Functional impairment and the economic consequences of female breast cancer.

Recent trends in breast cancer diagnosis and mortality suggest that long-term survivors are now more likely to be functionally impaired and, hence, more likely to experience adverse economic outcomes. This study tests whether women who have survived breast cancer for at least five years exhibit more, or more severe, functional impairments than otherwise similar women without breast cancer. It also tests whether women with more severe impairments experience poorer economic outcomes attributable to their functional status. A group of 105 breast cancer survivors was interviewed to obtain data on health and economic changes in the five-year period since diagnosis and initial treatment. An age- and work-matched group of 105 women without cancer was also interviewed to obtain the same data over the same time period. Key changes in the functional status of the subjects as well as economic outcomes such as changes in market earnings, household income, and insurance coverage were measured. Whether impairment is more severe in the breast cancer group than the comparison group was then tested statistically; whether economic outcomes are more adverse in more impaired than less impaired women regardless of their breast cancer status was also tested. The analysis turned up statistically significant evidence in regard to each of these relationships. Breast cancer survivors were more likely than controls to be functionally impaired at the five-year benchmark. Impaired women, in turn, were more likely to reduce work effort and experience downturns in market earnings, among other things. Policy and research implications are discussed.

Indirect economic effects of long-term breast cancer survival.

PURPOSE: The indirect morbidity/disability costs of breast cancer may be rising as a consequence of the growth in the population of long-term survivors. This study was conducted to test whether women who have survived breast cancer for at least 5 years experience long-lasting or continuing economic consequences that are attributable to their disease. DESCRIPTION OF STUDY: A group of 105 women who initially had been treated for breast cancer approximately 5 years before were interviewed to obtain data on economic, demographic, and health changes in the period since diagnosis. An age-matched and work-matched group of 105 women without cancer also was interviewed to obtain the same data for the same time period. Key changes in the economic position of subjects and their families were measured, including changes in work effort, pay rates, and annual earnings of working women and changes in household earnings, income, and assets of all women. RESULTS: These preliminary empirical findings suggest that breast cancer exacts an economic toll from long-term survivors. In particular, survivors who were working at the time of their diagnosis experienced significantly larger reductions in annual market earnings over the 5-year study period than did working control subjects. These losses appear to arise mostly from reduced work effort, not changes in pay rates. Also, changes in total household earnings were lower for survivors, suggesting the presence of family adjustments to the disease. However, no significant differences were detected between the groups in changes in total income or assets over the study period. CLINICAL IMPLICATIONS: Clinicians and policy makers must seek ways to minimize the indirect economic losses that are attributable to breast cancer.

A human immunoglobulin G1 antibody originating from an in vitro-selected Fab phage antibody binds avidly to tumor-associated MUC1 and is efficiently internalized.

We describe the engineering and characterization of a whole human antibody directed toward the tumor-associated protein core of human MUC1. The antibody PH1 originated from the in vitro selection on MUC1 of a nonimmune human Fab phage library. The PH1 variable genes were reformatted for expression as a fully human IgG1. The resulting PH1-IgG1 human antibody displays a 160-fold improved apparent kd (8.7 nmol/L) compared to the kd of the parental Fab (1.4 micromol/L). In cell-binding studies with flow cytometry and immunohistochemistry, PH1-IgG1 exhibits staining patterns typical for antibodies recognizing the tumor-associated tandem repeat region on MUC1, eg, it binds the tumor-associated glycoforms of MUC1 in breast and ovarian cancer cell lines, but not the heavily glycosylated form of MUC1 on colon carcinoma cell lines. In many tumors PH1-IgG1 binds to membranous and cytoplasmic MUC1, with often intense staining of the whole-cell membrane (eg, in adenocarcinoma). In normal tissues staining is either absent or less intense, in which case it is found mostly at the apical side of the cells. Finally, fluorescein isothiocyanate-labeled PH1-IgG1 internalizes quickly after binding to human OVCAR-3 cells, and to a lesser extent to MUC1 gene-transfected 3T3 mouse fibroblasts. The tumor-associated binding characteristics of this antibody, its efficient internalization, and its human nature, make PH1-IgG1 a valuable candidate for further studies as a cancer-targeting immunotherapeutic.