medicinal Plant for Cancer Theraby." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0124.

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Introduction: Elaeagnus angustifolia (EA) is a medicinal plant that has been used for centuries in treating many human diseases, in the Middle East, including fever, amoebic dysentery, gastrointestinal problems. However, the effect of EA plant extract on human cancer progression especially oral malignancy has not been investigated yet. Thus, first we examined the effect of EA flower extract on angiogenesis in ovo, and on selected parameters in human oral cancer cells. Materials and methods: Chorioallantoic membranes (CAMs) of chicken embryos at 3-7 days of incubation were used to assess the effect EAflower plant extract on angiogenesis. Meanwhile, cell proliferation, soft agar, cell cycle, cell invasion and cell wounding assays were performed to explore the outcome of EA plant extract on FaDu and SCC25 oral cancer cell lines. On the other hand, western blot analysis was carried out to evaluate E-cadherin and Erk1/Erk2 expression and activation, respectively, in FaDu and SCC25 under the effect of EA extract. Results: Our data show that EA extract inhibits cell proliferation and colony formation, in addition to the initiation of Scell cycle arrest and reductionof G1/G2 phases. In parallel, EA extract provokes differentiation to an epithelial phenotype “mesenchymal-epithelial transition: MET” which is the opposite of “epithelial-mesenchymal transition, EMT”: an important event in cell invasion and metastasis. Thus, EA extract causes a dramatic decrease in cell motility and invasion abilities of FaDu and SCC25 cancer cells in comparison with their controls. These changes are accompanied by an up-regulation of E-cadherin expression. The molecular pathway analysis of the EA flower extract reveals that it can inhibit the phosphorylation of Erk1/Erk2, which could be behind the inhibition of angiogenesis, the initiation of MET event and the overexpression of E-cadherin. Conclusions: Our findings indicate that EA plant extract can downgrade human oral cancer progression by the inhibition of angiogenesis and cell invasion via Erk1/Erk2 signaling pathways.
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Shattil, S. J., J. A. Hoxie, M. Cunningham, C. S. Abrahms, J. O’Brien, and Z. Budzynski. "DETECTION OF ACTIVATED PLATELETS IN WHOLE BLOOD BY FLOW CYTOMETRY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643830.

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Platelets may become activated in a number of clinical disorders and participate in thrombus formation. We have developed a direct test for activated platelets in whole blood that utilizes dual-color flow cytometry and requires no washing steps. Platelets were distinguished from erythrocytes and white blood cells in the flow cytometer by labeling the platelets with biotin-AP1, an antibody specific for membrane glycoprotein lb, and analyzing the cells for phycoerythrin-streptavidin fluorescence. Membrane surface changes resulting from platelet activation were detected with three different FITC-labeled monoclonal antibodies: 1) PAC1, an antibody specific for the fibrinogen receptor on activated platelets; 2) 9F9, which binds to the D-domain of fibrinogen and detects platelet-bound fibrinogen; and 3) S12, which binds to an alpha-granule membrane protein that associates with the platelet surface during secretion. Unstimulated platelets demonstrated no PAC1, 9F9, or S12-specific fluorescence, indicating that they did not bind these antibodies. Upon stimulation with agonists, however, the platelets demonstrated a dose-dependent increase in FITC-fluorescence. The binding of 9F9 to activated platelets required fibrinogen. Low concentrations of ADP and epinephrine, which induce fibrinogen receptors but little secretion, stimulated near-maximal PAC1 or 9F9 binding but little S12 binding. On the other hand, a concentration of phorbol myristate acetate that evokes full platelet aggregation and secretion induced maximal binding of all three antibodies. When blood samples containing activated and non-activated platelets were mixed, as few as 0.8% activated platelets could be detected by this technique. There was a direct correlation between ADP-induced FITC-PAC1 binding and binding determined in a conventional 125I-PAC1 binding assay (r = 0.99; p < 0.001). These studies demonstrate that activated platelets can be reliably detected in whole blood using activation-dependent monoclonal antibodies and flow cytometry. This method may be useful to assess the degree of platelet activation and the efficacy platelet inhibitor therapy in thrombotic disorders.
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