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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 (May 1, 1995): 801. http://dx.doi.org/10.1136/gut.36.5.801-b.

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2

Shirakami, Yohei, Takayuki Nakanishi, Noritaka Ozawa, Takayasu Ideta, Takahiro Kochi, Masaya Kubota, Hiroyasu Sakai, Takashi Ibuka, Takuji Tanaka, and Masahito Shimizu. "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 (May 18, 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 colorectum was decreased following RQ-15986 treatment. RQ-15986 also suppressed the expression of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-6, interleukin-18, and monocyte chemotactic protein-1, in the colon mucosa. In addition, the expression levels of indoleamine 2,3-dioxygenase, which is involved in immune tolerance, were decreased in the colorectal epithelium and tumors of the RQ-15986-treated group. These findings indicate that RQ-15986 inhibits colitis-associated colorectal tumorigenesis by attenuating inflammation, suppressing cell proliferation, and modulating the expression of indoleamine 2,3-dioxygenase. Targeting prostaglandin E2/EP4 signaling might be a useful strategy for chemoprevention of inflammation-related colorectal cancer.
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3

Li, Tao, Guoliang Liu, Jiannan Li, Jian Cui, Xinyu Wang, Wei Li, Zeyun Zhao, Kai Zhang, and Tongjun Liu. "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 (April 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 recurrence up to 2 years after treatment. These cases indicate that patients should be monitored closely for gastric tumorigenesis after treatment for colorectal cancer. Early detection and active surgical treatment can provide satisfactory results for colorectal cancer followed by gastric tumorigenesis. Long-term follow-up and regular examinations, especially gastroscopy, are necessary to detect gastric tumorigenesis after colorectal cancer. The focus on monitoring colorectal cancer alone in colorectal cancer patients should be changed to include a broader range of cancers in addition to precancers and other tumors, such as gastric stromal tumor.
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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 (November 5, 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, Young-Soon Na, Tae Won Kim, Se Jin Jang, Yong Sung Kim, and Jin Cheon Kim. "Upregulation of SPRR3 Promotes Colorectal Tumorigenesis." Molecular Medicine 16, no. 7-8 (March 17, 2010): 271–77. http://dx.doi.org/10.2119/molmed.2009.00187.

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6

Tanaka, N., N. Matsubara, M. Ikeda, H. Takashima, T. Fujiwara, J. Shao, M. Ogawa, T. Fukazawa, and A. Hizuta. "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 (July 23, 1996): 7950–54. http://dx.doi.org/10.1073/pnas.93.15.7950.

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8

Cross, William, Michal Kovac, Ville Mustonen, Daniel Temko, Hayley Davis, Ann-Marie Baker, Sujata Biswas, et al. "The evolutionary landscape of colorectal tumorigenesis." Nature Ecology & Evolution 2, no. 10 (August 31, 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 (June 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 (February 23, 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, Konstanti-nos Triantafyllou, Basil Xourgias, Ioannis Elemenoglou, and Demetrios George Karamanolis. "Apoptosis through different stages of colorectal tumorigenesis." Gastroenterology 118, no. 4 (April 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 (April 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 (January 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, Tracy M. Bryan, Stanley R. Hamilton, Stephen N. Thibodeau, Bert Vogelstein, and Kenneth W. Kinzler. "APC mutations occur early during colorectal tumorigenesis." Nature 359, no. 6392 (September 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 (September 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 (February 2005): 244–49. http://dx.doi.org/10.1309/9qvrhdjuk6h2turb.

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19

Caldwell, Germaine M., Carolyn Jones, Karl Gensberg, Shamem Jan, Robert G. Hardy, Philip Byrd, Shaheen Chughtai, Yvonne Wallis, Glenn M. Matthews, and Dion G. Morton. "The Wnt Antagonist sFRP1 in Colorectal Tumorigenesis." Cancer Research 64, no. 3 (February 1, 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 (April 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 (June 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, Katia Tsioupra, Sioban Sen-Gupta, Alistair Gunn, Mike Bradburn, and Joy Delhanty. "Analysis of familial and sporadic colorectal tumorigenesis." Cancer Genetics and Cytogenetics 63, no. 2 (October 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, Vijaykumar Chennupati, Hristina Bega, Chi Wang Yu, Dominique Velin, Pascal Schneider, and Kendle M. Maslowski. "Epithelial NAIPs protect against colonic tumorigenesis." Journal of Experimental Medicine 212, no. 3 (March 2, 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/Δ mice were protected from severe colitis and displayed increased antiapoptotic and proliferation-related gene expression. Naip1-6Δ/Δ mice also displayed increased tumorigenesis in an inflammation-independent model of colorectal cancer. Moreover, Naip1-6Δ/Δ mice, but not Nlrc4-null mice, displayed hyper-activation of STAT3 and failed to activate p53 18 h after carcinogen exposure. This suggests that NAIPs protect against tumor initiation in the colon by promoting the removal of carcinogen-elicited epithelium, likely in a NLRC4 inflammasome-independent manner. Collectively, we demonstrate a novel epithelial-intrinsic function of NAIPs in protecting the colonic epithelium against tumorigenesis.
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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 (December 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 (February 1, 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 adjacent normal tissues were obtained from 49 patients with primary colorectal cancer undergoing complete surgical resection of tumors and lymph nodes, followed by adjuvant systemic therapy in some cases. All tissue samples were stored at -80°C until use. The 49 colorectal specimens comprised 26 well-differentiated and 23 moderately-differentiated adenocarcinoma. Corresponding extraneoplastic normal colon tissues from the same 49 patients were also examined. The pathological stages of the patients were as follows: stage I, 9 patients; stage II, 16 patients and stage III, 24 patients by pTNM classification. The post-surgical treatment observation period was from 277 to 3,631 days (1625.0 ± 1033.0 days). Results: In 34 cases out of 49 (69%) colorectal tumor tissues, greater than a 50% reduction of the ALEX1 mRNA level was observed in comparison to adjacent normal mucosa tissues. ALEX1 mRNA was significantly reduced in colorectal tumor tissues than those in normal mucosa (p=0.01459, Mann–Whitney U-test). The 17 cases with higher ALEX1 gene expression (tumor/normal value ³a0.20) significantly revealed a better disease-free survival rate than the other 32 cases (< 0.20; p = 0.045, log-rank test), which showed significant correlations between ALEX1 expression and better prognosis. There was no significant relationship between ALEX1 expression and the other clinicopathological features. Conclusions: Our findings may support that ALEX1 functions as a tumor suppressor in colorectal cancer progression. Examination of ALEX1 expression might be helpful for predicting the prognosis of patients with curative resected colorectal cancer.
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26

Chell, S., H. A. Patsos, D. Qualtrough, A. M. H-Zadeh, D. J. Hicks, A. Kaidi, I. R. Witherden, A. C. Williams, and C. Paraskeva. "Prospects in NSAID-derived chemoprevention of colorectal cancer." Biochemical Society Transactions 33, no. 4 (August 1, 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 chemopreventive, has some side effects, as do some conventional COX-2-selective NSAIDs. As PGE2 is thought to be the major PG species responsible for promoting colorectal tumorigenesis, research is being directed to a number of protein targets downstream of COX-2 that might allow the selective inhibition of the tumour-promoting activities of PGE2, while minimizing the associated adverse events. The PGE synthases and E-prostanoid receptors (EP1–4) have therefore recently attracted considerable interest as potential novel targets for the prevention/therapy of colorectal cancer. Selective (and possibly combinatorial) inhibition of the synthesis and signalling of those PGs most highly associated with colorectal tumorigenesis may have some advantages over COX-2-selective inhibitors.
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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 (March 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 cell surface. Neutralization of surface-bound galectin-4 with anti-galectin-4 antibody resulted in increased cell proliferation with concomitant secretion of several chemokines into the extracellular medium. Neutralization of the surface-bound galectin-4 also resulted in the up-regulation of transcription of 29 genes, several of which are components of multiple inflammation signaling pathways. In an alternate experiment, binding of recombinant galectin-4 protein to cell surface of the galectin-4-negative colorectal cancer cells resulted in increased p27, and decreased cyclin D1 and c-Myc levels, leading to cell cycle arrest and apoptosis. Together, these data demonstrated that surface-bound galectin-4 is a dual function protein—down-regulating cell proliferation and chemokine secretion in galectin-4-expressing colorectal cancer cells on one hand and inducing apoptosis in galectin-4-negative colorectal cancer cells on the other hand.
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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 epithelium tissue (P<0.01). The correlation between the expression of nuclear PPAR-αand clinicopathological factors was evaluated in human colorectal carcinoma tissues, and the nuclear expression of PPAR-αwas significantly higher in well-to-moderately differentiated adenocarcinoma than in mucinous adenocarcinoma (P<0.05). These findings indicate that activation of PPAR-αmay be involved in anticancer effects in colorectal carcinomas, and nuclear expression of PPAR-αmay be a therapeutic target for colorectal adenocarcinoma treatment.
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29

Hibino, Sana, Tetsuro Kawazoe, Hidenori Kasahara, Shinji Itoh, Takatsugu Ishimoto, Mamiko Sakata-Yanagimoto, and Koji Taniguchi. "Inflammation-Induced Tumorigenesis and Metastasis." International Journal of Molecular Sciences 22, no. 11 (May 21, 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, Tiago Donizetti Silva, Sarhan Sydney Saad, Helena Bonciani Nader, Nora Manoukian Forones, and Leny Toma. "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 upregulated and increases cell migration. Moreover, expression of syndecan-1 and syndecan-4, generally antitumor molecules, is reduced. Levels of glypicans and perlecan are also altered in colorectal cancer; however, their role in tumor progression is not fully understood. In addition, studies have reported increased heparan sulfate remodeling enzymes, as the endosulfatases. Therefore, heparan sulfate proteoglycans are candidate molecules to clarify colorectal cancer tumorigenesis, as well as important targets to therapy and diagnosis.
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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 (December 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, Tianxiang Wang, Xu Feng, Yi-Ping Sun, Yue Xiong, Hai-Xin Yuan, and Kun-Liang Guan. "Endothelin Promotes Colorectal Tumorigenesis by Activating YAP/TAZ." Cancer Research 77, no. 9 (March 1, 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, Laurent Pays, Ségolène Arnaud, Christian Gespach, Dale E. Bredesen, Jean-Yves Scoazec, and Patrick Mehlen. "Netrin-1 controls colorectal tumorigenesis by regulating apoptosis." Nature 431, no. 7004 (September 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 important insights into the underlying molecular mechanisms. These studies have highlighted how epigenetic modifications influencePPARGgene expression in colorectal tumorigenesis. In this paper, we take a comprehensive look at the current understanding of the relationship between PPARγand cancer development. The role that epigenetic mechanisms play is also addressed disclosing novel crosstalks betweenPPARGsignaling and the epigenetic machinery and suggesting how this dysregulation may contribute to colon cancer development.
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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 (April 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, M. Guadagnoli, M. Jansen, M. Burggraaf, M. Versloot, et al. "The TNF family member APRIL promotes colorectal tumorigenesis." Cell Death & Differentiation 19, no. 11 (June 15, 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, Lu Chen, Jinxian Chen, Sheng-Li Yang, Hao-Yan Chen, Jie Hong, and Jing-Yuan Fang. "TEAD4 promotes colorectal tumorigenesis via transcriptionally targeting YAP1." Cell Cycle 17, no. 1 (January 2, 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 (July 2016): e249-e249. http://dx.doi.org/10.1038/emm.2016.58.

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41

Shi, Yingpeng, Hui Lin, Jing Cui, Haili Qi, Jon Florholmen, Zhanju Liu, and Guanglin Cui. "The Role of Interleukin-17A in Colorectal Tumorigenesis." Cancer Biotherapy and Radiopharmaceuticals 28, no. 6 (July 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 (October 8, 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 (August 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 genes, at least in some colon carcinoma cell lines, suggest the unusual effects of some signalling pathways in colonic epithelial cells. The results obtained to date indicate that distinct sets of genetic changes may underlie the development of colorectal tumors.
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44

Wang, Ke, Zuojian Hu, Cuiping Zhang, Lujie Yang, Li Feng, Pengyuan Yang, and Hongxiu Yu. "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 activation and demonstrated that SIRT5 played a pivotal role in regulating the differentiation of CD4+ regulatory T (Treg) cells and T helper 1 (Th1) cells. An imbalance in the lineages of immunosuppressive Treg cells and the inflammatory Th1 subsets of helper T cells leads to the development of colon cancer. Our results revealed a regulatory role of SIRT5 in T cell activation and colorectal tumorigenesis.
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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 progression of nonsmall cell lung carcinoma, colorectal cancer, and lymphoma. Together these studies suggest UCH-L1 has a potent oncogenic role and drives tumor development. Conversely, others have observed promoter methylation-mediated silencing of UCH-L1 in certain tumor subtypes, suggesting a potential tumor suppressor role for UCH-L1. In this paper, we provide an overview of the evidence supporting the involvement of UCH-L1 in tumor development and discuss the potential mechanisms of action of UCH-L1 in oncogenesis.
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Behrens, J. "The role of the Wnt signalling pathway in colorectal tumorigenesis." Biochemical Society Transactions 33, no. 4 (August 1, 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 will summarize the biochemical interactions occurring in Wnt signalling and describe how alterations in Wnt pathway components lead to CRC.
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Wu, William K., Sarah Kraus, and Nadir Arber. "Tu1648 CD24 Impaired Autophagic Flux to Promote Colorectal Tumorigenesis." Gastroenterology 146, no. 5 (May 2014): S—809. http://dx.doi.org/10.1016/s0016-5085(14)62924-3.

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Lv, You, Tao Ye, Hui-Peng Wang, Jia-Ying Zhao, Wen-Jie Chen, Xin Wang, Chen-Xia Shen, Yi-Bin Wu, and Yuan-Kun Cai. "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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Gong, Yanling, Rong Dong, Xiaomeng Gao, Jin Li, Li Jiang, Jiale Zheng, Sunliang Cui, 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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Shureiqi, Imad, Dongning Chen, R. Sue Day, Xiangsheng Zuo, Fredric Lyone Hochman, William A. Ross, Rhonda A. Cole, et al. "Profiling Lipoxygenase Metabolism in Specific Steps of Colorectal Tumorigenesis." Cancer Prevention Research 3, no. 7 (June 22, 2010): 829–38. http://dx.doi.org/10.1158/1940-6207.capr-09-0110.

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