scholarly journals SMAD4 Gene

2020 ◽  
Author(s):  
Keyword(s):  

2017 ◽  
Vol 23 (2) ◽  
pp. 17-19
Author(s):  
Aleksandra Nikolic ◽  
Filip Opincal ◽  
Momcilo Ristanovic ◽  
Jovanka Trifunovic ◽  
Srbislav Knezevic ◽  
...  

Background. Promoter hypermethylation of the SMAD4 gene has been registered in some cancer types, but in general doesn?t appear to be a frequent event in carcinogenesis. However, only a few published studies deal with this topic and not many cancer types have been analyzed. The aim of this study was to establish SMAD4 gene promoter methylation status in pancreatic and endometrial cancers. Methods. Patients included in the study (62 subjects) were diagnosed and surgically treated at the University of Belgrade, Clinical Center of Serbia. Patients with pancreatic carcinoma (17 subjects) underwent surgical removal of the pancreatic adenocarcinoma at the First Surgical Clinic, while the patients with endometrial carcinoma (45 subjects) underwent hysterectomy with adnexectomy at the Institute for Gynecology and Obstetrics. Extraction of DNA from fresh tissue samples was performed and the methylation status of the SMAD4 gene promoter was studied by a previously designed PCR-based HpaII and MspI restriction enzyme assay. The resulting PCR products were analyzed by electrophoresis in 2% agarose gels. Results. Neither of the analyzed samples was found to be hypermethylated. Conclusion. This is the first report on SMAD4 methylation status in pancreatic and endometrial tumor specimens, and supports the viewpoint that SMAD4 hypermethylation is not a common event in malignant tumors. Nevertheless, promoter hypermethylation remains a candidate mechanism for SMAD4 inactivation in malignant tissue as a potential cause of decreased or lost SMAD4 expression in certain tumor types, and should be further investigated in different tumor types and larger cohorts of patients.



Oncogene ◽  
1999 ◽  
Vol 18 (14) ◽  
pp. 2367-2371 ◽  
Author(s):  
Detlef Bartsch ◽  
Stephan A Hahn ◽  
Kirill D Danichevski ◽  
Annette Ramaswamy ◽  
Daniel Bastian ◽  
...  




Genes ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 766 ◽  
Author(s):  
Yao-Yu Hsieh ◽  
Tsang-Pai Liu ◽  
Chia-Jung Chou ◽  
Hsin-Yi Chen ◽  
Kuen-Haur Lee ◽  
...  

Pancreatic ductal adenocarcinoma (PDAC) is the most common and aggressive type of pancreatic cancer. The five-year survival rate of PDAC is very low (less than 8%), which is associated with the late diagnosis, high metastatic potential, and resistance to therapeutic agents. The identification of better prognostic or therapeutic biomarker may have clinical benefits for PDAC treatment. SMAD4, a central mediator of transforming growth factor beta (TGFβ) signaling pathway, is considered a tumor suppressor gene. SMAD4 inactivation is frequently found in PDAC. However, its role in prognosis and therapeutics of PDAC is still unclear. In this study, we applied bioinformatics approaches, and integrated publicly available resources, to investigate the role of SMAD4 gene deletion in PDAC. We found that SMAD4 deletion was associated with poorer disease-free, but not overall, survival in PDAC patients. Cancer hallmark enrichment and pathway analysis suggested that the upregulation of cell cycle-related genes in SMAD4-deleted PDAC. Chemotherapy response profiling of PDAC cell lines and patient-derived organoids revealed that SMAD4-deleted PDAC was sensitive to gemcitabine, the first-line treatment for PDAC, and specific cell cycle-targeting drugs. Taken together, our study provides an insight into the prognostic and therapeutic roles of SMAD4 gene deletion in PDAC, and SMAD4 gene copy numbers may be used as a therapeutic biomarker for PDAC treatment.



Oncogene ◽  
1999 ◽  
Vol 18 (34) ◽  
pp. 4879-4883 ◽  
Author(s):  
M C Yakicier ◽  
M B Irmak ◽  
A Romano ◽  
M Kew ◽  
M Ozturk


2018 ◽  
Vol 44 (5) ◽  
pp. 684-692 ◽  
Author(s):  
Takashi Mizuno ◽  
Jordan M. Cloyd ◽  
Diego Vicente ◽  
Kiyohiko Omichi ◽  
Yun Shin Chun ◽  
...  


2008 ◽  
Vol 144 (2) ◽  
pp. 196-197
Author(s):  
J. Joshua Smith ◽  
Bonnie LaFleur ◽  
Kay Washington ◽  
Nipun Merchant ◽  
Robert Coffey ◽  
...  


2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 180-180
Author(s):  
Olfa Derbel ◽  
Arnaud de la Fouchardière ◽  
Julien Peron ◽  
Francoise Desseigne ◽  
Pierre Heudel ◽  
...  

180 Background: Pancreatic adenocarcinoma remains resistant to many key cytotoxic chemotherapeutic agents and novel targeted therapies. The molecular heterogeneity of this cancer may account for therapy failures to date, although the growing arsenal of novel targeted agents could translate into patient survival. A better understanding of the cellular and molecular features of advanced disease will afford new opportunities for investigation, therapeutic intervention and clinical management of patients afflicted with pancreatic cancer. Methods: Data of 46 patients with pancreatic adenocarcinoma were analyzed. The clinicopathological parameters, the histologic features were determined and correlated to the stage at initial diagnosis and patterns of failure (locally advanced v metastatic disease). Using tissue microarray, we assessed the relationship of SMAD4 expression with the overall survival of patients. Results: Among the 46 treated patients, 32 underwent pancreaticoduodenectomy. 40% of patients died with metastatic disease and 15 % died with locally advance evolution. Loss of SMAD4 expression was found in 22% of patients and seems to be correlated with a high grade histologic features and progression to metastasis disease. Complementary data about correlation between the mutational status of SMAD4 and survival will be presented during congress. Conclusions: SMAD4 gene inactivation seems to be associated with poorer prognosis and disease progression. Prospective validation of SMAD4 as a predictive biomarker may personalize treatment strategies for patients with pancreatic cancer.



2018 ◽  
Vol 18 (2) ◽  
pp. 165-172
Author(s):  
Maurizio Ponz de Leon ◽  
Monica Pedroni ◽  
Alessandra Viel ◽  
Claudio Luppi ◽  
Rita Conigliaro ◽  
...  


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