Steroid hormone receptors in normal and malignant human renal tissue: Relationship with progestin therapy

Ronchi, E.; Pizzocaro, Giorgio; Miodini, Patrizia; Piva, Luigi; Salvioni, Roberto; Fronzo, G. Di

doi:10.1016/0022-4731(84)90287-5

Cited by 43 publications

(22 citation statements)

References 39 publications

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“…A number of findings support the concept that pregnancy-associated hormonal changes, and, particularly, high oestrogen levels, may promote malignant changes by stimulating renal cell proliferation either directly or via growth factors (Concolino et al, 1993). These findings include the fact that administration of potent oestrogens has been shown to induce renal cancers in the Syrian hamster (Kirkman, 1959;Reznik-Schuller, 1979;Li and Li, 1990;Cavalieri et al, 2001), the presence of oestrogen and progesterone receptors in normal and malignant renal cells (Concolino et al, 1976;Ronchi et al, 1984), and the observed association with obesity, which provides a major source of oestrogen in postmenopausal women. However, the evidence supporting a role of exposure to endogenous or exogenous oestrogens in renal cell carcinogenesis is conflicting.…”

Section: Discussionmentioning

confidence: 90%

“…First, over the past 30 years, incidence rates of renal cell cancer have been increasing more rapidly in women than in men in the USA and the UK (Katz et al, 1994;Chow et al, 1999;Tate et al, 2003), suggesting a possible association with exposure to exogenous hormones. Second, steroid hormone receptors have been found in both normal and cancerous renal cell tissue, suggesting hormonal regulation (Ronchi et al, 1984;Siiteri, 1987;Vugrin, 1987). Third, renal tumours can be induced in experimental animals with diethylstilbestrol and oestradiol (Kirkman, 1959;Reznik-Schuller, 1979;Li and Li, 1990).…”

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confidence: 99%

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A cohort study of reproductive and hormonal factors and renal cell cancer risk in women

et al. 2007

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We examined the association of reproductive and hormonal factors with renal cell cancer risk in a cohort study of 89 835 Canadian women. Compared with nulliparous women, parous women were at increased risk (hazard ratio (HR) 1.78, 95% confidence interval (CI) 1.02 -3.09), and there was a significant gradient of risk with increasing levels of parity: relative to nulliparous women, women who had X5 pregnancies lasting 4 months or more had a 2.4-fold risk (HR ¼ 2.41, 95% CI ¼ 1.27 -4.59, P for trend 0.01). Ever use of oral contraceptives was associated with a modest reduction in risk. No associations were observed for age at first live birth or use of hormone replacement therapy. The present study provides evidence that high parity may be associated with increased risk of renal cell cancer, and that oral contraceptive use may be associated with reduced risk.

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Section: Discussionmentioning

confidence: 90%

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confidence: 99%

A cohort study of reproductive and hormonal factors and renal cell cancer risk in women

et al. 2007

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“…High doses of potent estrogens have been shown to induce renal cancers in the Syrian hamster (43). The expression of estrogen and progesterone receptors in both normal and malignant renal tissues also suggests that endocrine regulation could directly influence kidney cancer development (44,45). On the other hand, obesity is a known risk factor for kidney cancer and is associated with pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Parity and Kidney Cancer Risk: Evidence from Epidemiologic Studies

Guan

Gong

2013

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Observational studies have reported conflicting results between parity and kidney cancer risk. To our knowledge, a comprehensive and quantitative assessment of the association between parity and kidney cancer has not been reported. Thus, we conducted a systematic review and dose-response meta-analysis of published epidemiologic studies to summarize the evidence of this association.Methods: Relevant published studies of parity and kidney cancer were identified using MEDLINE (PubMed) database through end of June 2013. Two authors independently assessed eligibility and extracted data. Six prospective and eight case-control studies reported relative risk (RR) estimates and 95% confidence intervals (CI) of kidney cancer associated with parity or parity number. Fixed-or random-effects models were used to estimate summary relative risk.Results: The summary relative risk of kidney cancer for the parity versus nulliparous was 1.23 (95% CI, 1.10-1.36; Q ¼ 12.41; P ¼ 0.413; I 2 ¼ 3.3%). In addition, significant association was also found for the highest

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“…Pregnancy-associated hormonal changes, particularly high oestrogen levels, may act as promotors of malignant change by stimulating renal cell proliferation either directly or via paracrine growth factors (Concolino et al, 1993). Both oestrogen and progesterone receptors are present in normal and malignant renal cells (Ronchi et al, 1984). High doses of potent oestrogens have been shown to induce renal cell tumours in laboratory rodents (Li and Li, 1990).…”

Section: Epidemiologymentioning

confidence: 99%

Pregnancy and risk of renal cell cancer: a population-based study in Sweden

et al. 2002

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Epidemiological findings indicate that hormonal influences may play a role in the etiology of renal cell cancer (RCC). The possible effect of childbearing remains enigmatic; while some investigators have reported a positive association between number of births and renal cell cancer risk, others have not. A case -control study, nested within a nation-wide Fertility Register covering Swedish women born 1925 and later, was undertaken to explore possible associations between parity and age at first birth and the risk of renal cell cancer. Among these women a total of 1465 cases of RCC were identified in the Swedish Cancer Register between 1958 and 1992 and information on the number of live childbirths and age at each birth was obtained by linkage to the Fertility Database. For each case, five age-matched controls were randomly selected from the same register. Compared to nulliparous women, ever-parous women were at a 40% increased risk of RCC (Odds Ratio [OR]=1.42; 95% CI 1.19-1.69). The corresponding OR for women of high parity (five or more live births) was 1.91 (95% CI 1.40 -2.62). After controlling for age at first birth among parous women, each additional birth was associated with a 15% increase in risk (OR=1.15; 95% CI 1.08 -1.22). The observed positive association between parity and renal cell cancer risk is unlikely to be fully explained by uncontrolled confounding, but warrants further evaluation in large studies, with allowance for body mass index.

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Steroid hormone receptors in normal and malignant human renal tissue: Relationship with progestin therapy

Cited by 43 publications

References 39 publications

A cohort study of reproductive and hormonal factors and renal cell cancer risk in women

A cohort study of reproductive and hormonal factors and renal cell cancer risk in women

Parity and Kidney Cancer Risk: Evidence from Epidemiologic Studies

Pregnancy and risk of renal cell cancer: a population-based study in Sweden

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