Increased cancer risks for relatives of very early-onset breast cancer cases with and without BRCA1 and BRCA2 mutations.

BACKGROUND: Little is known regarding cancer risks for relatives of women with very early-onset breast cancer. METHODS: We studied 2208 parents and siblings of 504 unselected population-based Caucasian women with breast cancer diagnosed before age 35 years (103 from USA, 124 from Canada and 277 from Australia), 41 known to carry a mutation (24 in BRCA1, 16 in BRCA2 and one in both genes). Cancer-specific standardised incidence ratios (SIRs) were estimated by comparing the number of affected relatives (50% verified overall) with that expected based on incidences specific for country, sex, age and year of birth. RESULTS: For relatives of carriers, the female breast cancer SIRs were 13.13 (95% CI 6.57-26.26) and 12.52 (5.21-30.07) for BRCA1 and BRCA2, respectively. The ovarian cancer SIR was 12.38 (3.1-49.51) for BRCA1 and the prostate cancer SIR was 18.55 (4.64-74.17) for BRCA2. For relatives of non-carriers, the SIRs for female breast, prostate, lung, brain and urinary cancers were 4.03 (2.91-5.93), 5.25 (2.50-11.01), 7.73 (4.74-12.62), 5.19 (2.33-11.54) and 4.35 (1.81-10.46), respectively. For non-carriers, the SIRs remained elevated and were statistically significant for breast and prostate cancer when based on verified cancers. CONCLUSION: First-degree relatives of women with very early-onset breast cancer are at increased risk of cancers not explained by BRCA1 and BRCA2 mutations.

Cancer incidence in Mormons and non-Mormons in Utah during 1967--75.

Data from the Utah Cancer Registry were used to compare cancer incidence in Mormons and non-Mormons in Utah for the period 1967--75. Church membership was identified for 97.8% of the 20,379 cases in Utah by a search of the central membership files of the Church of Jesus Christ of Latter-Day Saints (or Mormon Church). Sites associated with smoking (lung, larynx, pharynx, oral cavity, esophagus, and urinary bladder) showed an incidence in Mormons at about one-half that of non-Mormons. Rates of cancers of the breast, cervix, and ovary were low in Mormon women; the rate for cervical cancer was about one-half of that observed in non-Mormons. Cancers of the stomach, colon-rectum, and pancreas were about one-third lower in Mormons than in others who are not members of this religious group. Most of the differences seen in cancer incidence can be explained by Mormon teachings regarding sexual activity and alcohol and tobacco use, but some differences (e.g., colon and stomach) remain unexplained.

Cancer risk factors: an analysis of Utah Mormons and non-Mormons.

In a comparison of Mormons and non-Mormons in Utah, more Mormon men and women married spouses of the same faith, were religiously active, were of Northern Europe ancestry, lived in rural areas, had fewer exposures to occupational hazards, were less likely to smoke cigarettes or drink coffee, tea, and alcohol, used fats in cooking, and were more often married that was the cohort of other religions. No differences existed in occupation, but Mormon men had completed more years of schooling. Mormon women were less likely to be college graduates, had fewer sexual partners, had more pregnancies, were older at first pregnancy, were less likely to use birth control pills, had fewer miscarriages and hysterectomies, examined their breasts more often, and had more breast X-rays. For women, there was only a small difference by religion for age at first intercourse and no difference for age at which they began using birth control pills. Religious activity was examined for Mormons, and in most instances inactive Mormons were more like the non-Mormon population in respect to the variables measured.

Cancer in Utah: risk by religion and place of residence.

We compared cancer incidence during 1967--75 between Mormons and non-Mormons living in urban and rural areas of Utah. The non-Mormon urban men had a 34% higher risk of cancer compared with their rural counterparts. Most of this increase in risk occurred in sites associated with tobacco and for cancers of the stomach, colon, and prostate gland. Urban Mormon males had no significant increase in risk. The urban female population was at higher risk than was the rural regardless of religion. The increase was not as striking as that observed in non-Mormon men (8 vs. 34%); cancers of the respiratory and gastrointestinal tracts and female genitalia contributed to the elevated risk. We concluded that personal habits such as smoking and drinking and reproductive factors were possible explanations for the previously observed urban-rural gradients in cancer risk.

Coffee drinking and risk of bladder cancer.

The relationship between coffee drinking and risk of bladder cancer was assessed with the use of data from a case-control study of bladder cancer. Incident cases (2,982) and general population controls (5,782) were interviewed. Overall, the relative risk (RR) of bladder cancer for subjects who had ever drunk coffee was estimated as 1.4 (95% confidence interval = 1.1-1.8). There was no consistent relation between the RR estimate and the current consumption level. Among men who drank coffee, those who drank more than 49 cupfuls of coffee per week had an apparent excess in risk, but women who drank that much had an apparent deficit in risk.

Energy intake: its relationship to colon cancer risk.

A case-control study was conducted to assess the role of diet in the etiology of colon cancer. Diet was measured by means of a comprehensive quantifiable food frequency history instrument in 246 cases and 484 controls drawn from the general population of Utah. Each subject's diet was described by major nutrient groups and total energy based on the nutritional content of foods reported. Cases reported higher daily food intake 5 years preceding diagnosis than controls [men, rate ratio (RR) = 2.5; women, RR = 3.6], as measured by total energy content of the diet. Higher risk of colon cancer with increasing energy intake was independent of stage of disease at diagnosis and obesity, as measured by body mass. Fat, protein, and carbohydrate intake all had elevated RRs but could not be assessed as risk factors independent of energy intake because of their strong correlations with total calories. Due to the higher energy intake of the cases, odds ratios for the daily intake of dietary fiber and vitamins A and C were also greater than 1. However, adjusting for caloric intake removed this effect, and dietary fiber showed a weak protective effect. Total energy intake must be evaluated before attempting to assign a causal role to any food or nutrient that may be postulated to play a role in colon cancer.

Relative weight, weight change, height, and breast cancer risk in Asian-American women.

BACKGROUND: Breast cancer incidence rates have historically been four to seven times higher in the United States than in China or Japan, although the reasons remain elusive. When Chinese, Japanese, or Filipino women migrate to the United States, their breast cancer risk rises over several generations and reaches that for white women in the United States, indicating that modifiable exposures are involved. In a previous report on this case-control study of breast cancer in Asian-American women, designed to take advantage of their diversity in risk and lifestyle, we demonstrated a sixfold gradient in risk by migration history, comparable to the international differences in breast cancer incidence rates. PURPOSE: In this analysis, we have examined the roles of adult height, adiposity, and weight change in breast cancer etiology. METHODS: A population-based, case-control study of breast cancer was conducted among women of Chinese, Japanese, and Filipino ethnicities, aged 20-55 years, living in San Francisco-Oakland (CA), Los Angeles (CA), and Oahu (HI) during the period from April 1, 1983, through June 30, 1987. We successfully interviewed 597 (70%) of 852 eligible case subjects and 966 (75%) of 1287 eligible control subjects from August 1985 through February 1989. Subjects were asked about current height, usual adult weight, and usual weight in each decade of life, excluding the most recent 3 years and any periods of pregnancy. RESULTS: Height, recent adiposity (weight in the current decade of life/height 1.5), and recent weight change (between the current and preceding decades of life) were strong predictors of breast cancer risk after adjustment was made for accepted breast cancer risk factors. Risk doubled (relative risk [RR] = 2.01; 95% confidence interval [CI] = 1.16-3.49) over the 7-inch (17.8-cm) range in height (two-sided P for trend = .003), with comparable effects in both premenopausal and postmenopausal women. Except for reduced risk in the heavy, younger women (weight/height 1.5 > 29 kg/m 1.5 and < 40 years old), risk was positively associated with usual adult adiposity. Trends in risk became more striking as adiposity in each succeeding decade of adult life was considered. Women in their 50s and in the top quintile for their age group had twice the breast cancer risk (RR = 2.13; 95% CI = 1.17-3.87) of women in the bottom quintile (two-sided P for trend = .004). Women in their 50s, above the median adiposity for their age group, and with a recent gain of more than 10 pounds had three times the risk (RR = 3.01; 95% CI = 1.45-6.25) of women below the median adiposity and with no recent weight change. Recent weight loss was consistently associated with reduced risk (RRs of approximately 0.7) relative to no recent weight change. CONCLUSIONS: Adult adiposity, weight change, and height are critical determinants of breast cancer risk. Increased adiposity and weight gain in the decade preceding diagnosis are especially influential, suggesting that excess weight may function as a late stage promoter. IMPLICATIONS: Weight maintenance and/or reduction as an adult, possibly accompanied by specific changes in diet and physical activity, may have a significant and rapid impact on breast cancer risk.

Migration patterns and breast cancer risk in Asian-American women.

BACKGROUND: Breast cancer incidence rates have historically been 4-7 times higher in the United States than in China or Japan, although the reasons remain elusive. When Chinese, Japanese, or Filipino women migrate to the United States, breast cancer risk rises over several generations and approaches that among U.S. Whites. PURPOSE: Our objective was to quantify breast cancer risks associated with the various migration patterns of Asian-American women. METHODS: A population-based, case-control study of breast cancer among women of Chinese, Japanese, and Filipino ethnicities, aged 20-55 years, was conducted during 1983-1987 in San Francisco-Oakland, California, Los Angeles, California, and Oahu, Hawaii. We successfully interviewed 597 case subjects (70% of those eligible) and 966 control subjects (75%). RESULTS: A sixfold gradient in breast cancer risk by migration patterns was observed. Asian-American women born in the West had a breast cancer risk 60% higher than Asian-American women born in the East. Among those born in the West, risk was determined by whether their grandparents, especially grandmothers, were born in the East or the West. Asian-American women with three or four grandparents born in the West had a risk 50% higher than those with all grandparents born in the East. Among the Asian-American women born in the East, breast cancer risk was determined by whether their communities prior to migration were rural or urban and by the number of years subsequently lived in the West. Migrants from urban areas had a risk 30% higher than migrants from rural areas. Migrants who had lived in the West for a decade or longer had a risk 80% higher than more recent migrants. Risk was unrelated to age at migration for women migrating at ages less than 36 years. Ethnic-specific incidence rates of breast cancer in the migrating generation were clearly elevated above those in the countries of origin, while rates in Asian-Americans born in the West approximated the U.S. White rate. CONCLUSIONS: Exposure to Western lifestyles had a substantial impact on breast cancer risk in Asian migrants to the United States during their lifetime. There was no direct evidence of an especially susceptible period, during either menarche or early reproductive life. IMPLICATIONS: Because heterogeneity in breast cancer risk in these ethnic populations is similar to that in international comparisons and because analytic epidemiologic studies offer the opportunity to disentangle correlated exposures, this study should provide new insights into the etiology of breast cancer.

Vasectomy and prostate cancer: results from a multiethnic case-control study.

BACKGROUND: Vasectomy, a widely used form of contraception, has been associated in some studies with increased prostate cancer risk. PURPOSE: We assessed this association on the basis of data collected in a large multiethnic case-control study of prostate cancer that was conducted in the United States (Los Angeles, San Francisco, and Hawaii) and Canada (Toronto and Vancouver). METHODS: In home interviews conducted with newly diagnosed prostate cancer case patients and population control subjects, we obtained information on the participants' medical history, including a history of vasectomy and the age at which the procedure was performed, as well as other potential risk factors. Blood samples were collected from control subjects only and were assayed for concentration of sex hormones and sex hormone-binding globulin. RESULTS: The present analysis was based on 1642 prostate cancer patients and 1636 control subjects. A history of vasectomy was not significantly associated with prostate cancer risk among all racial/ethnic groups combined (odds ratio [OR] = 1.1; 95% confidence interval [CI] = 0.83-1.3), whites (OR = 0.94; 95% CI = 0.69-1.3), blacks (OR = 1.0; 95% CI = 0.59-1.8), or Chinese-Americans (OR = 0.96; 95% CI = 0.42-2.2). Among Japanese-Americans, the OR was 1.8 (95% CI = 0.97-3.4), but the statistically nonsignificant elevation in risk was limited to more educated men and those with localized cancers. ORs did not vary significantly by age at vasectomy or years since vasectomy. We found a lower serum concentration of sex hormone-binding globulin and a higher ratio of dihydrotestosterone to testosterone among vasectomized control subjects than among nonvasectomized control subjects. CONCLUSIONS: The findings of this study do not support previous reports of increased prostate cancer risk associated with vasectomy. However, the altered endocrine profiles of vasectomized control subjects seen in this cross-sectional comparison warrant further evaluation in longitudinal studies.

PIP: Vasectomy has been associated in some studies with increased prostate cancer risk. This association was assessed on the basis of data collected in a large multiethnic case control study of prostate cancer that was conducted in the United States (Los Angeles, San Francisco, and Hawaii) and Canada (Toronto and Vancouver). In home interviews conducted with newly diagnosed prostate cancer case patients (diagnosed between January 1, 1989 and December 31, 1991 as well as January 1, 1987 and December 31, 1988) and control subjects, information was obtained on the participants' medical history, including a history of vasectomy and the age at which the procedure was performed as well as other potential risk factors. Blood samples were collected from control subjects only and were assayed for concentration of total testosterone, percent of free testosterone, percent of bioavailable testosterone, dihydrotestosterone (DHT), and sex hormone-binding globulin (SHBG) using an automated, polyclonal-monoclonal immunochemiluminometric prostate-specific antigen (PSA) assay. The analysis was based on 1642 prostate cancer patients and 1636 control subjects. The analysis of PSA, androgens, and SHBG by vasectomy status was based on 850 control subjects with normal PSA concentrations. A history of vasectomy was not significantly associated with prostate cancer risk among all racial/ethnic groups combined (odds ratio [OR] = 1.1; Whites OR = 0.94; Blacks OR = 1.0; or Chinese-Americans OR = 0.96). Among Japanese-Americans, the OR was 1.8, but the statistically significant elevation in risk (OR = 4.1) was limited to more educated men with a history of vasectomy and those with localized cancers (OR = 5.3). ORs did not vary significantly by age at vasectomy or years since vasectomy. Lower serum concentration of SHBG and a higher ratio of DHT to testosterone was found among vasectomized control subjects than among nonvasectomized control subjects. The findings do not support previous reports of increased prostate cancer risk associated with vasectomy. However, the altered endocrine profiles of vasectomized control subjects warrant further evaluation in longitudinal studies.

Prostate cancer in relation to diet, physical activity, and body size in blacks, whites, and Asians in the United States and Canada.

BACKGROUND: International and interethnic differences in prostate cancer incidence suggest an environmental, potentially modifiable etiology for the disease. PURPOSE: We conducted a population-based case-control study of prostate cancer among blacks (very high risk), whites (high risk), and Asian-Americans (low risk) in Los Angeles, San Francisco, Hawaii, Vancouver, and Toronto. Our aim was to evaluate the roles of diet, physical activity patterns, body size, and migration characteristics on risk in these ethnic groups and to assess how much of the interethnic differences in risk might be attributed to interethnic differences in such lifestyle characteristics. METHODS: We used a common protocol and questionnaire to administer personal interviews to 1655 black, white, Chinese-American, and Japanese-American case patients diagnosed during 1987-1991 with histologically confirmed prostate carcinoma and to 1645 population-based control subjects matched to case patients by age, ethnicity, and region of residence. Sera collected from 1127 control subjects were analyzed for levels of prostate-specific antigen (PSA) to permit comparison of case patients with control subjects lacking serological evidence of prostate disease. Odds ratios were estimated using conditional logistic regression. We estimated the proportion of prostate cancer attributable to certain risk factors and the proportion of interethnic risk differences attributable to interethnic differences in risk-factor prevalence. RESULTS: A positive statistically significant association of prostate cancer risk and total fat intake was found for all ethnic groups combined. This association was attributable to energy from saturated fats; after adjusting for saturated fat, risk was associated only weakly with monounsaturated fat and was unrelated to protein, carbohydrate, polyunsaturated fat, and total food energy. Saturated fat intake was associated with higher risks for Asian-Americans than for blacks and whites. In all ethnic groups combined, the risk tended to be higher when only case patients with advanced disease were compared with control subjects with normal PSA levels. Among foreign-born Asian-Americans, risk increased independently with years of residence in North America and with saturated fat intake. Crude estimates suggest that differences in saturated fat intake account for about 10% of black-white differences and about 15% of white-Asian-American differences in prostate cancer incidence. Risk was not consistently associated with intake of any micronutrients, body mass, or physical activity patterns. CONCLUSIONS: These data support a causal role in prostate cancer for saturated fat intake but suggest that other factors are largely responsible for interethnic differences in risk.

Methodological issues in epidemiological studies of diet and cancer.

We review the goals of epidemiological nutritional studies and evaluate methods of dietary data collection in terms of these goals. Special problems for the cancer epidemiologist studying diet are then reviewed, including methods of data collection, quantification of food intake, and analysis of nutritional data. Food frequency methods are generally best for collection of dietary data in epidemiological studies, and the use of food data banks enables the study of specific dietary components. The major problems in analysis stem from the complex interrelationships among nutrients and their high correlation with each other.

Use of hair dyes and risk of bladder cancer.

The relation between use of hair dyes and risk of bladder cancer was assessed using data from a case-control study of bladder cancer. Incident cases (2982) and general population controls (5782) were interviewed. The overall estimate of relative risk of bladder cancer for users of hair dyes was 1.0 (95%) confidence interval, 0.9 to 1.2) compared to nonusers. No consistent pattern of association was detected between bladder cancer risk and various indices of timing or intensity of exposure to hair dyes. Various explanations of the lack of association are discussed.

Energy-dependent calcium sequestration activity in a Golgi apparatus fraction derived from lactating rat mammary glands.

A fraction isolated from lactating rat mammary glands was shown by marker enzyme assays to be rich in Golgi apparatus vesicles. This Golgi apparatus-rich fraction was shown to accumulate calcium in the presence of ATP but not in its absence. Other nucleoside triphosphates were only partially effective in promoting calcium transport. Mg2+ was required for the uptake which was also temperature and pH dependent. The uptake was sustained by the use of oxalate and phosphate as intravesicular trapping agents. In the presence of 10 mM oxalate the apparent Km for calcium uptake was 0.24 muM ionized calcium. The V was 4.45 nmol calcium/min per mg protein. Preloaded calcium could be rapidly released by the addition of the ionophore A23187 indicating an intravesicular location for the sequestered ion. Addition of ethylene glycol bis(beta-aminoethylether)-N,N'-tetraacetic acid resulted in a slower release of preaccumulated calcium, indicating the existence of one or more efflux routes by which calcium leaves the vesicles in the presence of MgATP. Ruthenium red partially inhibited the uptake but lanthanum and particularly the sulphydryl inhibitor p-hydroxy-mercuribenzoate were much more effective. The properties of the calcium-sequestering system in the Golgi apparatus-rich fraction were similar to those reported for other non-muscular tissues and lend support to the hypothesis that calcium is secreted into milk via the Golgi apparatus of the mammary gland secretory gland.

The effects of probucol and clofibrate alone and in combination on hepatic cholesterol metabolism in the male rat.

Male rats were fed for 10 days on a diet supplemented with either probucol or clofibrate, alone or in combination, and the effects of the drugs on hepatic cholesterol metabolism studied. Plasma triacylglycerols were significantly lowered (15.6%, P < 0.05) by the drugs in combination but not individually whereas plasma cholesterol levels were reduced by probucol alone (22.4%, P < 0.05) and the combined treatment effected a further decrease leading to a total reduction of 50.6% (P < 0.001). Probucol reduced hepatic cellular triacylglycerols (20.0%, P < 0.05) and cholesterol (15.3%, P < 0.05) but cholesteryl esters were unaffected. In combination with clofibrate, probucol accentuated the reductions in both cellular cholesterol and cholesteryl esters produced by clofibrate alone and lowered their levels by 22.8%, P < 0.01 and 38.5%, P < 0.001, respectively. Although probucol, on its own, did not affect the activity of acyl-coenzyme A:cholesterol acyltransferase (ACAT), its combination with clofibrate caused less inhibition (43.5%, P < 0.01) of this enzyme activity than clofibrate alone (65.7%, P < 0.001). Probucol had a similarly moderating effect on the clofibrate-induced reductions in microsomal cholesterol and cholesteryl esters. Neither the microsomal nor the cytosolic neutral cholesteryl ester hydrolase was affected by probucol alone although both enzymes were dramatically increased (between 350% and 550%) by clofibrate and the combined treatment. The activity of the hepatic cytosolic inhibitor of cholesteryl ester hydrolase was unaffected by clofibrate or probucol individually but the two drugs in combination increased the total activity of the inhibitor by 52.1%, P < 0.01. When allowance was made for this increased inhibitor activity, it was clear that probucol accentuated the stimulatory effect of clofibrate on the cytosolic nCEH.

Transient formation of the phosphoprotein during autophosphorylation of rat mammary gland Golgi vesicles.

Incubation with [gamma-32P] ATP of Golgi vesicles, prepared from the mammary tissue of lactating rats, resulted in the phosphorylation of four of the proteins in the preparation which were resolvable by sodium dodecyl sulphate (SDS)-polyacrylamide gel electrophoresis. Three of these had electrophoretic properties identical to the three major caseins of rat milk: their phosphorylation was approximately linear with respect to time during the course of the short (1 min) incubations analyzed. The fourth component (Mr,app. 70,000) behaved differently. It was very rapidly phosphorylated to a maximum level within 5 S at 0 degree C; its 32 P-content declined thereafter, with a t 1/2 for dephosphorylation of approx. 20 s. The extent of 32P incorporation into this component, measured after incubation for 20 s at 0 degree C with [gamma-32P] ATP, was sensitive to the concentration of Ca2+ in the incubation medium, being enhanced at low concentrations (less than 10-8 M) of Ca2+ and depressed at high (10-4 M) ones. Inclusion of ADP (100 microM) in such incubation also depressed 32P incorporation into the 70 kDa component. This phosphoprotein was further distinguished from the other three by virtue of the lability of its incorporated phosphorus to treatment with hot trichloroacetic acid. The properties and possible function of this phosphoprotein are discussed in relation to the ATP-dependent Ca2+ transport that occurs in this Golgi vesicle preparation.

A study of the enzymic dephosphorylation of beta-casein and a derived phosphopeptide.

beta-Casein, and the phosphate containing peptide derived from it by tryptic digestion, have been dephosphorylated by the action of two phosphatases. Escherichia coli alkaline phosphatase (EC 3.1.3.1) has been shown to remove the phosphates from these substrates in two distinct stages. Substrate molecules retaining three of the original phosphoseryl residues accumulate during the reaction and are resistant to further dephosphorylation at low enzyme concentrations. In contrast bovine spleen phosphoprotein phosphatase (EC 3.1.3.16) achieves complete dephosphorylation of these substrates sequentially without any of the intervening species showing resistance to the action of the enzyme. The phosphopeptide has been partially dephosphorylated by the action of the two phosphatases and the resultant peptides containing three phosphoseryl residues compared in their reactivity toward the E. coli alkaline phosphatase. The results obtained are discussed in relation to the mode of action of the two enzymes.

A kinetic analysis of the dephosphorylation, by bovine spleen phosphoprotein phosphatase (EC 3.1.3.16) of a phosphopeptide derived from beta-casein.

A peptide containing the four closely grouped phosphoseryl residues present in beta-casein has been enzymatically dephosphorylated with bovine spleen phosphoprotein phosphatase (EC 3.1.3.16). The course of the dephosphorylation reaction has been followed by cellulose acetate electrophoresis and the amount of partially phosphorylated peptides present at each stage quantified by the same method. The phosphate groups are shown to be removed in a sequential manner and the rate constants for each stage of the dephosphorylation have been computed from the data obtained. The rate constants indicate that interaction in the intact peptide results in an enhancement of the activity of the phosphoseryl cluster.

The esterification of cholesterol in the liver of the chick embryo.

The development of the chick embryo was characterised by the accumulation of large droplets of lipid in the cytoplasm of the embryonic liver, as revealed by electron microscopy. Analysis of the lipid composition of the livers indicated that this accumulation resulted from a dramatic increase in the cholesteryl ester content of the tissue during the the latter part of the embryonic period. This lipid is apparently derived from yolk cholesterol and may be taken up by the liver in the form of lipoprotein remnants. Significant levels of acyl-CoA: cholesterol acyltransferase (ACAT) activity were expressed in the liver throughout the second half of the developmental period, and this activity was maximal at the time when lipid transfer from the yolk was most intensive. The activity of microsomal cholesterol ester hydrolase (CEH) was very low throughout development, and no CEH activity was detected in the cytosolic fraction. In addition, substantial amounts of a cytosolic protein which inhibits CEH activity were present. Thus the relative activities of these enzymic systems are consistent with the net accumulation of cholesteryl ester which occurs in the liver during development.

Cholesterol ester hydrolysis and hormone-sensitive lipase in lactating rat mammary tissue.

Neutral cholesterol esterase activity is expressed in extracts of mammary epithelial cells. The identity of the enzyme catalyzing this hydrolysis was investigated. Anti-hormone-sensitive lipase immunoglobulin elicited the total inhibition of this activity and also immunoprecipitated a single phosphoprotein of Mr 84 kDa from mammary cell extracts previously phosphorylated in vitro with [gamma-32P]ATP and cyclic AMP-dependent protein kinase. It is concluded that mammary cell cholesterol esterase activity results from the presence of hormone-sensitive lipase.