Postmenopausal women who develop endometrial cancer are on the whole heavier than women who do not develop the disease. One possi- ble explanation is that heavy women are more exposed to endogenous estrogens which are produced in postmenopausal women by conversion of steroid precursors to active estrogens in peripheral fat. In the face of varying levels of endogenous estrogen production, one might ask whether the carcinogenic potential of exogenous estrogens would be the same in all women. A case-control study has been conducted to examine the relation among weight, replacement estrogen therapy, and endometrial cancer. The results are shown in Table E1.23.
Estrogen Replacement
|
Weight (kg)
|
Yes
|
No
|
|
57
|
|
|
|
Cases
|
20
|
12
|
|
Controls
|
61
|
183
|
|
57-75
|
|
|
|
Cases
|
37
|
45
|
|
Controls
|
113
|
378
|
|
>75
|
|
|
|
Cases
|
9
|
42
|
|
Controls
|
23
|
140
|
(a) Calculate separately for the three weight groups the odds ratio associated with estrogen replacement.
(b) Compare the three odds ratios in part (a). When the difference is confirmed properly, we have an effect modification.
(c) Assuming that the odds ratios for the three weight groups are equal (in other words, weight is not an effect modifier), calculate the Mantel-Haenszel estimate of this common odds ratio.