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Journal articles on the topic 'Field carcinogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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1

Jones, Timothy D., Mingsheng Wang, John N. Eble, et al. "Molecular Evidence Supporting Field Effect in Urothelial Carcinogenesis." Clinical Cancer Research 11, no. 18 (2005): 6512–19. http://dx.doi.org/10.1158/1078-0432.ccr-05-0891.

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2

Hashash, Jana G., Rajan K. Bista, Douglas J. Hartman, et al. "Nuclear Refractive Index Detects the Field Effect of Carcinogenesis." Gastroenterology 140, no. 5 (2011): S—339. http://dx.doi.org/10.1016/s0016-5085(11)61378-4.

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3

Frede, Julia, David J. Adams, and Philip H. Jones. "Mutation, clonal fitness and field change in epithelial carcinogenesis." Journal of Pathology 234, no. 3 (2014): 296–301. http://dx.doi.org/10.1002/path.4409.

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4

Piérard, Gérald E., Claudine Piérard-Franchimont, Philippe Paquet, and Pascale Quatresooz. "Emerging therapies for ionizing radiation-associated skin field carcinogenesis." Expert Opinion on Pharmacotherapy 10, no. 5 (2009): 813–21. http://dx.doi.org/10.1517/14656560902754060.

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5

Torezan, Luis Antonio Ribeiro, and Cyro Festa-Neto. "Cutaneous field cancerization: clinical, histopathological and therapeutic aspects." Anais Brasileiros de Dermatologia 88, no. 5 (2013): 775–86. http://dx.doi.org/10.1590/abd1806-4841.20132300.

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The concept of "field cancerization" was first introduced by Slaughter in 1953 when studying the presence of histologically abnormal tissue surrounding oral squamous cell carcinoma. It was proposed to explain the development of multiple primary tumors and locally recurrent cancer. Organ systems in which field cancerization has been described since then are: head and neck (oral cavity, oropharynx, and larynx), lung, vulva, esophagus, cervix, breast, skin, colon, and bladder. Recent molecular studies support the carcinogenesis model in which the development of a field with genetically altered ce
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6

WALI, RAMESH K., THOMAS A. HENSING, DANIEL W. RAY, et al. "Buccal microRNA dysregulation in lung field carcinogenesis: Gender-specific implications." International Journal of Oncology 45, no. 3 (2014): 1209–15. http://dx.doi.org/10.3892/ijo.2014.2495.

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7

Hernandez-Illan, Eva, Juan Jose Lozano, Míriam Juárez, et al. "Mo1978 - Comprehensive Analysis of Methylation Field Defect in Colorectal Carcinogenesis." Gastroenterology 154, no. 6 (2018): S—870. http://dx.doi.org/10.1016/s0016-5085(18)32941-x.

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8

HAYS, GRANVIL L., SCOTT M. LIPPMAN, CATHERINE M. FLAITZ, et al. "Co-carcinogenesis and field cancerization: oral lesions offer first signs." Journal of the American Dental Association 126, no. 1 (1995): 47–51. http://dx.doi.org/10.14219/jada.archive.1995.0023.

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9

Thomson, P. J. "Field change and oral cancer: new evidence for widespread carcinogenesis?" International Journal of Oral and Maxillofacial Surgery 31, no. 3 (2002): 262–66. http://dx.doi.org/10.1054/ijom.2002.0220.

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10

Radosevich, Andrew J., Nikhil N. Mutyal, Ji Yi, et al. "Ultrastructural alterations in field carcinogenesis measured by enhanced backscattering spectroscopy." Journal of Biomedical Optics 18, no. 9 (2013): 097002. http://dx.doi.org/10.1117/1.jbo.18.9.097002.

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11

Kunte, Dhananjay P., Mart DelaCruz, Ramesh K. Wali, et al. "Dysregulation of MicroRNAs in Colonic Field Carcinogenesis: Implications for Screening." PLoS ONE 7, no. 9 (2012): e45591. http://dx.doi.org/10.1371/journal.pone.0045591.

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12

Bauer, Greta M., Yolanda Stypula-Cyrus, Hariharan Subramanian, et al. "The transformation of the nuclear nanoarchitecture in human field carcinogenesis." Future Science OA 3, no. 3 (2017): FSO206. http://dx.doi.org/10.4155/fsoa-2017-0027.

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13

Momi, Navneet, Vadim Backman, Charles B. Brendler, and Hemant K. Roy. "Harnessing novel modalities: field carcinogenesis detection for personalizing prostate cancer management." Future Oncology 11, no. 20 (2015): 2737–41. http://dx.doi.org/10.2217/fon.15.182.

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14

Seybold, Paul G., and Kenny B. Lipkowitz. "Theperi effect in aromatic hydrocarbon carcinogenesis: An empirical force field examination." International Journal of Quantum Chemistry 31, no. 6 (1987): 847–53. http://dx.doi.org/10.1002/qua.560310602.

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15

Sinjab, Ansam, Guangchun Han, Linghua Wang, and Humam Kadara. "Field Carcinogenesis in Cancer Evolution: What the Cell Is Going On?" Cancer Research 80, no. 22 (2020): 4888–91. http://dx.doi.org/10.1158/0008-5472.can-20-1956.

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16

Subramanian, Hariharan, Hemant K. Roy, Prabhakar Pradhan, et al. "Nanoscale Cellular Changes in Field Carcinogenesis Detected by Partial Wave Spectroscopy." Cancer Research 69, no. 13 (2009): 5357–63. http://dx.doi.org/10.1158/0008-5472.can-08-3895.

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17

Majewski, Tadeusz, Hui Yao, Jolanta Bondaruk, et al. "Whole-Organ Genomic Characterization of Mucosal Field Effects Initiating Bladder Carcinogenesis." Cell Reports 26, no. 8 (2019): 2241–56. http://dx.doi.org/10.1016/j.celrep.2019.01.095.

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18

Tanaka, Takuji, and Rikako Ishigamori. "Understanding Carcinogenesis for Fighting Oral Cancer." Journal of Oncology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/603740.

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Oral cancer is one of the major global threats to public health. Oral cancer development is a tobacco-related multistep and multifocal process involving field cancerization and carcinogenesis. The rationale for molecular-targeted prevention of oral cancer is promising. Biomarkers of genomic instability, including aneuploidy and allelic imbalance, are able to measure the cancer risk of oral premalignancies. Understanding of the biology of oral carcinogenesis will give us important advances for detecting high-risk patients, monitoring preventive interventions, assessing cancer risk, and pharmaco
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19

Rosenfeld, Simon. "Are the Somatic Mutation and Tissue Organization Field Theories of Carcinogenesis Incompatible?" Cancer Informatics 12 (January 2013): CIN.S13013. http://dx.doi.org/10.4137/cin.s13013.

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Two drastically different approaches to understanding the forces driving carcinogenesis have crystallized through years of research. These are the somatic mutation theory (SMT) and the tissue organization field theory (TOFT). The essence of SMT is that cancer is derived from a single somatic cell that has successively accumulated multiple DNA mutations, and that those mutations occur on genes which control cell proliferation and cell cycle. Thus, according to SMT, neoplastic lesions are the results of DNA-level events. Conversely, according to TOFT, carcinogenesis is primarily a problem of tis
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20

Vineis, Paolo. "Diet, genetic susceptibility and carcinogenesis." Public Health Nutrition 4, no. 2b (2001): 485–91. http://dx.doi.org/10.1079/phn2001135.

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AbstractAt least six types of gene–environment interactions (GEI) have been proposed (Kouhry and Wagener, 1993) In the first type, neither the environmental exposure (EE) nor the genetic risk factor (GRF) have any effect by themselves, but interaction between them causes disease. This is the case of phenylalanine exposure and the phenylketonuria genotype. Type 2 is a situation in which the GRF has no effect on disease in the absence of exposure, but exacerbates the effects of the latter. This is the most important type of GEI in relation to metabolic susceptibility genes and human carcinogenes
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21

Roy, Hemant K., Thomas Hensing, and Vadim Backman. "Nanocytology for field carcinogenesis detection: novel paradigm for lung cancer risk stratification." Future Oncology 7, no. 1 (2011): 1–3. http://dx.doi.org/10.2217/fon.10.176.

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22

Backman, Vadim, and Hemant K. Roy. "Advances in Biophotonics Detection of Field Carcinogenesis for Colon Cancer Risk Stratification." Journal of Cancer 4, no. 3 (2013): 251–61. http://dx.doi.org/10.7150/jca.5838.

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23

Di Domenico, Marina, Angela Santoro, Carmela Ricciardi, et al. "Epigenetic fingerprint in endometrial carcinogenesis: The hypothesis of a uterine field cancerization." Cancer Biology & Therapy 12, no. 5 (2011): 447–57. http://dx.doi.org/10.4161/cbt.12.5.15963.

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24

Ruderman, Sarah, Vesta Valuckaite, Anas Almoghrabi, et al. "912 Early Angiogenic Changes Associated With Field Carcinogenesis in Experimental Colon Cancer." Gastroenterology 148, no. 4 (2015): S—172. http://dx.doi.org/10.1016/s0016-5085(15)30575-8.

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25

Rodriguez-Diaz, Eladio, Christopher S. Huang, Ashish Sharma, Lisa I. Jepeal, Irving J. Bigio, and Satish K. Singh. "Optical Sensing of Field Carcinogenesis in Colonic Mucosa Using Elastic-Scattering Spectroscopy." Gastroenterology 140, no. 5 (2011): S—751. http://dx.doi.org/10.1016/s0016-5085(11)63123-5.

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26

Konda, Vani, Lusik Cherkezyan, Hariharan Subramanian, et al. "Nanoscale markers of esophageal field carcinogenesis: potential implications for esophageal cancer screening." Endoscopy 45, no. 12 (2013): 983–88. http://dx.doi.org/10.1055/s-0033-1344617.

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27

Backman, Vadim, and Hemant K. Roy. "Light-Scattering Technologies for Field Carcinogenesis Detection: A Modality for Endoscopic Prescreening." Gastroenterology 140, no. 1 (2011): 35–41. http://dx.doi.org/10.1053/j.gastro.2010.11.023.

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28

Tanaka, Takuji, Mayu Tanaka, and Takahiro Tanaka. "Oral Carcinogenesis and Oral Cancer Chemoprevention: A Review." Pathology Research International 2011 (May 22, 2011): 1–10. http://dx.doi.org/10.4061/2011/431246.

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Oral cancer is one of the major global threats to public health. The development of oral cancer is a tobacco-related multistep and multifocal process involving field cancerization and carcinogenesis. The rationale for molecular-targeted prevention of oral cancer is promising. Biomarkers of genomic instability, including aneuploidy and allelic imbalance, are possible to measure the cancer risk of oral premalignancies. Understanding of the biology of oral carcinogenesis will yield important advances for detecting high-risk patients, monitoring preventive interventions, and assessing cancer risk
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29

Lippman, Scott M. "Head and Neck Chemoprevention: Recent Advances." Cancer Control 4, no. 2 (1997): 128–35. http://dx.doi.org/10.1177/107327489700400203.

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Background Head and neck cancers are important to human life and health in both developed and underdeveloped countries. Management of established cancers is difficult, and there is great interest in evaluating methods to prevent these tumors from developing. Methods The biology of carcinogenesis, including field carcinogenesis, is reviewed, together with the biology and pharmacology of the retinoids. Intervention studies of premalignant lesions have led to prospective clinical trials of the capability of various retinoids to reduce the incidence of new second cancers. Results High-dose 13-cis-
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30

Wei, Rui, Si Liu, Shutian Zhang, Li Min, and Shengtao Zhu. "Cellular and Extracellular Components in Tumor Microenvironment and Their Application in Early Diagnosis of Cancers." Analytical Cellular Pathology 2020 (January 8, 2020): 1–13. http://dx.doi.org/10.1155/2020/6283796.

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Tumors are surrounded by complex environmental components, including blood and lymph vessels, fibroblasts, endothelial cells, immune cells, cytokines, extracellular vesicles, and extracellular matrix. All the stromal components together with the tumor cells form the tumor microenvironment (TME). In addition, extracellular physical and chemical factors, including extracellular pH, hypoxia, elevated interstitial fluid pressure, and fibrosis, are closely associated with tumor progression, metastasis, immunosuppression, and drug resistance. Cellular and extracellular components in TME contribute t
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31

Joshua, A. M., B. Vukovic, I. Braude, A. Evans, J. Srigley, and J. A. Squire. "Telomere dysfunction in prostatic carcinogenesis." Journal of Clinical Oncology 24, no. 18_suppl (2006): 10021. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10021.

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10021 Background: Telomeres are composed of tandemly repeated DNA sequences (TTAGGG) and specific binding proteins located at the ends of eukaryotic chromosomes. They stabilize chromosomal ends; telomere shortening is an important mechanism of genomic instability and can lead to end-to-end chromosomal fusion, rearrangements and cell death. Here we evaluate the hypothesis that telomere shortening contributes to the development of prostate cancer (CaP). Methods: We used telomeric, centromeric and chromosome specific peptide-nucleic acid probes with z-stacked quantitative fluorescence in-situ hyb
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32

Schulz, Christian, Kerstin Schütte, Julia Mayerle, and Peter Malfertheiner. "The role of the gastric bacterial microbiome in gastric cancer: Helicobacter pylori and beyond." Therapeutic Advances in Gastroenterology 12 (January 2019): 175628481989406. http://dx.doi.org/10.1177/1756284819894062.

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A link between chronic inflammation and carcinogenesis has been depicted in many organ systems. Helicobacter pylori is the most prevalent bacterial pathogen, induces chronic gastritis and is associated with more than 90% of cases of gastric cancer (GC). However, the introduction of nucleotide sequencing techniques and the development of biocomputional tools have surpassed traditional culturing techniques and opened a wide field for studying the mucosal and luminal composition of the bacterial gastric microbiota beyond H. pylori. In studies applying animal models, a potential role in gastric ca
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33

Rivenbark, Ashley G., and William B. Coleman. "Field cancerization in mammary carcinogenesis — Implications for prevention and treatment of breast cancer." Experimental and Molecular Pathology 93, no. 3 (2012): 391–98. http://dx.doi.org/10.1016/j.yexmp.2012.10.018.

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34

Rodriguez-Diaz, Eladio, Theresa M. Lee, Irving J. Bigio, and Satish K. Singh. "716 Optical Sensing of Field Carcinogenesis in Colonic Mucosa Using Elastic-Scattering Spectroscopy." Gastroenterology 138, no. 5 (2010): S—96. http://dx.doi.org/10.1016/s0016-5085(10)60437-4.

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35

Gladstein, Scott, Dhwanil Damania, Luay M. Almassalha, et al. "Correlating colorectal cancer risk with field carcinogenesis progression using partial wave spectroscopic microscopy." Cancer Medicine 7, no. 5 (2018): 2109–20. http://dx.doi.org/10.1002/cam4.1357.

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36

Wolfsen, Herbert, Andrew Gomes, Abraham Panossian, Michael Wallace, and Vadim Backman. "Polarization-gated Spectroscopy (PGS) to Detect Tissue Microstructural Alterations in Esophageal Field Carcinogenesis." American Journal of Gastroenterology 108 (October 2013): S28—S29. http://dx.doi.org/10.14309/00000434-201310001-00085.

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37

Franklin, W. A., A. F. Gazdar, J. Haney, et al. "Widely dispersed p53 mutation in respiratory epithelium. A novel mechanism for field carcinogenesis." Journal of Clinical Investigation 100, no. 8 (1997): 2133–37. http://dx.doi.org/10.1172/jci119748.

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38

Almadori, Giovanni, Francesco Bussu, Gabriella Cadoni, et al. "Multistep laryngeal carcinogenesis helps our understanding of the field cancerisation phenomenon: a review." European Journal of Cancer 40, no. 16 (2004): 2383–88. http://dx.doi.org/10.1016/j.ejca.2004.04.023.

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39

Toruner, Murat, Martin E. Fernandez-Zapico, and Christopher L. Pin. "New Aspects of the Epigenetics of Pancreatic Carcinogenesis." Epigenomes 4, no. 3 (2020): 18. http://dx.doi.org/10.3390/epigenomes4030018.

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Pancreatic cancer remains among the deadliest forms of cancer with a 5 year survival rate less than 10%. With increasing numbers being observed, there is an urgent need to elucidate the pathogenesis of pancreatic cancer. While both contribute to disease progression, neither genetic nor environmental factors completely explain susceptibility or pathogenesis. Defining the links between genetic and environmental events represents an opportunity to understand the pathogenesis of pancreatic cancer. Epigenetics, the study of mitotically heritable changes in genome function without a change in nucleo
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40

MARCINIAK-CZOCHRA, ANNA, and MAREK KIMMEL. "MODELLING OF EARLY LUNG CANCER PROGRESSION: INFLUENCE OF GROWTH FACTOR PRODUCTION AND COOPERATION BETWEEN PARTIALLY TRANSFORMED CELLS." Mathematical Models and Methods in Applied Sciences 17, supp01 (2007): 1693–719. http://dx.doi.org/10.1142/s0218202507002443.

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The generally accepted Moolgavkar's theory of carcinogenesis assumes that all cancers are clonal, i.e. that they arise from progressive genetic deregulation in a cell pedigree originating from a single ancestral cell.18 However, recently the clonal theory has been challenged by the field theory of carcinogenesis, which admits the possibility of simultaneous changes in tissue subject to carcinogenic agents, such as tobacco smoke in lung cancer. Axelrod et al.1 formulated a more detailed framework, in which partially transformed cells depend in a mutualistic way on growth factors they produce, i
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41

Kunte, Dhananjay, Ramesh K. Wali, Mart DeLaCruz, et al. "Sa2005 C-Terminal SRC Kinase (CSK) As a Biomarker for Human Colonic Field Carcinogenesis." Gastroenterology 144, no. 5 (2013): S—357. http://dx.doi.org/10.1016/s0016-5085(13)61314-1.

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42

Momi, Navneet, Ramesh K. Wali, Christopher R. Weber, et al. "PRDM16-Mediated Metabolic Reprogramming in Colonic Field Carcinogenesis: Potential Role of Sonic Hedgehog Signaling." Gastroenterology 152, no. 5 (2017): S19. http://dx.doi.org/10.1016/s0016-5085(17)30438-9.

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43

Roy, Hemant K., Dhwanil P. Damania, Mart DelaCruz, et al. "Nano-Architectural Alterations in Mucus Layer Fecal Colonocytes in Field Carcinogenesis: Potential for Screening." Cancer Prevention Research 6, no. 10 (2013): 1111–19. http://dx.doi.org/10.1158/1940-6207.capr-13-0138.

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44

Rodriguez-Diaz, Eladio, Christopher S. Huang, Ashish Sharma, Lisa I. Jepeal, Irving J. Bigio, and Satish K. Singh. "550 Optical Sensing of Field Carcinogenesis in Colonic Mucosa Using Elastic-Scattering Spectroscopy (ESS)." Gastroenterology 142, no. 5 (2012): S—110. http://dx.doi.org/10.1016/s0016-5085(12)60415-6.

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45

Lehrbach, Dárcio Matenhauer, Marcelo Eidi Nita, and Ivan Cecconello. "Molecular aspects of esophageal squamous cell carcinoma carcinogenesis." Arquivos de Gastroenterologia 40, no. 4 (2003): 256–61. http://dx.doi.org/10.1590/s0004-28032003000400011.

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BACKGROUND: The development of human esophageal cancer is a multistep, progressive process. An early indicator of this process is an increased proliferation of esophageal epithelial cells morphologically including basal cell hyperplasia, dysplasia, carcinoma in situ and advanced esophageal squamous cell carcinoma. The process of tumorigenesis at cellular level is related to disorders of the control of cell proliferation and differentiation and controlled cell death (apoptosis). Most of cancer cells contain genetic alterations related to the control of these processes, including transcription f
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46

Assumpção, Monica B., Fabiano C. Moreira, Igor G. Hamoy, et al. "High-Throughput miRNA Sequencing Reveals a Field Effect in Gastric Cancer and Suggests an Epigenetic Network Mechanism." Bioinformatics and Biology Insights 9 (January 2015): BBI.S24066. http://dx.doi.org/10.4137/bbi.s24066.

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Field effect in cancer, also called “field cancerization”, attempts to explain the development of multiple primary tumors and locally recurrent cancer. The concept of field effect in cancer has been reinforced, since molecular alterations were found in tumor-adjacent tissues with normal histopathological appearances. With the aim of investigating field effects in gastric cancer (GC), we conducted a high-throughput sequencing of the miRnome of four GC samples and their respective tumor-adjacent tissues and compared them with the miRnome of a gastric antrum sample from patients without GC, assum
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47

Roy, Hemant K., Dhwanil Damania, Douglas K. Rex, et al. "Su1217 Nanocytological Analysis of Field Carcinogenesis As a Potential Guide for Post-Polypectomy Surveillance Colonoscopy." Gastroenterology 146, no. 5 (2014): S—404—S—405. http://dx.doi.org/10.1016/s0016-5085(14)61463-3.

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48

Stypula, Yolanda E., Dhwanil Damania, Dhananjay Kunte, et al. "Su1894 Nanoarchitectural Changes of Chromatin by Histone Deacetylase (HDAC) Dysregulation Occurs in Colorectal Field Carcinogenesis." Gastroenterology 142, no. 5 (2012): S—529. http://dx.doi.org/10.1016/s0016-5085(12)62033-2.

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49

Stypula, Yolanda, Nikhil Mutyal, Vladimir Turzhitsky, et al. "S1930 Biophotonic Detection of Colonic Field Carcinogenesis Spectral Slope Represents Fundamental Alterations in Crypt Architecture." Gastroenterology 138, no. 5 (2010): S—283. http://dx.doi.org/10.1016/s0016-5085(10)61301-7.

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50

Roy, Hemant K., Vladimir Turzhitsky, Young L. Kim, et al. "851 Field Carcinogenesis Detection By Rectal Spectral Markers Accurately Identifies Patients Harboring Proximal Advanced Adenomas." Gastroenterology 136, no. 5 (2009): A—129. http://dx.doi.org/10.1016/s0016-5085(09)60580-1.

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