Wang L, Banerjee S
CLEVELAND CLIN FDN,RES INST,DEPT CANC BIOL,CLEVELAND,OH 44195.
Int J Oncol. 1995 Feb;6(2):459-63.
To determine the tissue specificity of the potential mutations in DNA polymerase beta (pol beta), alterations in the pol beta were examined in breast, prostate, and colorectal primary tumors. The pol beta is known to contribute to mammalian base excision repair and replication. Similar to colorectal cancer, a high occurrence of mutations as 87-bp deletion in the catalytic domain of the pol beta removing 29 amino acids was observed in breast cancer. Contrary to breast and colorectal tumors, a low occurrence of mutation as a single base (T) deletion at the position coding for amino acid 181 of the pol beta was associated with prostate cancer. The missing T changed the codon from TTC to TCA (phenylalanine to serine), causing a frame shift.
为了确定DNA聚合酶β(polβ)潜在突变的组织特异性,在乳腺、前列腺和结肠直肠癌原发性肿瘤中检测了polβ的改变。已知polβ有助于哺乳动物碱基切除修复和复制。与结肠直肠癌相似,在乳腺癌中观察到polβ催化结构域中高发生率的突变,如87碱基对缺失,去除了29个氨基酸。与乳腺和结肠直肠肿瘤相反,polβ第181位氨基酸编码位置的单个碱基(T)缺失这种低发生率的突变与前列腺癌相关。缺失的T将密码子从TTC变为TCA(苯丙氨酸变为丝氨酸),导致移码。