Annals of Coloproctology

Original Articles

Anaphase-Promoting Complex 7 is a Prognostic Factor in Human Colorectal Cancer: Ik Yong Kim, Hye Yeon Kwon, Kwang Hwa Park, Dae Sung Kim; Ann Coloproctol. 2017;33(4):139-145. Published online August 31, 2017; DOI: https://doi.org/10.3393/ac.2017.33.4.139

3,990 View
59 Download
8 Web of Science
8 Citations

Purpose

The anaphase-promoting complex (APC) is a multiprotein complex with E3 ubiquitin ligase activity and is required for ubiquitination of securin and cyclin-B. Several APC-targeting molecules are reported to be oncogenes. Dysregulation of APC may be associated with tumorigenesis. This study examines the relationship between APC expression and clinicopathological factors and evaluates the possibility of an aberrant APC function in colorectal carcinomas (CRCs).

Methods

To determine whether the loss of APC7 expression is related to tumorigenesis, we used tissue micro-arrays in 114 resected CRCs to scrutinize the expressions of APC7 and Ki-67 immunohistochemistry and to find relations with clinocopathologic parameters. The expression of APC7 was defined as positive for summed scores of staining intensities from 0 to 3+.

Results

Forty-four cases (67.7%) of colon cancer and 38 cases (77.6%) of rectal cancer showed immunopositive reactions to APC. The grade of APC expression was not statistically correlated with tumor location, age, T or TNM stage, or differentiation. However, the expression of APC did correlate with the expression of Ki-67 and to the tumor recurrent. Higher APC expression showed the better 5-year overall survival rate in 74% of grades 2, 3 groups (high expression) than 57% of grades 0, 1 groups (lower expression) respectively (P = 0.042).

Conclusion

Positive APC expression may be a good prognostic factor for patients with CRC, and the loss of APC expression in tumor tissue may be related with the risk for recurrence and a poor survival rate compared to high APC expression. Further study of APC in controlling the cell cycle as aberrant function in CRC is needed.

Citations

Citations to this article as recorded by

Microbiota as the unifying factor behind the hallmarks of cancer
Iva Benešová, Ľudmila Křížová, Miloslav Kverka
Journal of Cancer Research and Clinical Oncology.2023; 149(15): 14429. CrossRef
Upregulation of anaphase promoting complex (APC) 7 as a prognostic marker for esophageal squamous cell carcinoma: A hospital based study
Eyashin Ali, Manash Jyoti Kalita, Simanta Kalita, Jayasree Talukdar, Ankur Jyoti Deka, Jasmin Sultana, Bikash Narayan Choudhury, Munindra Narayan Baruah, Sahana Bhattacharjee, Subhash Medhi
Heliyon.2022; 8(6): e09722. CrossRef
Gatekeepers of the Gut: The Roles of Proteasomes at the Gastrointestinal Barrier
Gayatree Mohapatra, Avital Eisenberg-Lerner, Yifat Merbl
Biomolecules.2021; 11(7): 989. CrossRef
Using BioPAX-Parser (BiP) to enrich lists of genes or proteins with pathway data
Giuseppe Agapito, Mario Cannataro
BMC Bioinformatics.2021;[Epub] CrossRef
Extensive loss of cell-cycle and DNA repair genes in an ancient lineage of bipolar budding yeasts
Jacob L. Steenwyk, Dana A. Opulente, Jacek Kominek, Xing-Xing Shen, Xiaofan Zhou, Abigail L. Labella, Noah P. Bradley, Brandt F. Eichman, Neža Čadež, Diego Libkind, Jeremy DeVirgilio, Amanda Beth Hulfachor, Cletus P. Kurtzman, Chris Todd Hittinger, Antoni
PLOS Biology.2019; 17(5): e3000255. CrossRef
Identification of Novel Molecular Network Expression in Acute Myocardial Infarction
Marwa Matboli, Ayman E. Shafei, Sara H.A. Agwa, Sherif Sammir Elzahy, Ahmed K. Anwar, Amr R. Mansour, Ahmed I. Gaber, Ali E.A. Said, Paula Lwis, Marwa Hamdy
Current Genomics.2019; 20(5): 340. CrossRef
Activating the Anaphase Promoting Complex to Enhance Genomic Stability and Prolong Lifespan
Troy A. A. Harkness
International Journal of Molecular Sciences.2018; 19(7): 1888. CrossRef
What is the Meaning of Anaphase-Promoting Complex 7 in Malignant Neoplasms?
Weon-Young Chang
Annals of Coloproctology.2017; 33(4): 123. CrossRef

Oncologic Outcome after Cessation or Dose Reduction of Capecitabine in Patients with Colon Cancer: Jung-A Yun, Hee Cheol Kim, Hyun-Sook Son, Hyoung Ran Kim, Hae Ran Yun, Yong Beom Cho, Seong Hyeon Yun, Woo Yong Lee, Ho-Kyung Chun; J Korean Soc Coloproctol. 2010;26(4):287-292. Published online August 31, 2010; DOI: https://doi.org/10.3393/jksc.2010.26.4.287

3,480 View
38 Download
6 Citations

Abstract PDF

Purpose

Oral capecitabine has been used as adjuvant therapy for colorectal cancer patients since the 1990s. Patient-initiated cessation or reduced use of capecitabine occurs widely for various reasons, yet the consequences of these actions are unclear. The present study sought to clarify treatment outcomes in such patients.

Methods

The study included 173 patients who had been diagnosed with stage II or III colon cancer according to the pathologic report after radical surgery at Samsung Medical Center from May 2005 to June 2007 and who had received capecitabine as adjuvant therapy. The patients were divided into groups according to whether the dose was reduced (I, dose maintenance; II, dose reduction) or stopped (A, cycle completion; B, cycle cessation). Recurrence and disease-free survival rates between the two groups each were analyzed.

Results

Of the 173 patients, 128 (74.6%) experienced complications, most frequently hand-foot syndrome (n = 114). Reduction (n = 35) or cessation (n = 18) of medication was most commonly due to complications. Concerning reduced dosage, both groups displayed no statistically significant differences in recurrence rate and 3-year disease-free survival rate. Concerning discontinued medication use, the cycle completion group showed an improved recurrence rate (P = 0.048) and 3-year disease-free survival rate (P = 0.028).

Conclusion

The results demonstrate that maintaining compliance with capecitabine as an adjuvant treatment for colon cancer to preventing complications positively affects patient prognosis.

Citations

Citations to this article as recorded by

Medication Perceptions Mediate the Association between Illness Perceptions and Adherence to Oral Anticancer Agents among Patients with Gastrointestinal Tract Cancer: A Cross-sectional Study
Yongfeng Chen, Marques Shek Nam Ng, Xulian Wei, LiYuan Zhang, Kai Chow Choi, Yan Ma, Fang Wang, Carmen Wing Han Chan
European Journal of Oncology Nursing.2024; : 102720. CrossRef
The Value of Pharmacogenetics to Reduce Drug-Related Toxicity in Cancer Patients
Doreen Z. Mhandire, Andrew K. L. Goey
Molecular Diagnosis & Therapy.2022; 26(2): 137. CrossRef
Global Cancer Burden and Natural Disasters: A Focus on Asia’s Vulnerability, Resilience Building, and Impact on Cancer Care
Roselle De Guzman, Monica Malik
Journal of Global Oncology.2019; (5): 1. CrossRef
Association Between Adjuvant Chemotherapy Duration and Survival Among Patients With Stage II and III Colon Cancer
Devon J. Boyne, Colleen A. Cuthbert, Dylan E. O’Sullivan, Tolulope T. Sajobi, Robert J. Hilsden, Christine M. Friedenreich, Winson Y. Cheung, Darren R. Brenner
JAMA Network Open.2019; 2(5): e194154. CrossRef
5-fluorouracil Toxicity Mechanism Determination in Human Keratinocytes: in vitro Study on HaCaT Cell Line
Jan Hartinger, Pavel Veselý, Martin Šíma, Irena Netíková, Eva Matoušková, Luboš Petruželka
Prague Medical Report.2017; 118(4): 128. CrossRef
An exploratory study to identify risk factors for the development of capecitabine‐induced Palmar Plantar Erythrodysesthesia (PPE)
Annie Law, Sue Dyson, Denis Anthony
Journal of Advanced Nursing.2015; 71(8): 1825. CrossRef

Effects of DCA on Cell Cycle Proteins in Colonocytes: Yun-Hyung Ha, Dong-Guk Park; J Korean Soc Coloproctol. 2010;26(4):254-259. Published online August 31, 2010; DOI: https://doi.org/10.3393/jksc.2010.26.4.254

3,231 View
42 Download
11 Citations

Abstract PDF

Purpose

Evidence that indicates bile acid is a promoter of colon cancer exists. Deoxycholic acid (DCA) modifies apoptosis or proliferation by affecting intracellular signaling and gene expression. However, because previous studies have been based on studies on colon cancer cell lines, the effect of DCA on normal colonocytes is unknown.

Methods

Normal colonocytes and Caco-2 and HCT116 cells were treated with 20 µM and 250 µM of DCA, and the effect of different concentrations of DCA was measured based on the expression of cell-cycle-related proteins by using Western blots.

Results

The expressions of CDK2 and cyclin D1 for different concentrations of DCA in normal colonocytes and colon cancer cells were similar, but the expressions of cyclin E and A were significantly different. In HCT116 colon cancer cells, the expression of cyclin E increased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin E was not changed or decreased. In HCT116 colon cancer cells, the expression of cyclin A was not changed or decreased regardless of the DCA concentration, but in normal colonocytes and Caco-2 cells, the expression of cyclin A was increased at a DCA concentration of 20 µM.

Conclusion

The effect of DCA on stimulating cell proliferation suggests that DNA synthesis is stimulated by an increased expression of cyclin E in colon cancer cells. Our results suggest that a low dose of DCA induces cellular proliferation through increased expression of cyclin A and that a high dose of DCA induces decreased expression of cyclin E and CDK2 in normal colonocytes.

Citations

Citations to this article as recorded by

Implication of gut microbes and its metabolites in colorectal cancer
Arun Kumar, Asgar Ali, Raj Kishore Kapardar, Ghulam Mehdi Dar, Nimisha, Apurva, Abhay Kumar Sharma, Renu Verma, Real Sumayya Abdul Sattar, Ejaj Ahmad, Bhawna Mahajan, Sundeep Singh Saluja
Journal of Cancer Research and Clinical Oncology.2023; 149(1): 441. CrossRef
Dissecting the role of the gut microbiome and fecal microbiota transplantation in radio- and immunotherapy treatment of colorectal cancer
Lena Van Dingenen, Charlotte Segers, Shari Wouters, Mohamed Mysara, Natalie Leys, Samir Kumar-Singh, Surbhi Malhotra-Kumar, Rob Van Houdt
Frontiers in Cellular and Infection Microbiology.2023;[Epub] CrossRef
Methyltransferase like 3 promotes colorectal cancer proliferation by stabilizing CCNE1 mRNA in an m6A‐dependent manner
Wei Zhu, Yan Si, Jun Xu, Yu Lin, Jing‐Zi Wang, Mengda Cao, Shanwen Sun, Qiang Ding, Lingjun Zhu, Ji‐Fu Wei
Journal of Cellular and Molecular Medicine.2020; 24(6): 3521. CrossRef
Microbiota in cancer development and treatment
Muhammad Hassan Raza, Kamni Gul, Abida Arshad, Naveeda Riaz, Usman Waheed, Abdul Rauf, Fahad Aldakheel, Shatha Alduraywish, Maqbool Ur Rehman, Muhammad Abdullah, Muhammad Arshad
Journal of Cancer Research and Clinical Oncology.2019; 145(1): 49. CrossRef
Secondary Bile Acids and Short Chain Fatty Acids in the Colon: A Focus on Colonic Microbiome, Cell Proliferation, Inflammation, and Cancer
Huawei Zeng, Shahid Umar, Bret Rust, Darina Lazarova, Michael Bordonaro
International Journal of Molecular Sciences.2019; 20(5): 1214. CrossRef
Dysbiosis of gut microbiota in promoting the development of colorectal cancer
Shaomin Zou, Lekun Fang, Mong-Hong Lee
Gastroenterology Report.2018; 6(1): 1. CrossRef
Oxidative stress: a key regulator of leiomyoma cell survival
Nicole M. Fletcher, Mohammed S. Abusamaan, Ira Memaj, Mohammed G. Saed, Ayman Al-Hendy, Michael P. Diamond, Ghassan M. Saed
Fertility and Sterility.2017; 107(6): 1387. CrossRef
Deoxycholic acid inhibits the growth of BGC-823 gastric carcinoma cells via a p53-mediated pathway
HAI-BO YANG, WEI SONG, MEI-DIE CHENG, HAI-FANG FAN, XU GU, YING QIAO, XIN LU, RUI-HE YU, LAN-YING CHEN
Molecular Medicine Reports.2015; 11(4): 2749. CrossRef
Differential Regulation of EGFR–MAPK Signaling by Deoxycholic Acid (DCA) and Ursodeoxycholic Acid (UDCA) in Colon Cancer
Sara M. Centuori, Jesse D. Martinez
Digestive Diseases and Sciences.2014; 59(10): 2367. CrossRef
Bile acids in the colon, from healthy to cytotoxic molecules
Juan I. Barrasa, Nieves Olmo, Ma Antonia Lizarbe, Javier Turnay
Toxicology in Vitro.2013; 27(2): 964. CrossRef
Sodium deoxycholate inhibits chick duodenal calcium absorption through oxidative stress and apoptosis
María A. Rivoira, Ana M. Marchionatti, Viviana A. Centeno, Gabriela E. Díaz de Barboza, María E. Peralta López, Nori G. Tolosa de Talamoni
Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology.2012; 162(4): 397. CrossRef

First
Prev
Page of 1
Next
Last

Search