BREAST-CANCER AND FAMILY HISTORY - LEVELS OF LIPID-ASSOCIATED SIALIC-ACID IN PLASMA AND ABSENT FAMILY HISTORY OF BREAST-CANCER IN WOMEN WHOHAVE BREAST-TUMORS

Citation
St. Brower et al., BREAST-CANCER AND FAMILY HISTORY - LEVELS OF LIPID-ASSOCIATED SIALIC-ACID IN PLASMA AND ABSENT FAMILY HISTORY OF BREAST-CANCER IN WOMEN WHOHAVE BREAST-TUMORS, The Mount Sinai journal of medicine, 62(6), 1995, pp. 419-421
Citations number
15
Categorie Soggetti
Medicine, General & Internal
ISSN journal
00272507
Volume
62
Issue
6
Year of publication
1995
Pages
419 - 421
Database
ISI
SICI code
0027-2507(1995)62:6<419:BAFH-L>2.0.ZU;2-K
Abstract
Background: Breast cancer has a strong genetic component, and at least two breast cancer genes exist. But these genes probably play little r ole in most breast cancers. Other factors, such as environmental estro gens and diet, may cause the genetic changes involved in the genesis o f sporadic breast cancer. A method of observing genetic changes indire ctly might be to measure tumor markers known to be associated with bre ast cancer. Methods: We measured, by biochemical extraction and partit ion, lipid-associated sialic acid in plasma (LASA-P), a circulating tu mor marker, in a group of 239 women with benign or malignant breast tu mors. Results: The concentration of LASA-P was elevated in women with both benign and malignant tumors and no family history of breast cance r (p = 0.046, one-way ANOVA). Because LASA-P levels rise with age and number of pregnancies, we analyzed our data using multiple linear regr ession. Benign versus malignant character of the tumor, family history of breast cancer, number of pregnancies, and age were the independent variables. Family history of breast cancer had a significant effect o n LASA-P levels (p = 0.0146) independent of the effects of age (p = 0. 011), number of pregnancies (0.012), and whether the tumor was benign or malignant (p = 0.31). Conclusions: We hypothesize that elevated LAS A-P in women with breast tumors and no family history of breast cancer is a result of the genetic changes occurring in nonfamilial breast ca ncer. These genetic changes, possibly related to environmental estroge ns or other environmental factors, are distinct from the changes due t o mutations of BRCA1 or other familial breast cancer genes. Moreover, the elevation of LASA-P suggests that the surface membranes of breast cancer may differ in composition. Further study may lead to exact char acterization of the genetic and cell membrane changes associated with familial and nonfamilial breast tumors, and perhaps to better methods of breast cancer prevention and treatment.