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Journal articles on the topic 'Colorectal tumorigenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Abbasi, A. M., I. C. Talbot, A. Forbes, and I. C. Talbot. "Colorectal tumorigenesis." Gut 36, no. 5 (1995): 801. http://dx.doi.org/10.1136/gut.36.5.801-b.

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2

Shirakami, Yohei, Takayuki Nakanishi, Noritaka Ozawa, et al. "Inhibitory effects of a selective prostaglandin E2 receptor antagonist RQ-15986 on inflammation-related colon tumorigenesis in APC-mutant rats." PLOS ONE 16, no. 5 (2021): e0251942. http://dx.doi.org/10.1371/journal.pone.0251942.

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Prostaglandin E2 receptor EP4 is involved in inflammation and related tumorigenesis in the colorectum. This study aimed to investigate the chemopreventive ability of RQ-15986, a selective EP4 antagonist, in colitis-related colorectal tumorigenesis. Male Kyoto APC delta rats, which have APC mutations, were treated with azoxymethane and dextran sulfate sodium and subsequently administered RQ-15986 for eight weeks. At the end of the experiment, the development of colorectal tumor was significantly inhibited in the RQ-15986-treated group. The cell proliferation of the crypts and tumors in the colo

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3

Li, Tao, Guoliang Liu, Jiannan Li, et al. "Gastric tumorigenesis after radical resection combined with adjuvant chemotherapy for colorectal cancer: two case reports and a literature review." Journal of International Medical Research 49, no. 4 (2021): 030006052110070. http://dx.doi.org/10.1177/03000605211007050.

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Radical resection with or without adjuvant chemotherapy is a common option for stage II and III colorectal cancer. Few reports exist regarding gastric tumorigenesis, including gastric cancer, gastric intraepithelial neoplasia, and gastric stromal tumor, in patients who received this protocol as the standard treatment for colorectal cancer. We present two cases of gastric tumorigenesis in patients with colorectal cancer following radical resection combined with adjuvant chemotherapy. Both patients underwent gastrectomy and D2 lymphadenectomy for their gastric tumors; neither patient developed r

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4

Yang, Lin-Sen, Xiao-Jian Zhang, Yin-Yin Xie, Xiao-Jian Sun, Ren Zhao, and Qiu-Hua Huang. "SUMOylated MAFB promotes colorectal cancer tumorigenesis." Oncotarget 7, no. 50 (2016): 83488–501. http://dx.doi.org/10.18632/oncotarget.13129.

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5

Cho, Dong-Hyung, Yoon Kyung Jo, Seon Ae Roh, et al. "Upregulation of SPRR3 Promotes Colorectal Tumorigenesis." Molecular Medicine 16, no. 7-8 (2010): 271–77. http://dx.doi.org/10.2119/molmed.2009.00187.

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6

Tanaka, N., N. Matsubara, M. Ikeda, et al. "Molecular colorectal tumorigenesis and gene therapy." Nippon Daicho Komonbyo Gakkai Zasshi 51, no. 9 (1998): 686–686. http://dx.doi.org/10.3862/jcoloproctology.51.686.

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7

Morin, P. J., B. Vogelstein, and K. W. Kinzler. "Apoptosis and APC in colorectal tumorigenesis." Proceedings of the National Academy of Sciences 93, no. 15 (1996): 7950–54. http://dx.doi.org/10.1073/pnas.93.15.7950.

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8

Cross, William, Michal Kovac, Ville Mustonen, et al. "The evolutionary landscape of colorectal tumorigenesis." Nature Ecology & Evolution 2, no. 10 (2018): 1661–72. http://dx.doi.org/10.1038/s41559-018-0642-z.

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9

Fearon, Eric R., and Bert Vogelstein. "A genetic model for colorectal tumorigenesis." Cell 61, no. 5 (1990): 759–67. http://dx.doi.org/10.1016/0092-8674(90)90186-i.

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10

Wang, W. S., P. M. Chen, and Y. Su. "Colorectal carcinoma: from tumorigenesis to treatment." Cellular and Molecular Life Sciences 63, no. 6 (2006): 663–71. http://dx.doi.org/10.1007/s00018-005-5425-4.

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11

Kawamura, M. "Expression of p53 Protein in Colorectal Tumorigenesis." Nippon Daicho Komonbyo Gakkai Zasshi 50, no. 4 (1997): 227–33. http://dx.doi.org/10.3862/jcoloproctology.50.227.

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12

Karin, M. "72: Inflammation in colorectal and liver tumorigenesis." European Journal of Cancer 50 (July 2014): S18. http://dx.doi.org/10.1016/s0959-8049(14)50072-x.

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13

Tzouvala, Maria, Nikiforos Kapranos, George Papatheodoridis, et al. "Apoptosis through different stages of colorectal tumorigenesis." Gastroenterology 118, no. 4 (2000): A1415. http://dx.doi.org/10.1016/s0016-5085(00)81549-8.

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14

Sugao, Yoriaki, Takehiko Koji, Takashi Yao, Takashi Ueki, and Masazumi Tsuneyoshi. "The Incidence of Apoptosis During Colorectal Tumorigenesis." International Journal of Surgical Pathology 8, no. 2 (2000): 123–32. http://dx.doi.org/10.1177/106689690000800207.

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15

Wong, J. J. L., N. J. Hawkins, and R. L. Ward. "Colorectal cancer: a model for epigenetic tumorigenesis." Gut 56, no. 1 (2007): 140–48. http://dx.doi.org/10.1136/gut.2005.088799.

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16

Powell, Steven M., Nathan Zilz, Yasmin Beazer-Barclay, et al. "APC mutations occur early during colorectal tumorigenesis." Nature 359, no. 6392 (1992): 235–37. http://dx.doi.org/10.1038/359235a0.

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17

Liu, Xiuli, Audrey J. Lazenby, and Gene P. Siegal. "Signal Transduction Cross-talk During Colorectal Tumorigenesis." Advances in Anatomic Pathology 13, no. 5 (2006): 270–74. http://dx.doi.org/10.1097/01.pap.0000213046.61941.5c.

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18

Akintola-Ogunremi, Olaronke, Qing Luo, Tong-Chuan He, and Hanlin L. Wang. "Is Cytomegalovirus Associated With Human Colorectal Tumorigenesis?" American Journal of Clinical Pathology 123, no. 2 (2005): 244–49. http://dx.doi.org/10.1309/9qvrhdjuk6h2turb.

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19

Caldwell, Germaine M., Carolyn Jones, Karl Gensberg, et al. "The Wnt Antagonist sFRP1 in Colorectal Tumorigenesis." Cancer Research 64, no. 3 (2004): 883–88. http://dx.doi.org/10.1158/0008-5472.can-03-1346.

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20

Tejpar, Sabine, and Eric Van Cutsem. "Molecular and genetic defects in colorectal tumorigenesis." Best Practice & Research Clinical Gastroenterology 16, no. 2 (2002): 171–85. http://dx.doi.org/10.1053/bega.2001.0279.

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21

Koike, Masahiko. "Significance of spontaneous apoptosis during colorectal tumorigenesis." Journal of Surgical Oncology 62, no. 2 (1996): 97–108. http://dx.doi.org/10.1002/(sici)1096-9098(199606)62:2<97::aid-jso5>3.0.co;2-l.

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22

Rees, Michele, Sarah Leigh, Luiza Bowles, et al. "Analysis of familial and sporadic colorectal tumorigenesis." Cancer Genetics and Cytogenetics 63, no. 2 (1992): 118. http://dx.doi.org/10.1016/0165-4608(92)90418-8.

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23

Allam, Ramanjaneyulu, Michel H. Maillard, Aubry Tardivel, et al. "Epithelial NAIPs protect against colonic tumorigenesis." Journal of Experimental Medicine 212, no. 3 (2015): 369–83. http://dx.doi.org/10.1084/jem.20140474.

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NLR family apoptosis inhibitory proteins (NAIPs) belong to both the Nod-like receptor (NLR) and the inhibitor of apoptosis (IAP) families. NAIPs are known to form an inflammasome with NLRC4, but other in vivo functions remain unexplored. Using mice deficient for all NAIP paralogs (Naip1-6Δ/Δ), we show that NAIPs are key regulators of colorectal tumorigenesis. Naip1-6Δ/Δ mice developed increased colorectal tumors, in an epithelial-intrinsic manner, in a model of colitis-associated cancer. Increased tumorigenesis, however, was not driven by an exacerbated inflammatory response. Instead, Naip1-6Δ

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24

Fearnhead, Nicola S., Jennifer L. Wilding, and Walter F. Bodmer. "Genetics of colorectal cancer: hereditary aspects and overview of colorectal tumorigenesis." British Medical Bulletin 64, no. 1 (2002): 27–43. http://dx.doi.org/10.1093/bmb/64.1.27.

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25

Takeda, Akihiko. "Role of overexpressions of ALEX1 gene in human colorectal tumorigenesis." Journal of Clinical Oncology 31, no. 4_suppl (2013): 443. http://dx.doi.org/10.1200/jco.2013.31.4_suppl.443.

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443 Background: Arm protein lost in epithelial cancers, on chromosome X (ALEX) is a novel subgroup within the armadillo family which has several ARM repeat domain. Our studies have revealed that overexpression of ALEX1 suppressed colony formation ability of stable human colorectal carcinoma cell lines. But clinical significance of ALEX1 expression in colorectal cancer patients is largely unknown. Methods: We examined the expression level of ALEX1 mRNA in matched tissue pairs of normal colorectal mucosa and colorectal tumor tissue by quantitative real-time RT-PCR Tumor specimens along with adja

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26

Chell, S., H. A. Patsos, D. Qualtrough, et al. "Prospects in NSAID-derived chemoprevention of colorectal cancer." Biochemical Society Transactions 33, no. 4 (2005): 667–71. http://dx.doi.org/10.1042/bst0330667.

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There is strong evidence for an important role for increased COX (cyclo-oxygenase)-2 expression and PG (prostaglandin) E2 production in colorectal tumorigenesis. PGE2 acts through four E-prostanoid receptors (EP1–4). COX-2 has therefore become a target for the potential chemoprevention and therapy of colorectal cancer. However, any therapeutic/preventive strategy has the potential to have an impact on physiological processes and hence result in side effects. General COX (COX-1 and -2) inhibition by traditional NSAIDs (non-steidal anti-inflammatory drugs), such as aspirin, although chemoprevent

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27

Rao, U. Subrahmanyeswara, and Prema S. Rao. "Surface-bound galectin-4 regulates gene transcription and secretion of chemokines in human colorectal cancer cell lines." Tumor Biology 39, no. 3 (2017): 101042831769168. http://dx.doi.org/10.1177/1010428317691687.

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One long-term complication of chronic intestinal inflammation is the development of colorectal cancer. However, the mechanisms linking inflammation to the colorectal tumorigenesis are poorly defined. Previously, we have demonstrated that galectin-4 is predominantly expressed in the luminal epithelia of the gastrointestinal tract, and its loss of expression plays a key role in the colorectal tumorigenesis. However, the mechanism by which galectin-4 regulates inflammation-induced tumorigenesis is unclear. Here, we show that galectin-4 secreted by the colorectal cancer cell lines was bound to the

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28

Morinishi, Tatsuya, Yasunori Tokuhara, Hiroyuki Ohsaki, Emi Ibuki, Kyuichi Kadota, and Eiichiro Hirakawa. "Activation and Expression of Peroxisome Proliferator-Activated Receptor Alpha Are Associated with Tumorigenesis in Colorectal Carcinoma." PPAR Research 2019 (July 3, 2019): 1–9. http://dx.doi.org/10.1155/2019/7486727.

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Peroxisome proliferator-activated receptor alpha (PPAR-α) belongs to the PPAR family and plays a critical role in inhibiting cell proliferation and tumorigenesis in various tumors. However, the role of PPAR-αin colorectal tumorigenesis is unclear. In the present study, we found that fenofibrate, a PPAR-αagonist, significantly inhibited cell proliferation and induced apoptosis in colorectal carcinoma cells. In addition, PPAR-αwas expressed in the nucleus of colorectal carcinoma cells, and the expression of nuclear PPAR-αincreased in colorectal carcinoma tissue compared with that of normal epith

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29

Hibino, Sana, Tetsuro Kawazoe, Hidenori Kasahara, et al. "Inflammation-Induced Tumorigenesis and Metastasis." International Journal of Molecular Sciences 22, no. 11 (2021): 5421. http://dx.doi.org/10.3390/ijms22115421.

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Inflammation, especially chronic inflammation, plays a pivotal role in tumorigenesis and metastasis through various mechanisms and is now recognized as a hallmark of cancer and an attractive therapeutic target in cancer. In this review, we discuss recent advances in molecular mechanisms of how inflammation promotes tumorigenesis and metastasis and suppresses anti-tumor immunity in various types of solid tumors, including esophageal, gastric, colorectal, liver, and pancreatic cancer as well as hematopoietic malignancies.

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30

Vicente, Carolina Meloni, Daiana Aparecida da Silva, Priscila Veronica Sartorio, et al. "Heparan Sulfate Proteoglycans in Human Colorectal Cancer." Analytical Cellular Pathology 2018 (June 20, 2018): 1–10. http://dx.doi.org/10.1155/2018/8389595.

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Colorectal cancer is the third most common cancer worldwide, accounting for more than 610,000 mortalities every year. Prognosis of patients is highly dependent on the disease stage at diagnosis. Therefore, it is crucial to investigate molecules involved in colorectal cancer tumorigenesis, with possible use as tumor markers. Heparan sulfate proteoglycans are complex molecules present in the cell membrane and extracellular matrix, which play vital roles in cell adhesion, migration, proliferation, and signaling pathways. In colorectal cancer, the cell surface proteoglycan syndecan-2 is upregulate

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31

Jaiswal, Aruna, S. "Involvement of adenomatous polyposis coli in colorectal tumorigenesis." Frontiers in Bioscience 10, no. 1-3 (2005): 1118. http://dx.doi.org/10.2741/1605.

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32

Kauffman, John, and Jacques Van Dam. "Mechanism underlying NSAID–mediated inhibition of colorectal tumorigenesis." Gastroenterology 115, no. 6 (1998): 1599–600. http://dx.doi.org/10.1016/s0016-5085(98)70049-6.

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33

Wang, Zhen, Peng Liu, Xin Zhou, et al. "Endothelin Promotes Colorectal Tumorigenesis by Activating YAP/TAZ." Cancer Research 77, no. 9 (2017): 2413–23. http://dx.doi.org/10.1158/0008-5472.can-16-3229.

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34

Mazelin, Laetitia, Agnès Bernet, Christelle Bonod-Bidaud, et al. "Netrin-1 controls colorectal tumorigenesis by regulating apoptosis." Nature 431, no. 7004 (2004): 80–84. http://dx.doi.org/10.1038/nature02788.

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35

Sabatino, Lina, Alessandra Fucci, Massimo Pancione, and Vittorio Colantuoni. "PPARGEpigenetic Deregulation and Its Role in Colorectal Tumorigenesis." PPAR Research 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/687492.

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Peroxisome proliferator-activated receptor gamma (PPARγ) plays critical roles in lipid storage, glucose metabolism, energy homeostasis, adipocyte differentiation, inflammation, and cancer. Its function in colon carcinogenesis has largely been debated; accumulating evidence, however, supports a role as tumor suppressor through modulation of crucial pathways in cell differentiation, apoptosis, and metastatic dissemination. Epigenetics adds a further layer of complexity to gene regulation in several biological processes. In cancer, the relationship with epigenetic modifications has provided impor

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36

Caldwell, G. M., C. E. Jones, Y. Soon, R. Warrack, D. G. Morton, and G. M. Matthews. "Reorganisation of Wnt-response pathways in colorectal tumorigenesis." British Journal of Cancer 98, no. 8 (2008): 1437–42. http://dx.doi.org/10.1038/sj.bjc.6604327.

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37

Laurent-Puig, P., H. Bons, and P.-H. cugnenc. "Sequence of molecular genetic events in colorectal tumorigenesis." European Journal of Cancer Prevention 8 (December 1999): S49. http://dx.doi.org/10.1097/00008469-199912001-00007.

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38

Lascano, V., L. F. Zabalegui, K. Cameron, et al. "The TNF family member APRIL promotes colorectal tumorigenesis." Cell Death & Differentiation 19, no. 11 (2012): 1826–35. http://dx.doi.org/10.1038/cdd.2012.68.

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39

Tang, Jia-Yin, Chen-Yang Yu, Yu-Jie Bao, et al. "TEAD4 promotes colorectal tumorigenesis via transcriptionally targeting YAP1." Cell Cycle 17, no. 1 (2018): 102–9. http://dx.doi.org/10.1080/15384101.2017.1403687.

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40

Lee, Young-Mi, Saluja Kaduwal, Kug Hwa Lee, Jong-Chan Park, Woo-Jeong Jeong, and Kang-Yell Choi. "Sur8 mediates tumorigenesis and metastasis in colorectal cancer." Experimental & Molecular Medicine 48, no. 7 (2016): e249-e249. http://dx.doi.org/10.1038/emm.2016.58.

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41

Shi, Yingpeng, Hui Lin, Jing Cui, et al. "The Role of Interleukin-17A in Colorectal Tumorigenesis." Cancer Biotherapy and Radiopharmaceuticals 28, no. 6 (2013): 429–32. http://dx.doi.org/10.1089/cbr.2012.1396.

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42

Tannergård, P., T. Liu, Adolf Weger, Magnus Nordenskjöld, and A. Lindblom. "Tumorigenesis in colorectal tumors from patients with hereditary non-polyposis colorectal cancer." Human Genetics 101, no. 1 (1997): 51–55. http://dx.doi.org/10.1007/s004390050585.

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43

Kopnin, Boris. "Genetic Events Responsible for Colorectal Tumorigenesis: Achievements and Challenges." Tumori Journal 79, no. 4 (1993): 235–43. http://dx.doi.org/10.1177/030089169307900401.

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Colorectal carcinogenesis is a multistep process that is accompanied by accumulation of changes in proto-oncogenes and tumor-suppressor genes. APC/MCC, RAS, DCC, p53 mutations and/or allelic losses, hyperexpression of c-MYC and RB genes, as well as other genomic alterations appear at characteristic stages of tumor development and are observed in most neoplasms. However, consideration of each of these abnormalities leaves many unanswered questions. The striking data on recurrent amplification of the RB tumor-suppressor gene as well as suppressive activities of protein kinase C and activated RAS

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44

Wang, Ke, Zuojian Hu, Cuiping Zhang, et al. "SIRT5 Contributes to Colorectal Cancer Growth by Regulating T Cell Activity." Journal of Immunology Research 2020 (September 1, 2020): 1–17. http://dx.doi.org/10.1155/2020/3792409.

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Over the past several years, SIRT5 has attracted considerable attention in metabolic regulation. However, the function of SIRT5 in tumorigenesis by regulating tumor microenvironment is poorly understood. In this work, we found that Sirt5 knockout mice were resistant to AOM and DSS-induced colitis-associated colorectal tumorigenesis and the level of IFN-γ in their tumor microenvironment was higher. Additionally, proteome and network analysis revealed that SIRT5 was important in the T cell receptor signaling pathway. Furthermore, we determined that a deficiency of Sirt5 induced stronger T cell a

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45

Hurst-Kennedy, Jennifer, Lih-Shen Chin, and Lian Li. "Ubiquitin C-Terminal Hydrolase L1 in Tumorigenesis." Biochemistry Research International 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/123706.

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Ubiquitin carboxyl-terminal hydrolase L1 (UCH-L1, aka PGP9.5) is an abundant, neuronal deubiquitinating enzyme that has also been suggested to possess E3 ubiquitin-protein ligase activity and/or stabilize ubiquitin monomersin vivo. Recent evidence implicates dysregulation of UCH-L1 in the pathogenesis and progression of human cancers. Although typically only expressed in neurons, high levels of UCH-L1 have been found in many nonneuronal tumors, including breast, colorectal, and pancreatic carcinomas. UCH-L1 has also been implicated in the regulation of metastasis and cell growth during the pro

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46

Behrens, J. "The role of the Wnt signalling pathway in colorectal tumorigenesis." Biochemical Society Transactions 33, no. 4 (2005): 672–75. http://dx.doi.org/10.1042/bst0330672.

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Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes. Mutations in the tumour suppressor APC (adenomatous polyposis coli) genes occur early in the development of CRC and lead to the stabilization of the Wnt pathway component β-catenin and to the constitutive activation of Wnt signalling. Stabilizing mutations of β-catenin can also lead to its accumulation, qualifying β-catenin as a proto-oncogene. Here I

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47

Wu, William K., Sarah Kraus, and Nadir Arber. "Tu1648 CD24 Impaired Autophagic Flux to Promote Colorectal Tumorigenesis." Gastroenterology 146, no. 5 (2014): S—809. http://dx.doi.org/10.1016/s0016-5085(14)62924-3.

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48

Lv, You, Tao Ye, Hui-Peng Wang, et al. "Suppression of colorectal tumorigenesis by recombinantBacteroides fragilisenterotoxin-2in vivo." World Journal of Gastroenterology 23, no. 4 (2017): 603. http://dx.doi.org/10.3748/wjg.v23.i4.603.

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49

Gong, Yanling, Rong Dong, Xiaomeng Gao, et al. "Neohesperidin prevents colorectal tumorigenesis by altering the gut microbiota." Pharmacological Research 148 (October 2019): 104460. http://dx.doi.org/10.1016/j.phrs.2019.104460.

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50

Shureiqi, Imad, Dongning Chen, R. Sue Day, et al. "Profiling Lipoxygenase Metabolism in Specific Steps of Colorectal Tumorigenesis." Cancer Prevention Research 3, no. 7 (2010): 829–38. http://dx.doi.org/10.1158/1940-6207.capr-09-0110.

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