TY - JOUR
T1 - Genetic analysis of prostatic atypical adenomatous hyperplasia (adenosis)
AU - Doll, Jennifer A.
AU - Zhu, Xiaopei
AU - Furman, Jaime
AU - Kaleem, Zahid
AU - Torres, Carlos
AU - Humphrey, Peter A.
AU - Donis-Keller, Helen
N1 - Funding Information:
Supported in part by an award from the CaPCURE foundation (to H. D. K.) and graduate student stipend support from Dr. William Catalona and the Division of Urology, Washington University.
PY - 1999/9
Y1 - 1999/9
N2 - Atypical adenomatous hyperplasia (AAH) of the prostate, a small glandular proliferation, is a putative precursor lesion to prostate cancer, in particular to the subset of well-differentiated carcinomas that arise in the transition zone, the same region where AAH lesions most often occur. Several morphological characteristics of AAH suggest a relationship to cancer; however, no definitive evidence has been reported. In this study, we analyzed DNA from 25 microdissected AAH lesions for allelic imbalance as compared to matched normal DNA, using one marker each from chromosome arms 1q, 6q, 7q, 10q, 13q, 16q, 17p, 17q, and 18q, and 19 markers from chromosome 8p. We observed 12% allelic imbalance, with loss only within chromosome 8p11- 12. These results suggest that genetic alterations in transition zone AAH lesions may be infrequent. This genotypic profile of AAH will allow for comparisons with well-differentiated carcinomas in the transition zone of the prostate.
AB - Atypical adenomatous hyperplasia (AAH) of the prostate, a small glandular proliferation, is a putative precursor lesion to prostate cancer, in particular to the subset of well-differentiated carcinomas that arise in the transition zone, the same region where AAH lesions most often occur. Several morphological characteristics of AAH suggest a relationship to cancer; however, no definitive evidence has been reported. In this study, we analyzed DNA from 25 microdissected AAH lesions for allelic imbalance as compared to matched normal DNA, using one marker each from chromosome arms 1q, 6q, 7q, 10q, 13q, 16q, 17p, 17q, and 18q, and 19 markers from chromosome 8p. We observed 12% allelic imbalance, with loss only within chromosome 8p11- 12. These results suggest that genetic alterations in transition zone AAH lesions may be infrequent. This genotypic profile of AAH will allow for comparisons with well-differentiated carcinomas in the transition zone of the prostate.
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U2 - 10.1016/S0002-9440(10)65196-6
DO - 10.1016/S0002-9440(10)65196-6
M3 - Article
C2 - 10487854
AN - SCOPUS:0032887984
VL - 155
SP - 967
EP - 971
JO - American Journal of Pathology
JF - American Journal of Pathology
SN - 0002-9440
IS - 3
ER -