Risk factors for breast cancer by oestrogen receptor status: a population-based case-control study

Abstract

Summary Data from a population-based case-control study conducted (Stanford et al., 1986). Complete absence of overlap between risk factors for the two types of breast cancer would provide evidence against a progression from one to the other, while overlap would suggest either that there is a progression or that they are independent outcomes with overlapping aetiologies. The few case-control studies conducted to date (Hildreth et al., 1983;McTiernan et al., 1986;Hislop et al., 1986Hislop et al., , 1988Stanford et al., 1987) suggest that there is some overlap in risk factors for ER+ and ER-breast cancer. This possibility, and the others outlined above, are investigated further in the population-based case-control study reported here, in which risk of ER+ and ER -breast cancer is examined in association with menstrual and reproductive history, dietary intake and other factors. Materials and methods Study subjectsA detailed description of the study methods has been presented elsewhere (Rohan et al., 1988 of breast cancer, who were also resident in the Adelaide metropolitan area and who were registered on the electoral roll. (In South Australia, 97.2% of persons eligible to vote are registered (Australian Electoral Office, 1983).) For each case, one control, matched as closely as possible to the age of the case at diagnosis, was selected at random from the electoral roll. A total of 648 individuals were approached in order to enrol 451 controls. The total study population therefore comprised 451 case-control pairs. Reasons for nonparticipation were recorded during the recruitment of the first 100 controls, which required attempting to recruit 151 persons. Of the 51 who did not participate, 39 refused, 11 were untraceable and one had died.Data collection procedure Subjects were interviewed in their own homes by trained interviewers whose performance was monitored regularly. Interviewers were assigned randomly to case-control pairs. For cases, the average interval between diagnosis and interview was 4.8 months. Each control was interviewed as soon as possible after her case had been enrolled and in a few instances interview of the control preceded that of her case. Approximately 90% of controls were interviewed within two months of the corresponding case. Matching on date of interview was introduced in an attempt to minimise dietary differences between cases and controls due to seasonal influences.Socio-demographic and medical information was collected by use of an interviewer-administered questionnaire which sought basic biographic information, personal medical history, family history of cancer, gynaecological and reproductive history and history of hormone use.Information on usual dietary intake was collected from the study participants by means of a self-administered quantitative food frequency questionnaire. The questionnaire, which was designed to ascertain total daily intake of energy, several nutrients, alcohol and methylxanthines, has been described in detail elsewhere (Baghurst & Baghurst, 1981;Baghurst an...

Reproductive factors and subtypes of breast cancer defined by hormone receptor and histology

“…Consistent with our findings, three of these studies found evidence that late age at first birth was associated with receptor-positive tumours only (Potter et al, 1995;Huang et al, 2000;Cotterchio et al, 2003). Our results on breastfeeding are also consistent with the few previous studies that have addressed this (Hildreth et al, 1983;McTiernan et al, 1986;Cooper et al, 1989;Yoo et al, 1997;Huang et al, 2000;Britton et al, 2002;Cotterchio et al, 2003).…”

“…It has previously been proposed that hormonal breast cancer risk factors ought to be predominantly associated with tumours that express oestrogen (ER) and progesterone (PR) receptors, and less so with receptor-negative tumours (McTiernan et al, 1986;Stanford et al, 1987;Potter et al, 1995;Enger et al, 2000;Ursin et al, 2002). However, the studies that have addressed the effect of reproductive factors on breast tumours of different receptor status have yielded mixed results (Hildreth et al, 1983;McTiernan et al, 1986;Stanford et al, 1987;Cooper et al, 1989;Potter et al, 1995;Yoo et al, 1997;Huang et al, 2000;Britton et al, 2002;Cotterchio et al, 2003).…”

Smoking (active and passive) and breast cancer: Epidemiologic evidence up to June 2001

“…[Stanford et al, 1987] 0.9 (0.6-1. [Cooper et al, 1989] 1.6 e (1.0-2.7) 1.3 (0.7-2.5) 0.95 e (0.7-1.4) 1.3 (0.8-2.0) Manjer [Manjer et al, 2001] Some strong and biologically meaningful associations have been reported, but rarely reproduced, for NAT2 [Ambrosone et al, 1996;Hunter et al, 1997;Millikan et al, 1998a;Morabia et al, 2000b;Delfino et al, 2000;Chang-Claude et al, 2001], NAT1 [Millikan et al, 1998a;Zheng et al, 1999], Cyp1a1 [Ambrosone et al, 1995;Ishibe et al, 1998;Huang et al, 1999], COMT [Millikan et al, 1998b;Thompson et al, 1998;Yim et al, 2001], and BRCA1 and BRCA2 [Brunet et al, 1998;Couch et al, 2001]. With some exceptions, these studies belong to the first generation because they did not separate passive smokers from the nonexposed cohort.…”

Risk factors according to estrogen receptor status of breast cancer patients in Trivandrum, South India

“…Most of these studies were conducted in Western populations as early as 1980s. [1][2][3][4][5] Around the same time, it was also discovered that ER1 tumors that lacked progesterone receptor (PR) expression were less responsive to endocrine therapy compared to tumors that expressed PR. 8 This led to studies in the past decade that looked at the link of various risk factors of breast cancer and combined ER/PR information to better explain the underlying differences between the various subtypes of breast cancer.…”

“…[1][2][3][4][5][6][7] Numerous studies in the past have looked at differences in etiology and risk factors pertaining to presence or absence of ER-alpha. Most of these studies were conducted in Western populations as early as 1980s.…”