| Objective: 1.To determine the the presence of the K303R ERα mutant in normal breast tissues, Fibroadenoma,breast hyperplasia, ductal carcinorma in situ, invasive breast cancer and axillary lymph node of breast cancer. 2.To analysis the value of the K303R Estrogen Receptor αMutation in Breast Cancer.Methods: We divide all of the sample into 6 group: normal breast tissues, Fibroadenoma,breast hyperplasia, ductal carcinorma in situ, invasive breast cancer and axillary lymph node of breast cancer. Then we use the Goelz method to isolate the DNA from the sample. Using 3 kinds of method (including automatic sequence, manual sequence and Snapshot sequence) to sequence the K303R ERα?mutation of all the sample (including 20 cases of normal breast tissues, 21 cases of Fibroadenoma,59 cases of breast hyperplasia, 20 cases of ductal carcinorma in situ, 23 cases of invasive breast cancer and 10 cases of axillary lymph node of breast cancer. Result: We found that automatic sequence could not detect the K303R ERα?mutation. But laborious technique, manual dideoxynucleotide gel-based sequence analysis of genomic DNA could do it: the K303R ERαalteration could not found to be present in normal beast and fibroadenoma, but it was found to be present in a total of 20 of 59 (34%) of the hyperplasias , 11 of 20 (53%) of DCIS, 13 of 23 (62%) IBC and 10 of 10 (100%) of lymph node of breast cancer. And Snapshot sequence confirm the result above too.Conclusion: K303R ERαmutation is an A-to-G bp transition at nucleotide 908 of ERα. This mutation causes an amino acid change in the ER hinge domain (lysine 303 to arginine, K303R). It could not exist in normal breast and fibroadenoma but the exsiting rate is increasing from hyperplasia, DCIS, IBC to lymph node of breast cancer. It is demostrated that K303R ERα?mutation play a very important role in the progression of breast cancer. It accelerate the formation and the metastasis of breast cancer. Thus it could be a predictor and prognostic factor of breast cancer. |
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