Breast Cancer Risk Factors in Italian Women: A Multicentric Case-Control Study

Toti, A; Agugiaro, S; Amadori, Dino; Buzzi, G; Bruzzi, Paolo; Buiatti, Eva; Capelli, Maria Carla; Ciatto, Stefano; Delfino, Enrica; Foti, E

doi:10.1177/030089168607200304

Cited by 30 publications

(8 citation statements)

References 18 publications

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“…No significant associations were revealed between body mass index and breast cancer for pre-and postmenopausal women. This is of particular interest since several case-controls studies have demonstrated positive associations between BMI and breast cancer among postmenopausal women (2,4,7,8,15,17,18,(20)(21)(22)25,29) and inverse associations among premenopausal women (7,17,20). However, the reports from previous findings have not included African-Americans.…”

Section: Discussionmentioning

confidence: 99%

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The Relationship of Body Mass Index to Reproductive Factors in Pre‐ and Postmenopausal African‐American Women With and Without Breast Cancer

et al. 1996

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The relationship of body mass index to reproductive factors in pre-and postmenopausal AfricanAmerican women with and without breast cancer. Obes Res. 1996;4:451-456. To date, there are virtually no existing data on the relationship between obesity, menopausal status, and breast cancer in African-Americans. Therefore, the present study was designed to test the following hypotheses in an African-American population: (1) there exists a positive association between BMI and breast cancer among postmenopausal women; (2) there exists an inverse association between BMI and breast cancer among premenopausal women; and (3) similar associations between BMI and reproductive factors exist for both pre-and postmenopausal breast cancer cases. The study population comprised 357 African-American women (n=193 breast cancer cases; n=164 controls). No significant differences were observed between premenopausal cases and controls for BMI, obesity categories, and reproductive factors. Among the postmenopausal women, the cases had significantly lower weight and BMI levels than the controls. Age at first pregnancy and parity were significantly lower among postmenopausal cases than their controls. No significant associations were revealed between body mass index and breast cancer for pre-and postmenopausal women. In the present study, early age at menarche was the only reproductive factor that was an independent predictor of BMI for both pre-and postmenopausal women, irrespective of breast cancer status. Also, these fiidings strongly suggest the need to consider reproductive factors, particularly age at menarche, as a covariate of BMI and other obesityrelated diseases. ADAMS-CAMPBELL, LUCILE L, KYUNG SOOK

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Section: Discussionmentioning

confidence: 99%

“…The findings to date suggest that an interaction exists between BMI and menopausal status in relationship to breast cancer. Case-control studies have demonstrated relatively consistent positive findings between BMI and increased breast cancer risk for postmenopausal women (2,4,7,8,15,17,18,(20)(21)(22)25,29).…”

Section: Introductionmentioning

confidence: 96%

The Relationship of Body Mass Index to Reproductive Factors in Pre‐ and Postmenopausal African‐American Women With and Without Breast Cancer

et al. 1996

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“…In particular, the risk of developing the disease increases with higher calculated body mass index (BMI = body weight (kg) 7 height (m 2 )) [1][2][3][4][5][6][7]. Weight gain per se and body fat have also been implicated to play a role in breast cancer development [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Mammary tumor development from T47-D human breast cancer cells in obese ovariectomized mice with and without estradiol supplements

Nkhata

Ray

Doğan

et al. 2008

Breast Cancer Res Treat

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Obesity is a risk factor for postmenopausal breast cancer, particularly for development of estrogen-receptor (ER)-positive tumors. Additionally, obesity is implicated in breast cancer progression. However, few studies address mechanisms of action of how obesity mediates these responses. Our goal was to address how obesity and/or elevated serum leptin affects tumor formation from ER-positive T47-D cells. In Study 1 ovariectomized CD-1 nude female mice were injected with goldthioglucose (GTG) at 0.5 mg/g body weight in saline or the vehicle at 6 weeks of age. At 10 weeks of age mice were inoculated with T47-D cells and implanted with estrogen pellets. In Study 2 mice were injected with 0.3 mg/g GTG or the vehicle. At 10 weeks of age cells were inoculated and mice were implanted with estrogen or placebo pellets. Mice were followed until 30 weeks of age. Some GTG mice became obese and others were non-responders. In Study 1 no mice developed tumors. In Study 2 mice with placebo pellets developed more tumors than mice with estrogen pellets, 50% vs. 13%. GTG-obese mice with placebo pellets had a 100% tumor incidence compared to 50% and 20% for GTG-lean and controls without estrogen. Serum leptin was higher in obese compared to lean mice and adiponectin was not affected by body weight. Adiponectin:leptin ratio was significantly reduced in obese compared to lean mice. Leptin, leptin receptor and signaling protein expression were determined in mammary and tumor tissue. Leptin and STAT3 were most abundant in tumors. These findings suggest that in vivo estrogen suppressed proliferation of T47-D cells but without supplemental estrogen obesity enhanced tumor development. The exact reason for this is not presently clear.

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“…However, only 14 of 2 reliability studies4, 5 showed an important difference in reporting errors between cases and controls. Furthermore, the distribution of estimates of effect abstracted from such case‐control studies6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32 does not differ substantially from the distribution of estimates of effect abstracted from studies that assessed termination status by prospective self‐report or by retrospective record‐based report in which the record of termination status predated diagnosis33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45 (Fig. 1).…”

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confidence: 99%

Null association between pregnancy termination and breast cancer in a registry‐based study of parous women

Lash

Fink

2004

Intl Journal of Cancer

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Studies suggesting a positive association between pregnancy termination and breast cancer risk have often been of retrospective case-control design, so subject to selection and recall biases. We undertook a registry-based analysis with minimal selection bias and prospective record-based ascertainment of terminations. The source population comprised Massachusetts women with a record of giving birth between 1987 and 1999 in the Massachusetts Vital Statistics Registry. Primary breast cancer cases were 25-55 years old at diagnosis between 1988 and 2000 and had a record of the diagnosis in the Massachusetts Cancer Registry. We matched 3 controls to each case on maternal age, year of giving birth and birth facility. Information on terminations (induced and spontaneous) before the birth of record, the matched factors and potential confounders were collected from the birth certificate. After adjustment for the matched factors, age, parity and maternal and paternal education, the odds ratio associating any termination history with breast cancer risk equaled 0.91 (95% CI ‫؍‬ 0.79 -1.05). The marginally protective adjusted odds ratio largely derived from a protective effect among women with parity equaled to 1 (OR for any termination ‫؍‬ 0.68; 95% CI ‫؍‬ 0.45-1.03), suggesting a protective effect of terminated pregnancy among women with one live birth. © 2004 Wiley-Liss, Inc. Key words: breast neoplasm etiology; spontaneous abortion; induced abortionThe effect of pregnancy termination on subsequent breast cancer risk has been the subject of a substantial number of epidemiologic investigations. Some have argued that retrospective case-control studies with termination status assessed by self-report are more likely to yield nonnull estimates of effect because of the potential for selection bias and recall bias. 1-3 However, only 1 4 of 2 reliability studies 4,5 showed an important difference in reporting errors between cases and controls. Furthermore, the distribution of estimates of effect abstracted from such case-control studies 6 -32 does not differ substantially from the distribution of estimates of effect abstracted from studies that assessed termination status by prospective self-report or by retrospective record-based report in which the record of termination status predated diagnosis [33][34][35][36][37][38][39][40][41][42][43][44][45] (Fig. 1). Both distributions are centered on the null and have, on average, the more precisely measured estimates of effect nearest the null. Thus, studies of both designs yield null estimates of effect, on average, with mostly imprecise estimates of effect yielding nonnull results. Given the larger number of retrospective case-control studies (27) than studies of the other 2 designs (13), it is to be expected that more studies by the former design, particularly studies with imprecise estimates of effect, have been reported with nonnull results.Others have argued that the effect of spontaneous abortion on breast cancer risk is different from the effect of induced abortion, either for...

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Breast Cancer Risk Factors in Italian Women: A Multicentric Case-Control Study

Cited by 30 publications

References 18 publications

The Relationship of Body Mass Index to Reproductive Factors in Pre‐ and Postmenopausal African‐American Women With and Without Breast Cancer

The Relationship of Body Mass Index to Reproductive Factors in Pre‐ and Postmenopausal African‐American Women With and Without Breast Cancer

Mammary tumor development from T47-D human breast cancer cells in obese ovariectomized mice with and without estradiol supplements

Null association between pregnancy termination and breast cancer in a registry‐based study of parous women

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