Preferential occurrence of breast carcinomas with loss of chromosome 16q and der (16) t (1;16) / der (1;16) in middle-aged patients with hyperplasia of mammary glands.
Structural and numerical alterations of chromosome 16 are considered to be commonly involved in the genesis of breast cancer. To reveal etiological factors that predispose cells to these alterations, we examined the frequencies of chromosome 16 aneusomy, 16q loss and 1;16 fusion indicating der (16) t (1;16) / der (1;16) by multi-color fluorescence in situ hybridization in 46 tumors resected mostly from young ( </= 34 years old) or elderly ( >/= 75 years old) women, and compared the results with those in a patient group representing a common age distribution of Japanese patients in whom chromosome 16 status in the tumor had already been studied. The correlation of these chromosome 16 alterations with age, hyperplasia in adjacent mammary glands, cancer history, and obesity indices was investigated in a total of 244 patients. In the present 46 tumors, the frequency of 16q loss and der (16) t (1;16) did not differ between 20 younger patients (30% and 15%) and 23 elderly patients (43% and 13%). However, the incidences of 16q loss and der (16) t (1;16) were low in comparison with the values of 64% and 38% in the 198 Japanese patients representing the common age distribution (P < 0.001). In addition, 16q loss and der (16) t (1;16) were more frequent in tumors arising in hyperplastic mammary glands (68%, 44%) than in those without (52%, 24%) (P < 0.01). Such correlations were not evident for 16cen aneusomy. Other etiological factors examined were not correlated with these chromosome 16 alterations. The 16q loss and der (16) t (1;16) formation were more frequently involved in the development of breast cancer in middle-aged patients than in young and elderly patients. High-level estrogens and / or sensitivity of mammary glandular cells to estrogens might induce breast cancers with structural changes of chromosome 16.
Tsuda
H
H
Pathology Division, National Cancer Center Research Institute and Hospital, Chuo-ku, Tokyo 104-0045, Japan. hstsuda@gan2.ncc.go.jp
Takarabe
T
T
Fukutomi
T
T
Hirohashi
S
S
D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D000782:Aneuploidy; D015992:Body Mass Index; D001940:Breast / Q000473:pathology*; D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology; D002869:Chromosome Aberrations / Q000235:genetics*; D002872:Chromosome Deletion; D002878:Chromosomes, Human, Pair 1 / Q000235:genetics*; D002885:Chromosomes, Human, Pair 16 / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D006801:Humans; D006965:Hyperplasia / Q000473:pathology; D017404:In Situ Hybridization, Fluorescence; D008593:Menopause / Q000502:physiology; D008875:Middle Aged; D014178:Translocation, Genetic / Q000235:genetics