Incidence rates for pancreatic cancer are consistently lower in women than in men. Previous studies suggested that reproductive factors, particularly parity, may reduce   pancreatic   cancer   risk   in   women.  During   a   study   on   115,474 women (follow-up:  22 years),  243 cases of pancreatic cancer were identified.

Compared with nulliparous women, the relative risk of pancreatic cancer was 0.86 for women with 1-2 births, 0.75 for 3-4 births, and 0.58 for those with 5 or more births, after adjusting for other factors.  The analysis for linear trend indicated a 10%  reduction in risk for each birth.

Other reproductive factors and exogenous hormone use were not significantly,  related to pancreatic cancer risk ⁽¹²¹⁾.

Compared with women who were premenopausal at baseline,  postmenopausal women were at significantly increased risk of pancreatic cancer (odds ratio = 2.44). Age at first live birth, parity, age at menarche, use of oral contraceptive, and use of hormone replacement therapy (HRT)  were not associated with altered pancreatic cancer risk in studies population. 

However,  among parous women, later age at first full-term pregnancy ,significantly increases the risk of this cancer (adjusted OR =  4.05).

Other than the increased risk among postmenopausal women,  this cohort study provides little support for associations with hormonal factors.  Additional   prospective   data   are   needed. 

However,  growing epidemiological evidence that aspects of reproductive history and hormonal exposure are associated with risk of this disease could induce to support the hypothesis that pancreatic cancer is, at least in part, an estrogen-dependent disease ⁽¹²²⁾.  Prolonged lactation and increased parity seem associated with a reduced risk for pancreatic cancer ⁽¹²³⁾.

In a parallel fashion, risk of pancreatic cancer was decreased   for   women   with   intact   ovaries   compared   to   those   who   had oophorectomy:  hazard ratio was 0.70. These results indicate that older age at menopause are associated with reduced pancreatic cancer risk,  but further research is warranted. ⁽¹²⁴⁾. 

It was observed no association between any other reproductive factors examined (age at first birth, menarche, or menopause; type of menopause;  diethylstilbestrol (DES)  use;  or duration of oral contraceptive or estrogen replacement therapy use)  and pancreatic cancer mortality ⁽¹²⁵⁾.  In summary, literature data support the observation that high parity is associated with lower risk of pancreatic cancer but do not show a linear trend with increasing parity. 

Furthermore,  we find no evidence that other reproductive factors are associated with pancreatic cancer mortality. ⁽¹²⁶⁾.  It is of interest to report that clinically attainable concentrations of Medroxyprogesterone acetate   ^(MPA)  can inhibit the growth of some human pancreatic carcinoma cells,  in vitro,  by inducing   apoptosis,  probably   through   their   PR,  in   association   with   the phosphorylation of bcl-2 ⁽¹²⁷⁾.
—
Rosa Sabatini and Giuseppe Loverro
Dept. Obstetrics and Gynecology,
General Hospital Policlinico-University of Bari, Italy
—

REFERENCES

1.   La Vecchiam, C., Negri, E., Franceschi, S., Parazzini, F. (1993). Long-term impact of reproductive factors on cancer risk. Int J Cancer, Jan 21, 53(2), 215-9.
2.   Medard,  M.L.,  Ostrowska, L.  (2007).Combined oral contraception and the risk of reproductive organs cancer in women .Ginekol Pol, Aug,78(8), 637-41. 
3.   Casey, P.M., Cerhan, J.R., Pruthi, S. (2008). Oral contraceptive use and risk of breast cancer. Mayo Clin Proc,Jan,83),86-90
4.   Deligeoroglou, E., Michailidis, E., Creatsas, G. (2003).Oral contraceptives and reproductive system cancer. Ann N Y Acad Sci,Nov,997,199-208.
5.   White,  E.,  Malone,  K.E.,  Weiss,  N.S.,  Daling,  J.R.  (1994). Breast cancer among young US women in relation to oral contraceptive use.  J.  Nati Cancer Inst, 86(7), 505-14
6.   Brohet,  R.M.,  Goldgar,  D.E.,  Easton,  D.F.,  Antoniou,  A.C.,  Andrieu,  N., Chang-Claude,  J.,  Peock,  S.,  Eeles,  R.A.,  Cook,  M.,  Chu,  C.,  Nogue`s,  C., Lasset,  C.,  Berthet,  P.,  Meijers-Heijboer,  H.,  Gerdes,  A.M.,  Olsson,  H., Caldes,  T.,  van Leeuwen,  F.E.,  Rookus,  M.A.  (2007). Oral contraceptives and breast cancer risk in the international BRCA1/2 carrier cohort study: a report   from   EMBRACE,  GENEPSO,  GEO-HEBON,  and   the   IBCCS Collaborating Group.J Clin Oncol, Sep 1,25(25), 3831-6.
7.   Haile,  R.W., Thoma,  D.C.,  McGuire,  V.,  Felberg,  A.,  John,  E.M.,  Milne, R.L., Hopper, J.L. et.al. (2006). BRCA1 and BRCA2 mutation carriers, oral contraceptives use,and breast cancer before age 50. Cancer Epidemiol.Biomarker Prev, 15(10), 1863-70.
8.   Daling, J.R., Brinton, L.A., Voigt, L.F., Weiss, N.S., Coates, R.J., Malone, K.E., Schoenberg, J.B., Gammon, M. (1996). Risk of breast cancer among white women following induced abortion. Am J Epidemiol, Aug 15,144(4), 373-80. 
9.   Daling, J.R., Malone, K.E., Voigt, L.F., White, E., Weiss, N.S. (1997). Risk of breast cancer among young women:  relationship Med to induced abortion. N Engl J, 336(2), 81-5
10.   Rookus,  M.A.,  van Leeuwen,  F.E.  (1996).Induced abortion and risk for breast cancer:  reporting (recall)  bias in a Dutch case-control study.  J Natl Cancer Inst, 88 (23),1759-64
11.   Van   Leeuwen,  F.E.  (1991). Epidemiologic   aspects   of   exogenous progestagens in relation to their role in pathogenesis of human breast cancer. Acta Endocrinol, 125(1), 13.

Full References

Provided by ArmMed Media