Title of article :
Evaluation of PDE5 and PDE9 Expression in Benign and Malignant Breast Tumors
Author/Authors :
Karami-Tehrani، نويسنده , , Fatemeh and Moeinifard، نويسنده , , Marzieh and Aghaei، نويسنده , , Mahmoud and Atri، نويسنده , , Morteza، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2012
Pages :
6
From page :
470
To page :
475
Abstract :
Background and Aims odiesterases 5 and 9 (PDE5, PDE9) are enzymes responsible for regulating second messenger signaling by hydrolyzing 3’,5’ cyclic guanosine monophosphate (cGMP). PDE isoforms are deregulated in some types of human cancer. The present study was carried out to evaluate the expression of phosphodiesterase isoenzymes, PDE5 and PDE9, in benign and malignant breast tumors. s pression levels of PDE5 and PDE9 were assayed in malignant and benign breast tumors and corresponding normal breast tissues using quantitative real-time RT-PCR. Moreover, the correlation between PDE5, PDE9 relative expression and clinicopathological characteristics were analyzed. s lative expressions of PDE5 and PDE9 in malignant tumors were significantly higher than those of respective normal breast tissues and benign tumors (5.5-fold, p <0.001 and 6-fold, p <0.001, respectively). Furthermore, a significant positive correlation was found between PDE5 and PDE9 overexpression and tumor grade, stage, and lymph node involvement. However, a negative correlation was observed with age. sions on the present results, it is concluded that assessment of PDE5 and PDE9 expression may be useful in the differential diagnosis of benign and malignant breast disease and successful treatment of breast cancer. To the best of our knowledge, this is the first study to show that PDE5 and PDE9 expression levels are higher in malignant breast tumors than those of normal and benign breast tissue.
Keywords :
PDE5 and PDE9 expression , Benign Breast Disease , breast cancer
Journal title :
Archives of Medical Research
Serial Year :
2012
Journal title :
Archives of Medical Research
Record number :
1797799
Link To Document :
بازگشت