Cancer Causes & Control

, Volume 23, Issue 3, pp 473–485 | Cite as

Body size and the risk of postmenopausal breast cancer subtypes in the California Teachers Study cohort

  • Alison J. CancholaEmail author
  • Hoda Anton-Culver
  • Leslie Bernstein
  • Christina A. Clarke
  • Katherine Henderson
  • Huiyan Ma
  • Giske Ursin
  • Pamela L. Horn-Ross
Original paper



To evaluate how the association between body size and breast cancer risk varies by tumor receptor subtype, host factors, and other exposures among women in the California Teachers Study cohort.


Among 52,642 postmenopausal women, 2,321 developed invasive breast cancer with known estrogen- and progesterone-receptor status (1,652 ER+PR+, 338 ER+PR−, and 312 ER−PR−) between 1995 and 2007. In a subset of 35,529 with waist circumference data, 1,377 developed invasive breast cancer with known ERPR status (991 ER+PR+, 208 ER+PR−, 169 ER−PR−) between 1997 and 2007. Multivariate Cox regression was performed to estimate relative risks (RR) and 95% confidence intervals (CI).


Obesity, adult weight gain of ≥40 pounds, greater abdominal adiposity, and greater height increased the risk of ER+PR+ breast cancer. The increased risk associated with postmenopausal obesity was limited to those who did not use hormone therapy (HT) at cohort entry (RR = 1.37; 95% CI, 1.05–1.78 for BMI ≥ 30 vs. < 25 kg/m2; p-interaction = 0.14) and those who were not overweight or obese at age 18 (p-interaction = 0.06). The increased risk associated with greater abdominal adiposity was limited to those who were not also overweight or obese (p-interaction = 0.01). Neither obesity, abdominal adiposity, nor height was associated with the risk of ER−PR− tumors.


The effects of body size on postmenopausal breast cancer risk differed by hormone receptor subtype, and among women with ER+PR+ tumors, by HT use and early adult body size.


Breast cancer Obesity Hormone receptor status Abdominal adiposity Hormone therapy 



Body mass index


California Teachers Study


Combined estrogen plus progesterone therapy


Estrogen receptor


Estrogen-only therapy


Hormone therapy


Progesterone receptor



This research was supported by grant R01 CA77398 from the National Cancer Institute and contract 97-10500 from the California Breast Cancer Research Fund. The funding sources did not contribute to the design or conduct of the study, nor to the writing or submission of this manuscript. The collection of cancer incidence data used in this study was supported by the California Department of Health Services as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885; the National Cancer Institute’s Surveillance, Epidemiology and End Results Program under contract HHSN261201000036C awarded to the Cancer Prevention Institute of California, contract HHSN261201000035C awarded to the University of Southern California, and contract HHSN261201000034C awarded to the Public Health Institute; and the Centers for Disease Control and Prevention’s National Program of Cancer Registries, under agreement # 1U58 DP000807-01 awarded to the Public Health Institute. The ideas and opinions expressed herein are those of the authors, and endorsement by the State of California, Department of Health Services, the National Cancer Institute, and the Centers for Disease Control and Prevention or their contractors and subcontractors is not intended nor should be inferred. The authors would like to thank Jane Sullivan-Halley for substantial technical assistance with quality control work on the height and weight variables and the CTS Steering Committee who are responsible for the formation and maintenance of the cohort within which this study was conducted but who are not included as authors on the current paper: Ellen T. Chang, Dennis Deapen, James Lacey, Jr, David Nelson, Susan Neuhausen, Peggy Reynolds, Frederick Schumacher, Sophia Wang, and Argyrios Ziogas.

Conflict of interest

The authors declare that they have no conflict of interest.


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Copyright information

© Springer Science+Business Media B.V. 2012

Authors and Affiliations

  • Alison J. Canchola
    • 1
    Email author
  • Hoda Anton-Culver
    • 2
  • Leslie Bernstein
    • 3
  • Christina A. Clarke
    • 1
  • Katherine Henderson
    • 3
  • Huiyan Ma
    • 3
  • Giske Ursin
    • 4
    • 5
    • 6
  • Pamela L. Horn-Ross
    • 1
  1. 1.Cancer Prevention Institute of CaliforniaFremontUSA
  2. 2.Department of Epidemiology, School of MedicineUniversity of CaliforniaIrvineUSA
  3. 3.Division of Cancer Etiology, Department of Population SciencesBeckman Research Institute, City of HopeDuarteUSA
  4. 4.Department of Preventive Medicine, Keck School of MedicineUniversity of Southern CaliforniaLos AngelesUSA
  5. 5.Department of NutritionUniversity of OsloOsloNorway
  6. 6.Cancer Registry of NorwayOsloNorway

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