BACKGROUND AND OBJECTIVES: The circadian rhythm regulates the cell cycle progression and DNA damage response. The aim of our study was to investigate the association between polymorphisms in the CLOCK1, PER2, and PER3 genes with the colorectal cancer (CRC) susceptibility and clinicopathological variables. METHODS: Four hundred two CRC patients and 480 healthy controls were included in a case-control study. Genotype and allelic frequencies of 311T>C (rs1801260) in CLOCK1 gene, G3853A (rs934945) in PER2 gene and 4/5 repeats polymorphisms in PER3 gene were evaluated by the polymerase chain reaction (PCR) restriction fragment length polymorphism method in the DNA extracted from the peripheral blood of patients and controls. RESULTS: The frequencies of the 311T>C CLOCK1 gene, CC genotype and C allele were significantly higher among CRC patients compared to controls (P < 0.0001) elevating the CRC risk by 2.78- and 1.78-fold respectively. No correlation was found between G3853A and 4/5 repeats polymorphisms and CRC risk. The C/G/5 and C/G/4 repeats haplotypes were higher in CRC patients (P = 0.0009 and P = 0.038) elevating the CRC risk by 60% and 89% respectively. No correlation was found between any polymorphism and clinicopathological characteristics of CRC patients. CONCLUSION: The 311T>C polymorphism in the CLOCK1 gene significantly increases the risk for CRC development while it does not affect the outcome of CRC patients.
BACKGROUND AND OBJECTIVES: The circadian rhythm regulates the cell cycle progression and DNA damage response. The aim of our study was to investigate the association between polymorphisms in the CLOCK1, PER2, and PER3 genes with the colorectal cancer (CRC) susceptibility and clinicopathological variables. METHODS: Four hundred two CRC patients and 480 healthy controls were included in a case-control study. Genotype and allelic frequencies of 311T>C (rs1801260) in CLOCK1 gene, G3853A (rs934945) in PER2 gene and 4/5 repeats polymorphisms in PER3 gene were evaluated by the polymerase chain reaction (PCR) restriction fragment length polymorphism method in the DNA extracted from the peripheral blood of patients and controls. RESULTS: The frequencies of the 311T>C CLOCK1 gene, CC genotype and C allele were significantly higher among CRC patients compared to controls (P < 0.0001) elevating the CRC risk by 2.78- and 1.78-fold respectively. No correlation was found between G3853A and 4/5 repeats polymorphisms and CRC risk. The C/G/5 and C/G/4 repeats haplotypes were higher in CRC patients (P = 0.0009 and P = 0.038) elevating the CRC risk by 60% and 89% respectively. No correlation was found between any polymorphism and clinicopathological characteristics of CRC patients. CONCLUSION: The 311T>C polymorphism in the CLOCK1 gene significantly increases the risk for CRC development while it does not affect the outcome of CRC patients.
Authors: Melannie Alexander; James B Burch; Susan E Steck; Chin-Fu Chen; Thomas G Hurley; Philip Cavicchia; Meredith Ray; Nitin Shivappa; Jaclyn Guess; Hongmei Zhang; Shawn D Youngstedt; Kim E Creek; Stephen Lloyd; Xiaoming Yang; James R Hébert Journal: Oncol Rep Date: 2014-12-11 Impact factor: 3.906
Authors: Heather S L Jim; Hui-Yi Lin; Jonathan P Tyrer; Kate Lawrenson; Joe Dennis; Ganna Chornokur; Zhihua Chen; Ann Y Chen; Jennifer Permuth-Wey; Katja Kh Aben; Hoda Anton-Culver; Natalia Antonenkova; Fiona Bruinsma; Elisa V Bandera; Yukie T Bean; Matthias W Beckmann; Maria Bisogna; Line Bjorge; Natalia Bogdanova; Louise A Brinton; Angela Brooks-Wilson; Clareann H Bunker; Ralf Butzow; Ian G Campbell; Karen Carty; Jenny Chang-Claude; Linda S Cook; Daniel W Cramer; Julie M Cunningham; Cezary Cybulski; Agnieszka Dansonka-Mieszkowska; Andreas du Bois; Evelyn Despierre; Weiva Sieh; Jennifer A Doherty; Thilo Dörk; Matthias Dürst; Douglas F Easton; Diana M Eccles; Robert P Edwards; Arif B Ekici; Peter A Fasching; Brooke L Fridley; Yu-Tang Gao; Aleksandra Gentry-Maharaj; Graham G Giles; Rosalind Glasspool; Marc T Goodman; Jacek Gronwald; Philipp Harter; Hanis N Hasmad; Alexander Hein; Florian Heitz; Michelle A T Hildebrandt; Peter Hillemanns; Claus K Hogdall; Estrid Hogdall; Satoyo Hosono; Edwin S Iversen; Anna Jakubowska; Allan Jensen; Bu-Tian Ji; Beth Y Karlan; Melissa Kellar; Lambertus A Kiemeney; Camilla Krakstad; Susanne K Kjaer; Jolanta Kupryjanczyk; Robert A Vierkant; Diether Lambrechts; Sandrina Lambrechts; Nhu D Le; Alice W Lee; Shashi Lele; Arto Leminen; Jenny Lester; Douglas A Levine; Dong Liang; Boon Kiong Lim; Jolanta Lissowska; Karen Lu; Jan Lubinski; Lene Lundvall; Leon F A G Massuger; Keitaro Matsuo; Valerie McGuire; John R McLaughlin; Ian McNeish; Usha Menon; Roger L Milne; Francesmary Modugno; Lotte Thomsen; Kirsten B Moysich; Roberta B Ness; Heli Nevanlinna; Ursula Eilber; Kunle Odunsi; Sara H Olson; Irene Orlow; Sandra Orsulic; Rachel Palmieri Weber; James Paul; Celeste L Pearce; Tanja Pejovic; Liisa M Pelttari; Malcolm C Pike; Elizabeth M Poole; Eva Schernhammer; Harvey A Risch; Barry Rosen; Mary Anne Rossing; Joseph H Rothstein; Anja Rudolph; Ingo B Runnebaum; Iwona K Rzepecka; Helga B Salvesen; Ira Schwaab; Xiao-Ou Shu; Yurii B Shvetsov; Nadeem Siddiqui; Honglin Song; Melissa C Southey; Beata Spiewankiewicz; Lara Sucheston-Campbell; Soo-Hwang Teo; Kathryn L Terry; Pamela J Thompson; Ingvild L Tangen; Shelley S Tworoger; Anne M van Altena; Ignace Vergote; Christine S Walsh; Shan Wang-Gohrke; Nicolas Wentzensen; Alice S Whittemore; Kristine G Wicklund; Lynne R Wilkens; Anna H Wu; Xifeng Wu; Yin-Ling Woo; Hannah Yang; Wei Zheng; Argyrios Ziogas; Ernest Amankwah; Andrew Berchuck; Joellen M Schildkraut; Linda E Kelemen; Susan J Ramus; Alvaro N A Monteiro; Ellen L Goode; Steven A Narod; Simon A Gayther; Paul D P Pharoah; Thomas A Sellers; Catherine M Phelan Journal: J Genet Genome Res Date: 2015-09-15