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Journal articles on the topic 'Transformed growth'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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1

MORSE, PAIGE MARIE. "TRANSFORMED DSM TARGETS GROWTH." Chemical & Engineering News Archive 89, no. 11 (March 14, 2011): 24–27. http://dx.doi.org/10.1021/cen-v089n011.p024.

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2

Yang, Bo, Haguy Wolfenson, Vin Yee Chung, Naotaka Nakazawa, Shuaimin Liu, Junqiang Hu, Ruby Yun-Ju Huang, and Michael P. Sheetz. "Stopping transformed cancer cell growth by rigidity sensing." Nature Materials 19, no. 2 (October 28, 2019): 239–50. http://dx.doi.org/10.1038/s41563-019-0507-0.

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3

Macek, T., and K. Green. "Growth Studies Using Transformed Roots ofSolanum aviculareandS. nigrum." Planta Medica 59, S 1 (December 1993): A659. http://dx.doi.org/10.1055/s-2006-959923.

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4

Reed, M. L. E., and Bernard R. Glick. "Growth of canola (Brassica napus) in the presence of plant growth-promoting bacteria and either copper or polycyclic aromatic hydrocarbons." Canadian Journal of Microbiology 51, no. 12 (December 1, 2005): 1061–69. http://dx.doi.org/10.1139/w05-094.

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Growth of canola (Brassica napus) seeds treated with plant growth-promoting bacteria in copper-contaminated and polycyclic aromatic hydrocarbon (PAH)-contaminated soils was monitored. Pseudomonas asplenii AC, isolated from PAH-contaminated soil, was transformed to express a bacterial gene encoding 1-aminocyclopropane-1-carboxylate (ACC) deaminase, and both native and transformed bacteria were tested for growth promotion. Inoculation of seeds, grown in the presence of copper or creosote, with either native or transformed P. asplenii AC significantly increased root and shoot biomass. Native and transformed P. asplenii AC and transformed P. asplenii AC encapsulated in alginate were equally effective at promoting plant growth in copper-contaminated soils. In creosote-contaminated soils the native bacterium was the least effective, and the transformed encapsulated bacterium was the most effective in growth promotion.Key words: plant growth-promoting bacteria, phytoremediation, copper, polycyclic aromatic hydrocarbons, Brassica napus, ethylene, alginate encapsulation.
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5

Kuntz, Sabine, Silvia Rudloff, and Clemens Kunz. "Oligosaccharides from human milk influence growth-related characteristics of intestinally transformed and non-transformed intestinal cells." British Journal of Nutrition 99, no. 3 (March 2008): 462–71. http://dx.doi.org/10.1017/s0007114507824068.

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Human milk oligosaccharides (HMO) are considered to influence the composition of the gut microflora in breastfed infants. We investigated direct effects of milk HMO fractions or individual oligosaccharides on proliferation, differentiation and apoptosis in transformed human intestinal cells (HT-29 and Caco-2) and non-transformed small intestinal epithelial crypt cells of fetal origin (human intestinal epithelial cells; HIEC). We observed growth inhibition induced by neutral and acidic HMO fractions in HT-29, Caco-2 and HIEC cells in a dose dependent manner. However, the effects varied between cell lines, i.e. HT-29 and Caco-2 cells were more sensitive than HIEC cells. In HT-29, all 16 individual neutral and acidic oligosaccharides except from the two fucosyllactoses had an inhibitory effect on cell growth. Regarding the induction of differentiation in HT-29 and HIEC cells a threshold concentration was observed at 7·5 mg/ml for neutral and acidic HMO fractions. Among individual oligosaccharides, only sialyllactoses induced differentiation in HT-29 and HIEC cells; no effect neither of fractions nor of individual oligosaccharides was found in Caco-2 cells. A strong induction of apoptosis was only detected in HT-29 and HIEC cells for neutral oligosaccharide but not for acidic fractions. HMO were shown to induce growth inhibition in intestinal cells through two different mechanisms, by suppressing cell cycle progression through induction of differentiation and/or by influencing apoptosis. As the development and maturation of digestive and absorptive processes depend on differentiation our experiments show that oligosaccharides are effective at influencing various stages in gastrointestinal development in vitro.
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6

Burgess, Antony W. "Growth control mechanisms in normal and transformed intestinal cells." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 353, no. 1370 (June 29, 1998): 903–9. http://dx.doi.org/10.1098/rstb.1998.0254.

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The cells populating the intestinal crypts are part of a dynamic tissue system which involves the self–renewal of stem cells, a commitment to proliferation, lineage–specific differentiation, movement and cell death. Our knowledge of these processes is limited, but even now there are important clues to the nature of the regulatory systems, and these clues are leading to a better understanding of intestinal cancers. Few intestinal–specific markers have been described; however, homeobox genes such as cdx–2 appear to be important for morphogenic events in the intestine. There are several intestinal cell surface proteins such as the A33 antigen which have been used as targets for immunotherapy. Many regulatory cytokines (lymphokines or growth factors) influence intestinal development: enteroglucagon, IL–2, FGF, EGF family members. In conjunction with cell–cell contact and/or ECM, these cytokines lead to specific differentiation signals. Although the tissue distribution of mitogens such as EGF, TGFα, amphiregulin, betacellulin, HB–EGF and cripto have been studied in detail, the physiological roles of these proteins have been difficult to determine. Clearly, these mitogens and the corresponding receptors are involved in the maintenance and progression of the tumorigenic state. The interactions between mitogenic, tumour suppressor and oncogenic systems are complex, but the tumorigenic effects of multiple lesions in intestinal carcinomas involve synergistic actions from lesions in these different systems. Together, the truncation of apc and activation of the ras oncogene are sufficient to induce colon tumorigenesis. If we are to improve cancer therapy, it is imperative that we discover the biological significance of these interactions, in particular the effects on cell division, movement and survival.
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7

Rizzino, Angie, and Eric Ruff. "Fibroblast growth factor induces the soft agar growth of two non-transformed celllines." In Vitro Cellular & Developmental Biology 22, no. 12 (December 1986): 749–55. http://dx.doi.org/10.1007/bf02621092.

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8

Massagué, J. "Transforming growth factor-beta modulates the high-affinity receptors for epidermal growth factor and transforming growth factor-alpha." Journal of Cell Biology 100, no. 5 (May 1, 1985): 1508–14. http://dx.doi.org/10.1083/jcb.100.5.1508.

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The epidermal growth factor (EGF) receptor mediates the induction of a transformed phenotype in normal rat kidney (NRK) cells by transforming growth factors (TGFs). The ability of EGF and its analogue TGF-alpha to induce the transformed phenotype in NRK cells is greatly potentiated by TGF-beta, a polypeptide that does not interact directly with binding sites for EGF or TGF-alpha. Our evidence indicates that TGF-beta purified from retrovirally transformed rat embryo cells and human platelets induces a rapid (t 1/2 = 0.3 h) decrease in the binding of EGF and TGF-alpha to high-affinity cell surface receptors in NRK cells. No change due to TGF-beta was observed in the binding of EGF or TGF-alpha to lower affinity sites also present in NRK cells. The effect of TGF-beta on EGF/TGF-alpha receptors was observed at concentrations (0.5-20 pM) similar to those at which TGF-beta is active in promoting proliferation of NRK cells in monolayer culture and semisolid medium. Affinity labeling of NRK cells and membranes by cross-linking with receptor-bound 125I-TGF-alpha and 125I-EGF indicated that both factors interact with a common 170-kD receptor structure. Treatment of cells with TGF-beta decreased the intensity of affinity-labeling of this receptor structure. These data suggest that the 170 kD high-affinity receptors for EGF and TGF-alpha in NRK cells are a target for rapid modulation by TGF-beta.
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9

Nomura, Takahiro, Kazuo Ryoyama, Gensaku Okada, Sadaya Matano, Shinobu Nakamura, and Tadanori Kameyama. "Non-transformed, but notras/myc-transformed, Serum-free Mouse Embryo Cells Recover from Growth Suppression by Azatyrosine." Japanese Journal of Cancer Research 83, no. 8 (August 1992): 851–58. http://dx.doi.org/10.1111/j.1349-7006.1992.tb01990.x.

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10

Holzer, Claudia, Peter Maier, and Gerhard Zbinden. "Comparison of Exogenous Growth Stimuli for Chemically Transformed Cells: Growth Factors, Serum and Cocultures." Pathobiology 54, no. 5-6 (1986): 237–44. http://dx.doi.org/10.1159/000163362.

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11

KOSHIMIZU, Hajime. "Soil condition and tree growth on the transformed hill-site." Quaternary Research (Daiyonki-Kenkyu) 24, no. 3 (1985): 207–13. http://dx.doi.org/10.4116/jaqua.24.207.

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12

Ferriola, P. C., R. Steigerwalt, AT Robertson, and P. Nettesheim. "Abnormalities in Growth Regulation of Transformed Rat Tracheal Epithelial Cells." Pathobiology 58, no. 1 (1990): 28–36. http://dx.doi.org/10.1159/000163562.

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13

Toombs, Gordon L. "Book Review: Being Transformed: An Inner Way of Spiritual Growth." Journal of Pastoral Care 39, no. 1 (March 1985): 86–88. http://dx.doi.org/10.1177/002234098503900116.

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14

Spiegelman, Vladimir S., Irina V. Budunova, Steve Carbajal, and Thomas J. Slaga. "Resistance of transformed mouse keratinocytes to growth inhibition by glucocorticoids." Molecular Carcinogenesis 20, no. 1 (September 1997): 99–107. http://dx.doi.org/10.1002/(sici)1098-2744(199709)20:1<99::aid-mc11>3.0.co;2-4.

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15

Garry, Robert F., and Henry R. Bose. "Autogenous growth factor production by reticuloendotheliosis virus-transformed hematopoietic cells." Journal of Cellular Biochemistry 37, no. 3 (July 1988): 327–38. http://dx.doi.org/10.1002/jcb.240370307.

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16

Ciardiello, Fortunato, Eva M. Valverius, G. Luca Colucci-D'Amato, Nancy Kim, Robert H. Bassin, and David S.Salomon. "Differential growth factor expression in transformed mouse NIH-3T3 cells." Journal of Cellular Biochemistry 42, no. 1 (January 1990): 45–57. http://dx.doi.org/10.1002/jcb.240420105.

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17

Zhang, QiGuo, Fujiko Tsukahara, and Yoshiro Maru. "N-acetyl-cysteine enhances growth in BCR-ABL-transformed cells." Cancer Science 96, no. 4 (April 2005): 240–44. http://dx.doi.org/10.1111/j.1349-7006.2005.00038.x.

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18

Van der Ven, Leo T. M., Louk H. P. M. Rademakers, Alexander F. Angulo, Jacques C. Giltay, Iris Wills, Gerard H. Jansen, Irma M. Prinsen, Anne G. M. Rombouts, Paul J. M. Roholl, and Willem Den Otter. "Growth of mycoplasma transformed tTN129 cells depends on IGF-I." In Vitro Cellular & Developmental Biology - Animal 29, no. 7 (July 1993): 517–22. http://dx.doi.org/10.1007/bf02634142.

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19

Roth, Petra S., Thomas J. Bach, and Malcolm J. Thompson. "Brassinosteroids: Potent inhibitors of growth of transformed tobacco callus cultures." Plant Science 59, no. 1 (January 1989): 63–70. http://dx.doi.org/10.1016/0168-9452(89)90009-5.

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20

Levine, Alan E., Craig A. Crandall, and Michael G. Brattain. "Regulation of growth inhibitory activity in transformed mouse embryo fibroblasts." Experimental Cell Research 171, no. 2 (August 1987): 357–66. http://dx.doi.org/10.1016/0014-4827(87)90168-6.

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21

GONCALVES, E., C. VENTURA, T. YANO, M. RODRIGUESMACEDO, and S. GENARI. "Morphological and growth alterations in Vero cells transformed by cisplatin." Cell Biology International 30, no. 6 (June 2006): 485–94. http://dx.doi.org/10.1016/j.cellbi.2005.12.007.

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22

Kothapalli, Ravi, Najla Guthrie, Ann F. Chambers, and Kenneth K. Carroll. "Famesylamine: An inhibitor of famesylation and growth ofras-transformed cells." Lipids 28, no. 11 (November 1993): 969–73. http://dx.doi.org/10.1007/bf02537116.

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23

Esinduy, Canan B., Chia Cheng Chang, James E. Trosko, and Randall J. Ruch. "In vitro growth inhibition of neoplastically transformed cells by non-transformed cells: requirement for gap junctional intercellular communication." Carcinogenesis 16, no. 4 (1995): 915–21. http://dx.doi.org/10.1093/carcin/16.4.915.

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24

Neufeld, G., R. Mitchell, P. Ponte, and D. Gospodarowicz. "Expression of human basic fibroblast growth factor cDNA in baby hamster kidney-derived cells results in autonomous cell growth." Journal of Cell Biology 106, no. 4 (April 1, 1988): 1385–94. http://dx.doi.org/10.1083/jcb.106.4.1385.

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Growth factor over-production by responsive cells might contribute to their autonomous proliferation as well as their acquisition of a transformed phenotype in culture. Basic fibroblast growth factor (bFGF) has been shown to induce transient changes in cell behavior that resemble those encountered in transformed cells. In addition, several types of human tumor cells have been shown to produce bFGF. To determine directly the role that bFGF might play in the induction of the transformed phenotype, we have introduced a human bFGF cDNA expression vector into baby hamster kidney-derived (BHK-21) fibroblasts. One of the BHK transfectants, termed clone 19, expresses the bFGF mRNA and produces biologically active bFGF that accumulates to a high concentration inside the cells. These properties correlate with the ability of the cells to grow in serum-free medium without the addition of exogenous bFGF. Clone 19 cells also proliferated in soft agar, indicating that constitutive expression of the bFGF gene results in a loss of anchorage-dependent growth.
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25

Moscatelli, D., and N. Quarto. "Transformation of NIH 3T3 cells with basic fibroblast growth factor or the hst/K-fgf oncogene causes downregulation of the fibroblast growth factor receptor: reversal of morphological transformation and restoration of receptor number by suramin." Journal of Cell Biology 109, no. 5 (November 1, 1989): 2519–27. http://dx.doi.org/10.1083/jcb.109.5.2519.

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When NIH 3T3 cells were transfected with the cDNA for basic fibroblast growth factor (bFGF), most cells displayed a transformed phenotype. Acquisition of a transformed phenotype was correlated with the expression of high levels of bFGF (Quarto et al., 1989). Cells that had been transformed as a result of transfection with bFGF cDNA had a decreased capacity to bind 125I-bFGF to high affinity receptors. NIH 3T3 cells transfected with bFGF cDNA that expressed lower levels of bFGF were not transformed and had a normal number of bFGF receptors. NIH 3T3 cells transfected with the hst/Kfgf oncogene, which encodes a secreted molecule with 45% homology to bFGF, also displayed a transformed phenotype and decreased numbers of bFGF receptors. However, NIH 3T3 cells transfected with the H-ras oncogene were transformed but had a normal number of bFGF receptors. Thus, transformation by bFGF-like molecules resulted in downregulation of bFGF receptors. Receptor number was not affected by cell density for both parental NIH 3T3 cells and transformed cells. In the cells transfected with bFGF cDNA that were not transformed, the receptors could be downregulated in response to exogenous bFGF. Conditioned medium from transformed transfected cells contained sufficient quantities of bFGF to downregulate bFGF receptors on parental NIH 3T3 cells. Thus, the downregulation of bFGF receptors seemed related to the presence of bFGF in an extracytoplasmic compartment. Treatment of the transformed transfected NIH 3T3 cells with suramin, which blocks the interaction of bFGF with its receptor, reversed the morphological transformation and restored receptors almost to normal numbers. These results demonstrate that in these cells bFGF transforms cells by interacting with its receptor and that bFGF and hst/K-fgf may use the same receptor.
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26

Wang, Hong-Bei, Micah Dembo, and Yu-Li Wang. "Substrate flexibility regulates growth and apoptosis of normal but not transformed cells." American Journal of Physiology-Cell Physiology 279, no. 5 (November 1, 2000): C1345—C1350. http://dx.doi.org/10.1152/ajpcell.2000.279.5.c1345.

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One of the hallmarks of oncogenic transformation is anchorage-independent growth (27). Here we demonstrate that responses to substrate rigidity play a major role in distinguishing the growth behavior of normal cells from that of transformed cells. We cultured normal or H- ras-transformed NIH 3T3 cells on flexible collagen-coated polyacrylamide substrates with similar chemical properties but different rigidity. Compared with cells cultured on stiff substrates, nontransformed cells on flexible substrates showed a decrease in the rate of DNA synthesis and an increase in the rate of apoptosis. These responses on flexible substrates are coupled to decreases in cell spreading area and traction forces. In contrast, transformed cells maintained their growth and apoptotic characteristics regardless of substrate flexibility. The responses in cell spreading area and traction forces to substrate flexibility were similarly diminished. Our results suggest that normal cells are capable of probing substrate rigidity and that proper mechanical feedback is required for regulating cell shape, cell growth, and survival. The loss of this response can explain the unregulated growth of transformed cells.
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27

Djurhuus, R., A. M. Svardal, P. M. Ueland, J. R. Lillehaug, and R. Male. "Growth support, toxicity and some metabolic effects of homocysteine in non-transformed and chemically transformed C3H/10T1/2 cells." European Journal of Cancer and Clinical Oncology 23, no. 11 (November 1987): 1745. http://dx.doi.org/10.1016/0277-5379(87)90527-x.

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28

Wossning, Thomas, Sebastian Herzog, Fabian Köhler, Sonja Meixlsperger, Yogesh Kulathu, Gerhard Mittler, Akihiro Abe, Uta Fuchs, Arndt Borkhardt, and Hassan Jumaa. "Deregulated Syk inhibits differentiation and induces growth factor–independent proliferation of pre–B cells." Journal of Experimental Medicine 203, no. 13 (November 27, 2006): 2829–40. http://dx.doi.org/10.1084/jem.20060967.

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The nonreceptor protein spleen tyrosine kinase (Syk) is a key mediator of signal transduction in a variety of cell types, including B lymphocytes. We show that deregulated Syk activity allows growth factor–independent proliferation and transforms bone marrow–derived pre–B cells that are then able to induce leukemia in mice. Syk-transformed pre–B cells show a characteristic pattern of tyrosine phosphorylation, increased c-Myc expression, and defective differentiation. Treatment of Syk-transformed pre–B cells with a novel Syk-specific inhibitor (R406) reduces tyrosine phosphorylation and c-Myc expression. In addition, R406 treatment removes the developmental block and allows the differentiation of the Syk-transformed pre–B cells into immature B cells. Because R406 treatment also prevents the proliferation of c-Myc–transformed pre–B cells, our data indicate that endogenous Syk kinase activity may be required for the survival of pre–B cells transformed by other oncogenes. Collectively, our data suggest that Syk is a protooncogene involved in the transformation of lymphocytes, thus making Syk a potential target for the treatment of leukemia.
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29

Anzano, M. A., A. B. Roberts, J. E. De Larco, L. M. Wakefield, R. K. Assoian, N. S. Roche, J. M. Smith, J. E. Lazarus, and M. B. Sporn. "Increased secretion of type beta transforming growth factor accompanies viral transformation of cells." Molecular and Cellular Biology 5, no. 1 (January 1985): 242–47. http://dx.doi.org/10.1128/mcb.5.1.242.

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Cells transformed by Harvey or Moloney sarcoma virus secrete at least 40 times as much type beta transforming growth factor as their respective untransformed control cells. The transformed cells bind only 20 to 50% as much type beta transforming growth factor as the control cells, suggesting that transformation causes down-regulation of the type beta transforming growth factor receptor.
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30

Anzano, M. A., A. B. Roberts, J. E. De Larco, L. M. Wakefield, R. K. Assoian, N. S. Roche, J. M. Smith, J. E. Lazarus, and M. B. Sporn. "Increased secretion of type beta transforming growth factor accompanies viral transformation of cells." Molecular and Cellular Biology 5, no. 1 (January 1985): 242–47. http://dx.doi.org/10.1128/mcb.5.1.242-247.1985.

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Cells transformed by Harvey or Moloney sarcoma virus secrete at least 40 times as much type beta transforming growth factor as their respective untransformed control cells. The transformed cells bind only 20 to 50% as much type beta transforming growth factor as the control cells, suggesting that transformation causes down-regulation of the type beta transforming growth factor receptor.
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31

Rubin, Harry. "Deprivation of glutamine in cell culture reveals its potential for treating cancer." Proceedings of the National Academy of Sciences 116, no. 14 (March 15, 2019): 6964–68. http://dx.doi.org/10.1073/pnas.1815968116.

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The growth-stimulating capacity of calf serum (CS) in cell culture reaches a maximum of 10% with Balb 3T3 cells, remains at a plateau to 40% CS, and declines steeply to 100% CS. Growth capacity can be largely restored to the latter by a combination of cystine and glutamine. Glutamine is a conditionally essential amino acid that continues to function at very low concentrations to support the growth of nontransformed cells, but transformed cells require much larger concentrations to survive. These different requirements hold true over a 10-fold variation in background concentrations of CS and amino acids. The high requirement of glutamine for transformed cells applies to the development of neoplastically transformed foci. These observations have given rise to a novel protocol for cancer therapy based on the large difference in the need for glutamine between nontransformed and transformed cells. This protocol would stop the cumulative growth and survival of the transformed cells without reducing the growth rate of the nontransformed cells. The results call for studies of glutamine deprivation as a treatment for experimental cancer in rodents and clinical trials in humans.
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32

Song, Yuhong, Raymond S. Maul, C. Sachi Gerbin, and David D. Chang. "Inhibition of Anchorage-independent Growth of Transformed NIH3T3 Cells by Epithelial Protein Lost in Neoplasm (EPLIN) Requires Localization of EPLIN to Actin Cytoskeleton." Molecular Biology of the Cell 13, no. 4 (April 2002): 1408–16. http://dx.doi.org/10.1091/mbc.01-08-0414.

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Epithelial protein lost in neoplasm (EPLIN) is a cytoskeleton-associated protein characterized by the presence of a single centrally located lin-11, isl-1, and mec-3 (LIM) domain. We have reported previously that EPLIN is down-regulated in transformed cells. In this study, we have investigated whether ectopic expression of EPLIN affects transformation. In untransformed NIH3T3 cells, retroviral-mediated transduction of EPLIN did not alter the cell morphology or growth. NIH3T3 cells expressing EPLIN, however, failed to form colonies when transformed by the activated Cdc42 or the chimeric nuclear oncogene EWS/Fli-1. This suppression of anchorage-independent growth was not universal because EPLIN failed to inhibit the colony formation of Ras-transformed cells. Interestingly, the localization of EPLIN to the actin cytoskeleton was maintained in the EWS/Fli-1– or Cdc42-transformed cells, but not in Ras-transformed cells where it was distributed heterogeneously in the cytoplasm. Using truncated EPLIN constructs, we demonstrated that the NH2-terminal region of EPLIN is necessary for both the localization of EPLIN to the actin cytoskeleton and suppression of anchorage-independent growth of EWS/Fli-1–transformed cells. The LIM domain or the COOH-terminal region of EPLIN could be deleted without affecting its cytoskeletal localization or ability to suppress anchorage-dependent growth. Our study indicates EPLIN may function in growth control by associating with and regulating the actin cytoskeleton.
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33

Chan, L. F., L. F. O. Chen, H. Y. Lu, C. H. Lin, H. C. Huang, M. Y. Ting, Y. M. Chang, C. Y. Lin, and M. T. Wu. "Growth, yield and shelf-life of isopentenyltransferase (ipt)-gene transformed broccoli." Canadian Journal of Plant Science 89, no. 4 (July 1, 2009): 701–11. http://dx.doi.org/10.4141/cjps08156.

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Loss of chlorophyll leading to floret yellowing limits the post-harvest lifespan of broccoli (Brassica oleracea L. var. italica Plenck). Cytokinins are known to delay floral yellowing of plants. A transgene construct pSG766A, which results in the expression of isopentenyltransferase (ipt), the key enzyme for cytokinin synthesis, has been developed in broccoli. Expression of the ipt transgene is triggered by the senescence-associated gene promoter (SAG-13). Three selfed T5 lines of ipt transformed broccoli (lines 101, 102 and 103) have been obtained through selection for single copy insertion, acceptable horticultural traits and transgene ipt activity. These three transgenic inbred lines were evaluated in the field during 2004-2007 to determine their growth, yield and shelf-life after harvest, relative to a non-transgenic inbred line (104) and the parental variety Green King. For most of the vegetative growth parameters measured, year-to-year variability exceeded line-to-line variability. Inbreeding had little impact on the appearance or yield potential of the broccoli lines. Head yields of the transgenic inbred lines 102 and 103 were comparable to the parental variety Green King, but were significantly higher than the non-transgenic inbred line 104, as lines 102 and 103 produced more plants with heavier flower heads. Cytokinin content in the form of isopentenyladenosine was relatively higher in the transgenic lines than in the two non-transgenic controls. When flower heads were stored at 25 ± 2°C, the period required to cause 50% floret yellowing was 7.5 and 8.5 d for the transgenic lines 102 and 103, respectively, compared with 5.6 d for the non-transgenic line 104, and 5.1 d for the parental variety Green King. This study showed that the ipt-transformed inbred lines of broccoli combined acceptable appearance and yields with enhanced shelf-life.Key words: Brassica oleracea L. var. italica Plenck, transgenic broccoli, isopentenyltransferase gene, genetic characterization, shelf-life
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34

Burbee, David G., Catherine Morrissey, Yoshitaka Sekido, Kwun Fong, Michael White, Adi Gazdar, and John Minna. "O-176 Suppression of transformed lung cell growth by RASSF3A (NORE1A)." Lung Cancer 41 (August 2003): S53. http://dx.doi.org/10.1016/s0169-5002(03)91834-4.

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35

MELANI, RAFFAELLA, FABIO SALLUSTIO, PAOLO FARDIN, CRISTINA VANNI, MARZIA OGNIBENE, CATHERINE OTTAVIANO, GIOVANNI MELILLO, LUIGI VARESIO, and ALESSANDRA EVA. "Growth Arrest-Inducing Genes Are Activated in Dbl-Transformed Mouse Fibroblasts." Gene Expression 13, no. 3 (March 1, 2006): 155–65. http://dx.doi.org/10.3727/000000006783991845.

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36

Averbuch, M., D. Kazanov, D. Keret, M. Pick, L. Strier, H. Dvori-Sobol, V. Deutsch, T. Kunick, Z. Halpern, and N. Arber. "Rofecoxib Does not Inhibit the Growth of Transformed Cells In Vitro." Gastrointestinal Oncology 4, no. 2-3 (January 1, 2002): 71–75. http://dx.doi.org/10.1080/1475956021000041112.

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Vanhala, Leena, Manu Eeva, Seppo Lapinjoki, Raimo Hiltunen, and Kirsi-Marja Oksman-Caldentey. "Effect of growth regulators on transformed root cultures of Hyoscyamus muticus." Journal of Plant Physiology 153, no. 3-4 (January 1998): 475–81. http://dx.doi.org/10.1016/s0176-1617(98)80177-6.

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Dell'Era, Patrizia, Laura Coco, Roberto Ronca, Barbara Sennino, and Marco Presta. "Gene expression profile in fibroblast growth factor 2-transformed endothelial cells." Oncogene 21, no. 15 (April 2002): 2433–40. http://dx.doi.org/10.1038/sj.onc.1205301.

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Palamakumbura, Amitha H., Pascal Sommer, and Philip C. Trackman. "Autocrine Growth Factor Regulation of Lysyl Oxidase Expression in Transformed Fibroblasts." Journal of Biological Chemistry 278, no. 33 (June 4, 2003): 30781–87. http://dx.doi.org/10.1074/jbc.m305238200.

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Kratzsch, J., T. Selisko, and G. Birkenmeier. "Transformed α2-macroglobulin as a low-affinity growth hormone-binding protein." Acta Paediatrica 85, s417 (October 1996): 108–10. http://dx.doi.org/10.1111/j.1651-2227.1996.tb14315.x.

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O'Brien, W., G. Stenman, and R. Sager. "Suppression of tumor growth by senescence in virally transformed human fibroblasts." Proceedings of the National Academy of Sciences 83, no. 22 (November 1, 1986): 8659–63. http://dx.doi.org/10.1073/pnas.83.22.8659.

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Li, Jia, Todd A. Johnson, Laurie A. Hanson, and David G. Beer. "Loss of glucocorticoid-dependent growth inhibition in transformed mouse lung cells." Molecular Carcinogenesis 16, no. 4 (August 1996): 213–20. http://dx.doi.org/10.1002/(sici)1098-2744(199608)16:4<213::aid-mc5>3.0.co;2-g.

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Masui, Tohru, John F. Lechner, George H. Yoakum, James C. Willey, and Curtis C. Harris. "Growth and differentiation of normal and transformed human bronchial epithelial cells." Journal of Cellular Physiology 129, S4 (1986): 73–81. http://dx.doi.org/10.1002/jcp.1041290414.

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Cook, Jeffry R., and Jan-Kan Chen. "Enhancement of transformed cell growth in agar by serine protease inhibitors." Journal of Cellular Physiology 136, no. 1 (July 1988): 188–93. http://dx.doi.org/10.1002/jcp.1041360125.

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Nemeth, Jeffrey A., and Charles L. Goolsby. "TIMP-2, a Growth-Stimulatory Protein from SV40-Transformed Human Fibroblasts." Experimental Cell Research 207, no. 2 (August 1993): 376–82. http://dx.doi.org/10.1006/excr.1993.1204.

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Basset, P., J. Zwiller, M. O. Revel, and G. Vincendon. "Growth promotion of transformed cells by iron in serum-free culture." Carcinogenesis 6, no. 3 (1985): 355–59. http://dx.doi.org/10.1093/carcin/6.3.355.

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Navrátilová, Jarmila, Viktor Horváth, Alois Kozubík, Antonín Lojek, Joseph Lipsick, and Jan Šmarda. "p53 arrests growth and induces differentiation of v-Myb-transformed monoblasts." Differentiation 75, no. 7 (September 2007): 592–604. http://dx.doi.org/10.1111/j.1432-0436.2006.00158.x.

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Guyon, Pierre. "Transformed Plants Producing Opines Specifically Promote Growth of Opine-Degrading Agrobacteria." Molecular Plant-Microbe Interactions 6, no. 1 (1993): 92. http://dx.doi.org/10.1094/mpmi-6-092.

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Paolo Dotto, Gian, Luis F. Parada, and Robert A. Weinberg. "Specific growth response of ras-transformed embryo fibroblasts to tumour promoters." Nature 318, no. 6045 (December 5, 1985): 472–75. http://dx.doi.org/10.1038/318472a0.

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Dotto, G. P., L. F. Parada, and R. A. Weinberg. "Specific growth response of ras-transformed embryo fibroblasts to tumour promoters." Nature 321, no. 6067 (May 1986): 258. http://dx.doi.org/10.1038/321258a0.

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