CLONAL ORIGIN OF PITUITARY-ADENOMAS

被引:61
作者
JACOBY, LB
HEDLEYWHYTE, ET
PULASKI, K
SEIZINGER, BR
MARTUZA, RL
机构
[1] MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114
[2] MASSACHUSETTS GEN HOSP,PATHOL SERV,BOSTON,MA 02114
[3] HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115
[4] HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115
关键词
chromosome; X; clonal analysis; immunohistochemistry glycoprotein hormone; pituitary adenoma;
D O I
10.3171/jns.1990.73.5.0731
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Benign pituitary adenomas are among the most common neurosurgical tumors and account for a diversity of clinical syndromes due to their hormone content and release. To determine whether these tumors arise from a single cell or multiple cells, the authors studied X chromosome inactivation in deoxyribonucleic acid (DNA) isolated from pituitary adenomas in women. Tumors of three different hormonal subtypes were examined. One tumor contained cells immunoreactive for prolactin and human growth hormone; one tumor contained foci immunoreactive for the β-subunits of luteinizing hormone and follicle-stimulating hormone; and the third tumor had no immunoreactive prolactin, human growth hormone, β-subunits of thyroid-stimulating hormone, luteinizing hormone, or follicle-stimulating hormone, or the α-subunit. Analysis of the DNA revealed that, in each of the three pituitary tumors, one X chromosome was active in all cells and one X chromosome was inactive, indicating that each of these tumors was monoclonal in origin. It is concluded that clinically evident pituitary tumors arise from a genetic mutation in a single cell.
引用
收藏
页码:731 / 735
页数:5
相关论文
共 10 条
[1]  
[Anonymous], 1986, ATLAS TUMOR PATHOLOG
[2]   MONOCLONALITY AND ABNORMAL PARATHYROID-HORMONE GENES IN PARATHYROID ADENOMAS [J].
ARNOLD, A ;
STAUNTON, CE ;
KIM, HG ;
GAZ, RD ;
KRONENBERG, HM .
NEW ENGLAND JOURNAL OF MEDICINE, 1988, 318 (11) :658-662
[3]   HORMONE PRODUCTION IN CLINICALLY NONFUNCTIONING PITUITARY-ADENOMAS [J].
BLACK, PM ;
HSU, DW ;
KLIBANSKI, A ;
KLIMAN, B ;
JAMESON, JL ;
RIDGWAY, EC ;
HEDLEYWHYTE, ET ;
ZERVAS, NT .
JOURNAL OF NEUROSURGERY, 1987, 66 (02) :244-250
[4]   A TECHNIQUE FOR RADIOLABELING DNA RESTRICTION ENDONUCLEASE FRAGMENTS TO HIGH SPECIFIC ACTIVITY [J].
FEINBERG, AP ;
VOGELSTEIN, B .
ANALYTICAL BIOCHEMISTRY, 1983, 132 (01) :6-13
[5]   A 3-ALLELE RESTRICTION-FRAGMENT-LENGTH POLYMORPHISM AT THE HYPOXANTHINE PHOSPHORIBOSYLTRANSFERASE LOCUS IN MAN [J].
NUSSBAUM, RL ;
CROWDER, WE ;
NYHAN, WL ;
CASKEY, CT .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1983, 80 (13) :4035-4039
[6]   LOSS OF GENES ON CHROMOSOME-22 IN TUMORIGENESIS OF HUMAN ACOUSTIC NEUROMA [J].
SEIZINGER, BR ;
MARTUZA, RL ;
GUSELLA, JF .
NATURE, 1986, 322 (6080) :644-647
[7]   DETECTION OF SPECIFIC SEQUENCES AMONG DNA FRAGMENTS SEPARATED BY GEL-ELECTROPHORESIS [J].
SOUTHERN, EM .
JOURNAL OF MOLECULAR BIOLOGY, 1975, 98 (03) :503-+
[8]   USE OF RESTRICTION FRAGMENT LENGTH POLYMORPHISMS TO DETERMINE THE CLONAL ORIGIN OF HUMAN-TUMORS [J].
VOGELSTEIN, B ;
FEARON, ER ;
HAMILTON, SR ;
FEINBERG, AP .
SCIENCE, 1985, 227 (4687) :642-645
[9]  
VOGELSTEIN B, 1987, CANCER RES, V47, P4806
[10]   DIFFERENTIAL METHYLATION OF HYPOXANTHINE PHOSPHORIBOSYLTRANSFERASE GENES ON ACTIVE AND INACTIVE HUMAN X-CHROMOSOMES [J].
YEN, PH ;
PATEL, P ;
CHINAULT, AC ;
MOHANDAS, T ;
SHAPIRO, LJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1984, 81 (06) :1759-1763