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Articles by J. A Bennett
Total Records ( 2 ) for J. A Bennett
  H. I Jacobson , N Lemanski , A Agarwal , A Narendran , K. E Turner , J. A Bennett and T. T. Andersen

Parity in women is associated with reduced lifetime risk of breast cancer, and hormones of pregnancy [estrogen (E), progesterone (P), human chorionic gonadotropin (hCG)] are implicated. Parity also reduces mammary cancer risk in carcinogen-exposed rats, and administering pregnancy hormones to these animals is similarly effective. Because pregnancy hormones are also able to stimulate cancer growth, we proposed to resolve this dichotomy by determining whether administered pregnancy hormones elicit the cancer-inhibiting agent -fetoprotein (AFP) from the liver, which would implicate AFP as a proximal effector of hormonal anticancer activity. Accordingly, we treated groups of nitrosomethylurea-exposed rats with saline, E3, E2 + P, E3 + P, hCG, or allowed them to experience pregnancy, and then monitored mammary cancer incidence and serum levels of AFP over time. Each hormone treatment reduced mammary cancer incidence and elevated serum AFP levels. To challenge human tissues, human HepG2 liver cells in culture were treated with the same hormonal agents. Each hormone regimen increased the levels of AFP in the culture medium. Medium containing AFP elicited by hCG inhibited the E2-stimulated proliferation of cultured human MCF7 breast cancer cells, whereas hCG alone did not inhibit their growth. Furthermore, antibodies to AFP neutralized the growth-inhibiting effect of AFP-containing HepG2 medium. We conclude that in the treatment of carcinogen-exposed rats with the hormones of pregnancy, and by inference in women who have experienced pregnancy, that AFP is a proximal agent that inhibits mammary gland cancer. Cancer Prev Res; 3(2); 212–20

  M Day , J Poole , J. A Bennett and M. D. Peake

A previous study showed that lung cancer incidence in Leicester's South Asian (SA) population had increased between 1990 and 1999. We expanded the original data set to determine if this increase had continued in recent years.


All patients diagnosed with lung cancer in Leicester between 1990 and 2005 were identified. Ethnicity was assigned using Nam Pechan software, deprivation by Townsend score. Using Poisson regression, incidence rate ratios (IRRs) were calculated to assess variations in incidence by ethnicity, deprivation and period of diagnosis.


Comparing patients diagnosed in 2000–2005 with those in 1990–1994, the risk of lung cancer increased in the SA men (IRR: 1.67 (95% CI: 0.99, 2.78)) whereas in the non-South Asian (NSA) men, it had fallen (IRR: 0.84 (95% CI: 0.76, 0.94)). Comparing patients diagnosed in 2000–2005 with those in 1995–1999 an increase continued in the SA men (IRR: 1.11 (95% CI: 0.71–1.74)). A significant rise was observed in the NSA women comparing those diagnosed from 2000–2005 to 1995–1999 (IRR: 1.16 (95% CI: 1.01, 1.33)).


Lung cancer is an important public health issue amongst SAs in Leicester and has increased significantly since the early 1990s, with rates sustained in the more recent years of 2000–2005. Changes in the rates of lung cancer in SA and NSA populations are likely to be due to changing smoking habits.

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