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Journal articles on the topic 'Cellular Gene Expression'

Author: Grafiati

Published: 6 September 2023

Last updated: 7 September 2023

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1

Raven, John A., Charles A. Knight, and John Beardall. "Cell size has gene expression and biophysical consequences for cellular function." Perspectives in Phycology 6, no. 1-2 (July 1, 2019): 81–94. http://dx.doi.org/10.1127/pip/2019/0086.

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2

TSUDA, Masaaki. "Gene Expression and Cellular Function." YAKUGAKU ZASSHI 113, no. 8 (1993): 537–55. http://dx.doi.org/10.1248/yakushi1947.113.8_537.

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3

Smith, James R., and Olivia M. Pereira-Smith. "Altered gene expression during cellular aging." Genome 31, no. 1 (January 1, 1989): 386–89. http://dx.doi.org/10.1139/g89-058.

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The limited division potential of normal human diploid fibroblasts in culture represents a model system for cellular aging. Observations indicate cellular senescence is an active process. Senescent cells, although unable to divide, are actively metabolizing. Hybrids from fusion of normal and immortal human cells exhibit limited division potential, suggesting that the phenotype of cellular senescence is dominant and supporting the hypothesis that senescence is genetically programmed. Fusion of immortal human cell lines with each other has identified four complementation groups for indefinite division. This indicates that a limited number of specific genes or processes are involved in senescence. Senescent cells express highly abundant DNA synthesis inhibitory messenger RNAs and produce a surface membrane associated protein inhibitor of DNA synthesis not expressed in young cells. Senescent cell membranes were used as immunogen to generate three monoclonal antibodies reacting specifically with senescent but not young cells in several normal human cell lines. We have also found that fibronectin messenger RNA accumulates to high levels in senescent cells. The role of these changes in gene expression in senescence is being explored.Key words: cellular senescence, human cells.

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4

Misteli, Tom, and David L. Spector. "The cellular organization of gene expression." Current Opinion in Cell Biology 10, no. 3 (June 1998): 323–31. http://dx.doi.org/10.1016/s0955-0674(98)80007-0.

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5

Samson, Frederick E. "OXYGEN, GENE EXPRESSION, AND CELLULAR FUNCTION." Shock 8, no. 5 (November 1997): 389. http://dx.doi.org/10.1097/00024382-199711000-00014.

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6

Samadani, Uzma, Alexander R. Judkins, Albert Akpalu, Eleonora Aronica, and Peter B. Crino. "Differential Cellular Gene Expression in Ganglioglioma." Epilepsia 48, no. 4 (April 2007): 646–53. http://dx.doi.org/10.1111/j.1528-1167.2007.00925.x.

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7

Frenk, Stephen, and Jonathan Houseley. "Gene expression hallmarks of cellular ageing." Biogerontology 19, no. 6 (February 28, 2018): 547–66. http://dx.doi.org/10.1007/s10522-018-9750-z.

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8

Canaan, Allon, Izhak Haviv, Alexander E. Urban, Vincent P. Schulz, Steve Hartman, Zhengdong Zhang, Dean Palejev, et al. "EBNA1 regulates cellular gene expression by binding cellular promoters." Proceedings of the National Academy of Sciences 106, no. 52 (December 22, 2009): 22421–26. http://dx.doi.org/10.1073/pnas.0911676106.

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9

Airoldi, Edoardo M., Curtis Huttenhower, David Gresham, Charles Lu, Amy A. Caudy, Maitreya J. Dunham, James R. Broach, David Botstein, and Olga G. Troyanskaya. "Predicting Cellular Growth from Gene Expression Signatures." PLoS Computational Biology 5, no. 1 (January 2, 2009): e1000257. http://dx.doi.org/10.1371/journal.pcbi.1000257.

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10

Hutton, Guo, Birchall, and Pearson. "Mucin gene expression in OME: cellular localization." Clinical Otolaryngology and Allied Sciences 23, no. 3 (June 1998): 281–82. http://dx.doi.org/10.1046/j.1365-2273.1998.0138f.x.

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11

Daniel, Rachael, Zhiheng He, K. Paige Carmichael, Jaroslava Halper, and Andrew Bateman. "Cellular Localization of Gene Expression for Progranulin." Journal of Histochemistry & Cytochemistry 48, no. 7 (July 2000): 999–1009. http://dx.doi.org/10.1177/002215540004800713.

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12

Namy, Olivier, Jean-Pierre Rousset, Sawsan Napthine, and Ian Brierley. "Reprogrammed Genetic Decoding in Cellular Gene Expression." Molecular Cell 13, no. 2 (January 2004): 157–68. http://dx.doi.org/10.1016/s1097-2765(04)00031-0.

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13

Schibler, Ueli, and Felix Naef. "Cellular oscillators: rhythmic gene expression and metabolism." Current Opinion in Cell Biology 17, no. 2 (April 2005): 223–29. http://dx.doi.org/10.1016/j.ceb.2005.01.007.

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14

Repetti, Robert L., Jennifer Meth, Oluwatoni Sonubi, Daniel Flores, Lisa M. Satlin, and Rajeev Rohatgi. "Cellular cholesterol modifies flow-mediated gene expression." American Journal of Physiology-Renal Physiology 317, no. 4 (October 1, 2019): F815—F824. http://dx.doi.org/10.1152/ajprenal.00196.2019.

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Downregulation of heme oxygenase-1 (HO-1), cyclooxygenase-2 (COX2), and nitric oxide synthase-2 (NOS2) in the kidneys of Dahl rodents causes salt sensitivity, while restoring their expression aids in Na+ excretion and blood pressure reduction. Loading cholesterol into collecting duct (CD) cells represses fluid shear stress (FSS)-mediated COX2 activity. Thus, we hypothesized that cholesterol represses flow-responsive genes necessary to effectuate Na+ excretion. To this end, CD cells were used to test whether FSS induces these genes and if cholesterol loading represses them. Mice fed either 0% or 1% cholesterol diet were injected with saline, urine volume and electrolytes were measured, and renal gene expression determined. FSS-exposed CD cells demonstrated increases in HO-1 mRNA by 350-fold, COX2 by 25-fold, and NOS2 by 8-fold in sheared cells compared with static cells ( P < 0.01). Immunoblot analysis of sheared cells showed increases in HO-1, COX2, and NOS2 protein, whereas conditioned media contained more HO-1 and PGE2 than static cells. Cholesterol loading repressed the sheared mediated protein abundance of HO-1 and NOS2 as well as HO-1 and PGE2 concentrations in media. In cholesterol-fed mice, urine volume was less at 6 h after injection of isotonic saline ( P < 0.05). Urinary Na+ concentration, urinary K+ concentration, and osmolality were greater, whereas Na+ excretion was less, at the 6-h urine collection time point in cholesterol-fed versus control mice ( P < 0.05). Renal cortical and medullary HO-1 ( P < 0.05) and NOS2 ( P < 0.05) mRNA were repressed in cholesterol-fed compared with control mice. Cholesterol acts to repress flow induced natriuretic gene expression, and this effect, in vivo, may contribute to renal Na+ avidity.

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15

Singh, Anirudha, Tara L. Deans, and Jennifer H. Elisseeff. "Photomodulation of Cellular Gene Expression in Hydrogels." ACS Macro Letters 2, no. 3 (March 8, 2013): 269–72. http://dx.doi.org/10.1021/mz300591m.

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16

Pietropaolo, Massimo, Nick Giannoukakis, and Massimo Trucco. "Cellular environment and freedom of gene expression." Nature Immunology 3, no. 4 (April 2002): 335. http://dx.doi.org/10.1038/ni0402-335a.

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17

Kenneth, Niall Steven, and Sonia Rocha. "Regulation of gene expression by hypoxia." Biochemical Journal 414, no. 1 (July 29, 2008): 19–29. http://dx.doi.org/10.1042/bj20081055.

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Hypoxia induces profound changes in the cellular gene expression profile. The discovery of a major transcription factor family activated by hypoxia, HIF (hypoxia-inducible factor), and the factors that contribute to HIF regulation have greatly enhanced our knowledge of the molecular aspects of the hypoxic response. However, in addition to HIF, other transcription factors and cellular pathways are activated by exposure to reduced oxygen. In the present review, we summarize the current knowledge of how additional hypoxia-responsive transcription factors integrate with HIF and how other cellular pathways such as chromatin remodelling, translation regulation and microRNA induction, contribute to the co-ordinated cellular response observed following hypoxic stress.

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18

Sachit, Hayat Ghaith, Taghreed F. Almahbobi, Zahraa Muhsen M. Ali, Saad Hasan Mohammed Ali, and Shakir H. Mohammed Al-Alwany. "A Molecular Implicatory Propositioning Roles for Human Cytomegalovirus and P16 Gene Expression in Oral Squamous Cellular Carcinogenesis." Journal of Pure and Applied Microbiology 13, no. 4 (December 30, 2019): 2333–42. http://dx.doi.org/10.22207/jpam.13.4.49.

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19

Barski, Artem, Suresh Cuddapah, Andrey V. Kartashov, Hiromi Imamichi, Wenjing Yang, Weiqun Peng, H. Lane, and Keji Zhao. "Epigenetic regulation of gene expression and cellular differentiation." Molecular Pain 10, Suppl 1 (2014): O20. http://dx.doi.org/10.1186/1744-8069-10-s1-o20.

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20

Ejima, Miho, Koji Kadoi, and Ayae Honda. "Influenza virus infection induces cellular Ebp1 gene expression." Genes to Cells 16, no. 9 (July 28, 2011): 927–37. http://dx.doi.org/10.1111/j.1365-2443.2011.01541.x.

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21

Lehoux, Stéphanie, and Alain Tedgui. "Cellular mechanics and gene expression in blood vessels." Journal of Biomechanics 36, no. 5 (May 2003): 631–43. http://dx.doi.org/10.1016/s0021-9290(02)00441-4.

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22

Metzner, Christoph, Brian Salmons, Walter H. Gunzburg, Manfred Gemeiner, Ingrid Miller, Bernd Gesslbauer, Andreas Kungl, and John A. Dangerfield. "MMTV accessory factor Naf affects cellular gene expression." Virology 346, no. 1 (March 2006): 139–50. http://dx.doi.org/10.1016/j.virol.2005.10.029.

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23

Zhao, Hongxing, Fredrik Granberg, and Ulf Pettersson. "How adenovirus strives to control cellular gene expression." Virology 363, no. 2 (July 2007): 357–75. http://dx.doi.org/10.1016/j.virol.2007.02.013.

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24

Rausenberger, Julia, Christian Fleck, Jens Timmer, and Markus Kollmann. "Signatures of gene expression noise in cellular systems." Progress in Biophysics and Molecular Biology 100, no. 1-3 (September 2009): 57–66. http://dx.doi.org/10.1016/j.pbiomolbio.2009.06.003.

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25

Ntambi, J. M. "Cellular differentiation and dietary regulation of gene expression." Prostaglandins, Leukotrienes and Essential Fatty Acids 52, no. 2-3 (February 1995): 117–20. http://dx.doi.org/10.1016/0952-3278(95)90009-8.

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26

Jaggi, Rolf, Robert Friis, and Bernd Groner. "Oncogenes modulate cellular gene expression and repress glucocorticoid regulated gene transcription." Journal of Steroid Biochemistry 29, no. 5 (May 1988): 457–63. http://dx.doi.org/10.1016/0022-4731(88)90179-3.

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27

Satoh, Jun-ichi, and Takashi Yamamura. "Gene Expression Profile Following Stable Expression of the Cellular Prion Protein." Cellular and Molecular Neurobiology 24, no. 6 (December 2004): 793–814. http://dx.doi.org/10.1007/s10571-004-6920-0.

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28

Ray, Swagat, Pól Ó. Catnaigh, and Emma C. Anderson. "Post-transcriptional regulation of gene expression by Unr." Biochemical Society Transactions 43, no. 3 (June 1, 2015): 323–27. http://dx.doi.org/10.1042/bst20140271.

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Unr (upstream of N-ras) is a eukaryotic RNA-binding protein that has a number of roles in the post-transcriptional regulation of gene expression. Originally identified as an activator of internal initiation of picornavirus translation, it has since been shown to act as an activator and inhibitor of cellular translation and as a positive and negative regulator of mRNA stability, regulating cellular processes such as mitosis and apoptosis. The different post-transcriptional functions of Unr depend on the identity of its mRNA and protein partners and can vary with cell type and changing cellular conditions. Recent high-throughput analyses of RNA–protein interactions indicate that Unr binds to a large subset of cellular mRNAs, suggesting that Unr may play a wider role in translational responses to cellular signals than previously thought.

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29

Wen, X., H. H. Lin, and D. K. Ann. "Salivary Cellular Signaling and Gene Regulation." Advances in Dental Research 14, no. 1 (December 2000): 76–80. http://dx.doi.org/10.1177/08959374000140011201.

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Protein tyrosine kinase and protein serine kinase activation has been implicated in the regulation of salivary cell proliferation and differentiation. Aberrant expression and alterations of certain tyrosine or serine kinases, such as Raf or erbB2, are known to trigger salivary tumor development (Li et al., 1997; Cho et al., 1999). It has been estimated that there are about 1000 to 2000 protein kinases in the mammalian genome, with 100 to 200 of them ( i.e., 10%) being tyrosine kinase (Hanks and Hunter, 1995). At present, there are approximately 85 different tyrosine kinases identified in the GenBank database. Based on the relatively slow rate of discovery in the past few years, 100 is a better approximation of the total number of tyrosine kinases encoded by each mammalian genome. It is reasonable to assume that there are about 30 to 50 tyrosine kinases expressed in a given cell at a given differentiation/proliferation stage. This number is large enough to provide a characteristic tissue-specific tyrosine kinase expression profile, but small enough to be identified in a simple screening. The hope for tyrosine kinases as differentiation or proliferation markers rests with the possibility for the identification and characterization of a differentiation/proliferation stage-specific expression pattern in salivary cells. Several ligands that transmit signal through receptor tyrosine kinases and/or Ras/Raf/ERK kinases have been extensively studied in salivary cells. This review focuses mainly on the signaling pathways activated bv Raf and Etk.

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30

Wiesner, R. J., and R. Zak. "Quantitative approaches for studying gene expression." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 4 (April 1, 1991): L179—L188. http://dx.doi.org/10.1152/ajplung.1991.260.4.l179.

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The methods currently available for measuring mRNAs and proteins are reviewed, with a special emphasis on their application to physiological questions. The article focuses on the quantitative determination of cellular contents, but also on assessment of rates of synthesis and degradation, and turnover.

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31

Wildeman, Alan G. "Regulation of SV40 early gene expression." Biochemistry and Cell Biology 66, no. 6 (June 1, 1988): 567–77. http://dx.doi.org/10.1139/o88-067.

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The early promoter of the simian virus 40 (SV40) has been used as a model eukaryotic promoter for the study of DN A sequence elements and cellular factors that are involved in transcriptional control and initiation. Site-directed mutagenesis and cell-free transcription systems have enabled the dissection of the functional domains within the 21 bp upstream sequence element and the 72 bp enhancer, and a number of protein factors that bind to various "motifs" within these domains have been identified. This article summarizes recent observations that have led to the conclusion that the SV40 promoter, and particularly, the enhancer region, is composed of multiple sequence elements. Some of these elements are present in cellular genes, and may exhibit tissue-specificity in their action. Furthermore, the proteins that are being identified (e.g., Sp1) may have binding sites within these elements that are sufficiently specific to ensure that only certain sets of genes will be selectively expressed.

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32

Yang, B. S., T. J. Geddes, R. J. Pogulis, B. de Crombrugghe, and S. O. Freytag. "Transcriptional suppression of cellular gene expression by c-Myc." Molecular and Cellular Biology 11, no. 4 (April 1991): 2291–95. http://dx.doi.org/10.1128/mcb.11.4.2291-2295.1991.

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High levels of c-Myc in mouse 3T3-L1 cells specifically suppress the expression of three collagen genes. This effect is exerted through collagen promoter sequences and requires the leucine zipper motif of c-Myc. Our data suggest that an important aspect of c-Myc transforming activity is the ability to suppress specific cellular gene transcription.

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33

Strober, B. J., R. Elorbany, K. Rhodes, N. Krishnan, K. Tayeb, A. Battle, and Y. Gilad. "Dynamic genetic regulation of gene expression during cellular differentiation." Science 364, no. 6447 (June 27, 2019): 1287–90. http://dx.doi.org/10.1126/science.aaw0040.

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Genetic regulation of gene expression is dynamic, as transcription can change during cell differentiation and across cell types. We mapped expression quantitative trait loci (eQTLs) throughout differentiation to elucidate the dynamics of genetic effects on cell type–specific gene expression. We generated time-series RNA sequencing data, capturing 16 time points during the differentiation of induced pluripotent stem cells to cardiomyocytes, in 19 human cell lines. We identified hundreds of dynamic eQTLs that change over time, with enrichment in enhancers of relevant cell types. We also found nonlinear dynamic eQTLs, which affect only intermediate stages of differentiation and cannot be found by using data from mature tissues. These fleeting genetic associations with gene regulation may explain some of the components of complex traits and disease. We highlight one example of a nonlinear eQTL that is associated with body mass index.

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34

Yang, B. S., T. J. Geddes, R. J. Pogulis, B. de Crombrugghe, and S. O. Freytag. "Transcriptional suppression of cellular gene expression by c-Myc." Molecular and Cellular Biology 11, no. 4 (April 1991): 2291–95. http://dx.doi.org/10.1128/mcb.11.4.2291.

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High levels of c-Myc in mouse 3T3-L1 cells specifically suppress the expression of three collagen genes. This effect is exerted through collagen promoter sequences and requires the leucine zipper motif of c-Myc. Our data suggest that an important aspect of c-Myc transforming activity is the ability to suppress specific cellular gene transcription.

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35

Tan, Cheemeng, Saumya Saurabh, Marcel P. Bruchez, Russell Schwartz, and Philip LeDuc. "Molecular crowding shapes gene expression in synthetic cellular nanosystems." Nature Nanotechnology 8, no. 8 (July 14, 2013): 602–8. http://dx.doi.org/10.1038/nnano.2013.132.

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36

Peiró, Gloria, Joachim Diebold, and Udo Löhrs. "CAS(Cellular Apoptosis Susceptibility) Gene Expression in Ovarian Carcinoma." American Journal of Clinical Pathology 118, no. 6 (December 2002): 922–29. http://dx.doi.org/10.1309/xycb-uw8u-5541-u4qd.

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37

Zenilman, Michael E., Thomas H. Magnuson, Riccardo Perfetti, Jian Chen, and Alan R. Shuldiner. "Pancreatic reg Gene Expression Is Inhibited During Cellular Differentiation." Annals of Surgery 225, no. 3 (March 1997): 327–32. http://dx.doi.org/10.1097/00000658-199703000-00013.

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38

Sanchez, A., and I. Golding. "Genetic Determinants and Cellular Constraints in Noisy Gene Expression." Science 342, no. 6163 (December 5, 2013): 1188–93. http://dx.doi.org/10.1126/science.1242975.

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39

Engelberg-Kulka, Hanna, and Rachel Schoulaker-Schwarz. "Regulatory implications of translational frameshifting in cellular gene expression." Molecular Microbiology 11, no. 1 (January 1994): 3–8. http://dx.doi.org/10.1111/j.1365-2958.1994.tb00283.x.

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40

Frank, Steven A. "Evolution of Robustness and Cellular Stochasticity of Gene Expression." PLoS Biology 11, no. 6 (June 11, 2013): e1001578. http://dx.doi.org/10.1371/journal.pbio.1001578.

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41

Ziegler, K., S. Verma, T. Bui, RJ Frisque, R. Yanagihara, and V. Nerurkar. "Altered patterns of cellular gene expression by JC virus." Journal of Neurovirology 10, s2 (January 2004): 28. http://dx.doi.org/10.1080/13550280490469644.

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42

Campagnoni, Anthony T., and Wendy B. Macklin. "Cellular and molecular aspects of myelin protein gene expression." Molecular Neurobiology 2, no. 1 (March 1988): 41–89. http://dx.doi.org/10.1007/bf02935632.

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43

Rhoten, William B., and Sylvia Christakos. "Cellular gene expression for calbidin-D28k in mouse kidney." Anatomical Record 227, no. 2 (June 1990): 145–51. http://dx.doi.org/10.1002/ar.1092270202.

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44

Pietiäinen, Vilja, Pasi Huttunen, and Timo Hyypiä. "Effects of Echovirus 1 Infection on Cellular Gene Expression." Virology 276, no. 2 (October 2000): 243–50. http://dx.doi.org/10.1006/viro.2000.0551.

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45

Winter, Heather Y., and Susan J. Marriott. "Human T-Cell Leukemia Virus Type 1 Tax Enhances Serum Response Factor DNA Binding and Alters Site Selection." Journal of Virology 81, no. 11 (March 21, 2007): 6089–98. http://dx.doi.org/10.1128/jvi.02179-06.

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ABSTRACT Human T-cell leukemia virus type I (HTLV-1) is the etiological agent of adult T-cell leukemia. The viral transforming protein Tax regulates the transcription of viral and cellular genes by interacting with cellular transcription factors and coactivators. The effects of Tax on cellular gene expression have an important impact on HTLV-1-mediated cellular transformation. Expression of the c-fos cellular oncogene is regulated by serum response factor (SRF), and Tax is known to induce c-fos gene expression by activating SRF-responsive transcription. SRF activates cellular gene expression by binding to a consensus DNA sequence (CArG box) located within a serum response element (SRE). Since SRF activates transcription of many growth regulatory genes, this pathway is likely to have a significant impact on Tax-mediated transformation. Here we demonstrate that Tax interacts with SRF and enhances the binding of SRF to SREs located in the c-fos, Nur77, and viral promoters. Also, we establish that in the presence of Tax, SRF selects more divergent CArG box sequences than in the absence of Tax, revealing a novel mechanism for regulating SRF-responsive gene expression. Finally, increased association of SRF with chromatin and specific promoters was observed in Tax-expressing cells, correlating with increased c-fos and Nur77 mRNA levels in Tax-expressing cells. These results suggest that Tax activates SRF-responsive transcription by enhancing its binding affinity to multiple different SRE sequences.

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46

Jäger, J., C. Schulze, S. Rösner, and R. Martin. "IL7RA haplotype-associated alterations in cellular immune function and gene expression patterns in multiple sclerosis." Genes & Immunity 14, no. 7 (August 29, 2013): 453–61. http://dx.doi.org/10.1038/gene.2013.40.

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47

Santos-Berríos, C., G. A. Weisman, and F. A. Gonzalez. "P2X7 receptor induces gene expression." Journal of Neurochemistry 81 (June 28, 2008): 5–6. http://dx.doi.org/10.1046/j.1471-4159.81.s1.1_3.x.

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48

Siengdee, P., K. Nganvongpanit, P. Pothacharoen, S. Chomdej, S. Mekchay, and S. Ong-Chai. "Effects of bromelain on cellular characteristics and expression of selected genes in canine in vitro chondrocyte culture." Veterinární Medicína 55, No. 11 (December 1, 2010): 551–60. http://dx.doi.org/10.17221/3012-vetmed.

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The purpose of this study was to determine the effect of bromelain treatment on canine articular chondrocytes in vitro. This research evaluated cell viability, levels of apoptotis and mitotis, proteoglycan concentrations and the expression of certain genes. Chondrocytes were exposed to 50 μg/ml bromelain for 4, 16 and 32 h. The rate of apoptotis in the treatment groups was significantly lower than in the control groups that were incubated with media only (P < 0.05); and the mitotic rate in treatment groups was significantly higher than in the control groups (P < 0.05), at all durations of exposure. The effect of bromelain on gene expression was measured by the real-time PCR technique. It was found that bromelain significantly decreased (P < 0.05) TIMP-1 and MMP-3 expression. These experimental bromelain treatments have shown positive results, and have increased the basic knowledge in regard to the healing and modulation of osteoarthritis, prior to the general use of bromelain in clinical practice.

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49

Meng, Zhongji, Song Qiu, Xiaoyong Zhang, Jun Wu, Thomas Schreiter, Yang Xu, Dongliang Yang, Michael Roggendorf, Jörg Schlaak, and Mengji Lu. "Inhibition of woodchuck hepatitis virus gene expression in primary hepatocytes by siRNA enhances the cellular gene expression." Virology 384, no. 1 (February 2009): 88–96. http://dx.doi.org/10.1016/j.virol.2008.11.012.

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50

Der, C. J. "Cellular oncogenes and human carcinogenesis." Clinical Chemistry 33, no. 5 (May 1, 1987): 641–46. http://dx.doi.org/10.1093/clinchem/33.5.641.

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Abstract Experimental studies over the past decade have identified 30 or so cellular genes as potential oncogenes. The genetic events that lead to cellular oncogene activation may result in the excessive or inappropriate expression of the gene, or the expression of an aberrant gene product. Although the involvement of these putative cellular oncogenes in human oncogenesis has not been proven, the accumulation of considerable experimental evidence strongly implicates some role of these genes in the malignant process. The inactivation of certain genetic loci (suppressor genes) may also contribute to tumor progression.

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