AIM: To investigate the relationship between inactivation of p16 gene and gastric carcinoma, and the mechanism of inactivation of p16 gene in gastric carcinogenesis. METHODS: 40 fresh tumor tissue specimens were taken from primary gastric cancer patients. Expression of P16 protein was detected by immunohistochemical method. Deletion and point mutation of p16 gene were analyzed by polymerase chain reaction (PCR) and DNA sequencing, respectively. RESULTS: The frequency of loss of P16 protein expression in the gastric cancer tissue, adjacent nontumor tissue, and distal normal tissue was 77.5 % (31/40), 55.0 % (22/40), and 17.5 % (7/40), respectively (P<0.005). Homozygous deletion of exon 1 and exon 3 was observed in two and three cases, respectively, giving an overall frequency of homozygous deletion of 12.5 %. All five cases had diffuse type gastric carcinoma. No p16 gene point mutation was detected. CONCLUSION: These findings suggest a close correlation between inactivation of p16 gene and gastric carcinoma. Further investigations are needed to testify the mechanism of inactivation of p16 gene in gastric carcinogenesis.
AIM: To investigate the relationship between inactivation of p16 gene and gastric carcinoma, and the mechanism of inactivation of p16 gene in gastric carcinogenesis. METHODS: 40 fresh tumor tissue specimens were taken from primary gastric cancerpatients. Expression of P16 protein was detected by immunohistochemical method. Deletion and point mutation of p16 gene were analyzed by polymerase chain reaction (PCR) and DNA sequencing, respectively. RESULTS: The frequency of loss of P16 protein expression in the gastric cancer tissue, adjacent nontumor tissue, and distal normal tissue was 77.5 % (31/40), 55.0 % (22/40), and 17.5 % (7/40), respectively (P<0.005). Homozygous deletion of exon 1 and exon 3 was observed in two and three cases, respectively, giving an overall frequency of homozygous deletion of 12.5 %. All five cases had diffuse type gastric carcinoma. No p16 gene point mutation was detected. CONCLUSION: These findings suggest a close correlation between inactivation of p16 gene and gastric carcinoma. Further investigations are needed to testify the mechanism of inactivation of p16 gene in gastric carcinogenesis.
Authors: M Tsujie; H Yamamoto; N Tomita; Y Sugita; M Ohue; I Sakita; Y Tamaki; M Sekimoto; Y Doki; M Inoue; N Matsuura; T Monden; H Shiozaki; M Monden Journal: Oncology Date: 2000-02 Impact factor: 2.935
Authors: C T Liew; H M Li; K W Lo; C K Leow; J Y Chan; L Y Hin; W Y Lau; P B Lai; B K Lim; J Huang; W T Leung; S Wu; J C Lee Journal: Oncogene Date: 1999-01-21 Impact factor: 9.867
Authors: Ioana Cutcutache; Alice Yingting Wu; Yuka Suzuki; John Richard McPherson; Zhengdeng Lei; Niantao Deng; Shenli Zhang; Wai Keong Wong; Khee Chee Soo; Weng Hoong Chan; London Lucien Ooi; Roy Welsch; Patrick Tan; Steven G Rozen Journal: Gastric Cancer Date: 2015-07-24 Impact factor: 7.370
Authors: Miguel Cordova-Delgado; Mauricio P Pinto; Ignacio N Retamal; Matías Muñoz-Medel; María Loreto Bravo; María F Fernández; Betzabé Cisternas; Sebastián Mondaca; César Sanchez; Hector Galindo; Bruno Nervi; Carolina Ibáñez; Francisco Acevedo; Jorge Madrid; José Peña; Erica Koch; Maria José Maturana; Diego Romero; Nathaly de la Jara; Javiera Torres; Manuel Espinoza; Carlos Balmaceda; Yuwei Liao; Zhiguang Li; Matías Freire; Valentina Gárate-Calderón; Javier Cáceres; Gonzalo Sepúlveda-Hermosilla; Rodrigo Lizana; Liliana Ramos; Rocío Artigas; Enrique Norero; Fernando Crovari; Ricardo Armisén; Alejandro H Corvalán; Gareth I Owen; Marcelo Garrido Journal: Cancers (Basel) Date: 2019-08-30 Impact factor: 6.639