Ito T, Seyama T, Hayashi Y, Hayashi T, Dohi K, Mizuno T, Iwamoto K, Tsuyama N, Nakamura N, Akiyama M
RADIAT EFFECTS RES FDN,DEPT RADIOBIOL,5-2 HIJIYAMA PK,MINAMI KU,HIROSHIMA 732,JAPAN. HIROSHIMA CITY ASA HOSP,DEPT PATHOL,ASAKITA KU,HIROSHIMA 73102,JAPAN. HIROSHIMA UNIV,SCH MED,DEPT SURG,MINAMI KU,HIROSHIMA 734,JAPAN.
Int J Oncol. 1994 Mar;4(3):583-6. doi: 10.3892/ijo.4.3.583.
New cell lines, designated 8305C and 8505C, were established from undifferentiated thyroid carcinomas of a 67 year-old-female patient and a 78-year-old-female patient, respectively. Pathologically both these primary undifferentiated carcinoma tissues contained residual well differentiated components, suggesting well differentiated to undifferentiated carcinoma progression. Cell kinetic analysis indicate that the cell population doubling time is 43 h for 8305C and 36 h for 8505C. The saturation density at confluency is 5.7 x 10(4) cells/cm2 for 8305C and 1.1 x 10(5) cells/cm2 for 8505C. To identify genetic changes that may have occurred in these two cell lines, tumor suppressor genes p53, Rb, APC and MCC were analyzed. Sequence analysis confirmed a C:G to T:A transition at the first base of p53 gene codon 273 in 8305C and a C:G to G:C transversion at the first base of p53 codon 248 in 8505C. Polymerase chain reaction-loss of heterozygosity assays confirmed allelic deletion of p53 gene from the 8505C cell line. Loss of heterozygosity of other tumor suppressor genes were not observed. Given that p53 mutations associate with undifferentiated carcinoma but not with well differentiated carcinoma during multistep carcinogenesis of the thyroid, these cell lines should prove useful for research into the role of p53 gene mutations in malignant transformation.
分别从一名67岁女性患者和一名78岁女性患者的未分化甲状腺癌中建立了新的细胞系,命名为8305C和8505C。病理检查显示,这两种原发性未分化癌组织均含有残留的高分化成分,提示肿瘤由高分化向未分化进展。细胞动力学分析表明,8305C细胞群体倍增时间为43小时,8505C为36小时。汇合时的饱和密度,8305C为5.7×10⁴个细胞/cm²,8505C为1.1×10⁵个细胞/cm²。为了鉴定这两个细胞系中可能发生的基因变化,对肿瘤抑制基因p53、Rb、APC和MCC进行了分析。序列分析证实,8305C中p53基因密码子273的第一个碱基发生了C:G到T:A的转换,8505C中p53密码子248的第一个碱基发生了C:G到G:C的颠换。聚合酶链反应-杂合性缺失分析证实8505C细胞系中p53基因存在等位基因缺失。未观察到其他肿瘤抑制基因的杂合性缺失。鉴于在甲状腺多步骤致癌过程中,p53突变与未分化癌相关,而与高分化癌无关,这些细胞系将有助于研究p53基因突变在恶性转化中的作用。