N-RAS MUTATION OF THYROID-TUMOR WITH SPECIAL REFERENCE TO THE FOLLICULAR TYPE

被引:32
作者
OYAMA, T
SUZUKI, T
HARA, F
IINO, Y
ISHIDA, T
SAKAMOTO, A
NAKAJIMA, T
机构
[1] GUNMA UNIV,SCH MED,DEPT SURG 2,MAEBASHI,GUMMA 371,JAPAN
[2] UNIV TOKYO,FAC MED,DEPT PATHOL,TOKYO 113,JAPAN
关键词
FOLLICULAR CARCINOMA; N-RAS ONCOGENE; PCR-SSCP ANALYSIS; POINT MUTATION; THYROID;
D O I
10.1111/j.1440-1827.1995.tb03378.x
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Using the method of polymerase chain reaction-single strand conformation polymorphism, the point mutations of the ras oncogenes in a total of 33 thyroid tissues, including 12 follicular adenomas, 6 follicular carcinomas, 11 papillary carcinomas, and 4 undifferentiated carcinomas, were examined, The frequency of the mutation was 3% (1/33) in codon 12, 13 of Ki-ras and 18% (6/33) in codon 61 of N-ras, including 17% (2/12) in follicular adenoma, 50% (3/6) in follicular carcinoma, 0% (0/11) in papillary carcinoma and 25% (1/4) in undifferentiated carcinoma, In follicular adenoma, positivity was observed in microfollicular or trabecular subtypes. Furthermore, the mutation of ras was examined in histologically different parts, coexisting in the same tumor in a total of four cases, Both the undifferentiated carcinoma and coexisting follicular adenoma, and both the microfollicular adenoma and trabecular nodule growing in the tumor, had the same N-ras (61) mutation, Direct sequencing analysis showed that all mutations were CAA (Gln) to CGA (Arg) transition of codon 61, except for CAA to AAA transversion in one case of follicular carcinoma, A similar genetic abnormality of N-ras genes at codon 61 between follicular adenoma and follicular carcinoma suggests that the mutation of N-ras at codon 61 might play a part in oncogenesis in follicular tumors.
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页码:45 / 50
页数:6
相关论文
共 23 条
[1]   OVEREXPRESSION OF P53 AS A POSSIBLE PROGNOSTIC FACTOR IN HUMAN THYROID-CARCINOMA [J].
DOBASHI, Y ;
SAKAMOTO, A ;
SUGIMURA, H ;
MERNYEI, M ;
MORI, M ;
OYAMA, T ;
MACHINAMI, R .
AMERICAN JOURNAL OF SURGICAL PATHOLOGY, 1993, 17 (04) :375-381
[2]   STEPWISE PARTICIPATION OF P53 GENE MUTATION DURING DEDIFFERENTIATION OF HUMAN THYROID CARCINOMAS [J].
DOBASHI, Y ;
SUGIMURA, H ;
SAKAMOTO, A ;
MERNYEI, M ;
MORI, M ;
OYAMA, T ;
MACHINAMI, R .
DIAGNOSTIC MOLECULAR PATHOLOGY, 1994, 3 (01) :9-14
[3]  
EZAKI H, 1992, CANCER, V70, P808, DOI 10.1002/1097-0142(19920815)70:4<808::AID-CNCR2820700415>3.0.CO
[4]  
2-L
[5]   A GENETIC MODEL FOR COLORECTAL TUMORIGENESIS [J].
FEARON, ER ;
VOGELSTEIN, B .
CELL, 1990, 61 (05) :759-767
[6]   PURIFICATION OF DNA FROM FORMALDEHYDE FIXED AND PARAFFIN EMBEDDED HUMAN-TISSUE [J].
GOELZ, SE ;
HAMILTON, SR ;
VOGELSTEIN, B .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1985, 130 (01) :118-126
[7]   PTC IS A NOVEL REARRANGED FORM OF THE RET PROTO-ONCOGENE AND IS FREQUENTLY DETECTED INVIVO IN HUMAN THYROID PAPILLARY CARCINOMAS [J].
GRIECO, M ;
SANTORO, M ;
BERLINGIERI, MT ;
MELILLO, RM ;
DONGHI, R ;
BONGARZONE, I ;
PIEROTTI, MA ;
DELLAPORTA, G ;
FUSCO, A ;
VECCHIO, G .
CELL, 1990, 60 (04) :557-563
[8]  
HEDINGER CHR, 1988, WHO INT HISTOLOGICAL
[9]  
KARGA H, 1991, J CLIN ENDOCR METAB, V3, P832
[10]  
LEMOINE NR, 1989, ONCOGENE, V4, P159