Antidepressants and risk of prostate cancer: a nested case – control study

Hm, Tamim; Mahmud, Salaheddin M.; Ja, Hanley; Boivin, Jacky; Mr, Stang; Jp, Collet

doi:10.1038/sj.pcan.4501003

Cited by 20 publications

(20 citation statements)

References 35 publications

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“…Some of the above studies have controlled for some of these additional factors. 31,[33][34][35]52,56 With or without these controls, the 7 lines each provide circumstantial evidence that is consistent with the elevated NE etiological hypothesis. They are also to some degree independent of one another, further strengthening the hypothesis.…”

Section: Literature Search Detailssupporting

confidence: 53%

“…To provide the reader with a feel for the numbers, here are a few of the SIRs and odds ratios. In the prostate cancer study, 31 the rate ratios for tricyclics increasing prostate cancer risk were 1.31 (95% CI 1.14-1.51), 1.58 (95% CI 1.29-1.93) and 2.42 (95% CI 1.87-3.12) at the low, medium and high average daily dose levels, respectively. In the lung cancer study, 35 SSRI use during the year preceding the index date with treatment duration of at least 1 year had an odds ratio of 0.59 (95% CI 0.41-0.86).…”

Section: Literature Search Detailsmentioning

confidence: 99%

“…31 There is additional evidence that tricyclics increase the rate of other types of cancer, such as breast cancer, but this is controversial. [32][33][34] A recent lung cancer study showed that SSRIs may decrease the rate, whereas tricyclics increased the rate to a degree that was nearly statistically significant.…”

Section: Literature Search Detailsmentioning

confidence: 99%

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Is norepinephrine an etiological factor in some types of cancer?

Fitzgerald

2008

Intl Journal of Cancer

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I examine evidence that the signaling molecule norepinephrine (NE) is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) rodent studies of tumorigenesis in the context of NE manipulation; (ii) human studies of tricyclic antidepressant use and cancer rate; (iii) existence of pheochromocytoma, a cancer of the adrenal glands; (iv) cancer rate in families with individuals who have bipolar disorder; (v) hypertension and cancer risk; (vi) excessive body weight and cancer risk; and (vii) psychological stressors and cancer risk. Three aspects of the body's NE system are consistent with it playing an etiological role in various types of cancer: (i) NE circulates in the blood and can thereby access organ systems throughout the body, in addition to direct peripheral release by the sympathetic nervous system and being released within the brain; (ii) many of the body's organs possess NE receptors on the outer surface of at least some of their cells; (iii) by binding to its extracellular receptors, NE affects intracellular second messenger systems that could influence carcinogenesis. Most importantly, use of existing pharmaceutical drugs that either lower the level of NE (such as clonidine) or block NE receptors may lower the probability of an individual developing cancer, and this hypothesis could be tested immediately by an epidemiologist through examination of existing medical records. ' 2008 Wiley-Liss, Inc.Key words: norepinephrine; pharmacology; clonidine; adrenoceptor; rodent; hypertension; epidemiology; pheochromocytoma I present evidence that the signaling molecule norepinephrine (NE), which is a neurotransmitter and plays various roles in organs other than the brain, is an etiological factor in some types of cancer. In support of this hypothesis, I cite the following 7 lines of evidence: (i) in a series of rodent studies, increasing the level of NE in various organs increases tumorigenesis, whereas decreasing the level decreases tumorigenesis; (ii) in humans, tricyclic antidepressant use, which may boost the level of NE throughout the body, may be associated with increased rates of cancer; (iii) pheochromocytoma, which is a cancer of the adrenal glands, may be an example of NE causing cancer in the organ that releases it into the bloodstream; (iv) families with individuals who have bipolar disorder have elevated cancer rates, where bipolar disorder may be associated with a high level of NE; (v) hypertension is associated with an elevated level of NE in the bloodstream, and may be a cancer risk factor; (vi) excessive body weight is associated with elevated blood NE and is a cancer risk factor; and (vii) psychological stressors are associated with increased release of NE in the brain and bloodstream, and exposure to stress is potentially a cancer risk factor.In addition to the above evidence, including NE's role in the brain, several other aspects of the body's NE system are consistent with an etiological role in cancer: (i) In addition to relea...

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Section: Literature Search Detailssupporting

confidence: 53%

Section: Literature Search Detailsmentioning

confidence: 99%

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Is norepinephrine an etiological factor in some types of cancer?

Fitzgerald

2008

Intl Journal of Cancer

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“…Recent studies have demonstrated that antidepressants decrease the risk of breast cancer development (1)(2)(3)(4). On the other hand, several studies have reported that antidepressants increase the risk of nonHodgkin lymphoma and prostate cancer (5,6), and it is still controversial what effect tricyclic antidepressants have on lung, breast and colon cancer cells (7)(8)(9). Both in vitro and in vivo studies indicate antidepressants are cytotoxic to most malignant cells, particularly colon and breast cancer (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

“…For DNA fragmentation analysis, the cells were plated on a 10-mm culture dish at a density of 2x10 6 cells/dish and exposed to different concentrations of DMI for 24 h. The cells which attached to the bottom of the dish were scraped off and collected together with unattached cells by centrifuging at 800 x g for 5 min at 4˚C. The DNA was prepared from the pelleted cells and applied to a 2% agarose gel containing 0.5 mg/ml of ethidium bromide for electrophoretic analysis.…”

Section: Dna Fragmentation Analysismentioning

confidence: 99%

Effects of desipramine on the cell cycle and apoptosis in Ca3/7 mouse skin squamous carcinoma cells

Hanausek,¹

2010

Int J Mol Med

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Abstract. Desipramine (DMI) has been reported to induce glucocorticoid receptor-mediated signal transduction in recent studies. It has been suggested that a non-glucocorticoid receptor signaling pathway might play an important role in skin squamous carcinoma Ca3/7 cells. The aim of this study was to investigate the growth inhibitory effects of DMI on Ca3/7 cells by evaluating the mRNA expression of genes related to apoptosis and cell cycle progression. Hoechst nuclear staining and DNA fragmentation assays were used to detect apoptosis, and the cell cycle was analyzed by flow cytometry. Apoptotic bodies in the nuclei of cells and DNA fragmentation were observed when the Ca3/7 cells were treated with 20 μM DMI for 24 h. Quantitative RT-PCR (reverse transcriptional-polymerase chain reaction) showed that DMI caused a decrease in Bcl-2 and survivin but not Bcl-xL gene expression and an increase in the expression of Bax, Apaf-1, caspase-3 and caspase-7 in a dose-and timedependent manner. DMI also caused translocation of the apoptosis-inducing factor from the cytoplasm to the nucleus as well as cell cycle arrest in the Ca3/7 cells. Quantitative RT-PCR revealed that DMI decreased the expression of the PCNA gene and caused an increase in the expression of the p21 and p27 genes in the Ca3/7 cells. Our results showed that DMI inhibited the growth of Ca3/7 cells by inducing both apoptosis and cell cycle arrest.

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Incidence of cancer and antidepressant medication: Record linkage study

Haukka

Sankila

Klaukka

et al. 2009

Intl Journal of Cancer

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The consumption of antidepressants, especially selective serotonine reuptake inhibitors (SSRI) has been increasing. Because a large fraction of the population is exposed, even a small excess of risk with respect to cancer should be considered. We carried out a record linkage study in Finland utilizing nationwide databases of reimbursed medication and cancer. The study population included all antidepressant drug (AD) users in Finland who had purchased at least 1 prescription between 1998 and 2005, and who had no cancer diagnosis at the date of first purchase. A control population without AD usage (matched by age and sex) was also included. Data consisted of 418,588 pairs of individuals that cumulated 3.3 million person-years with an average of 4.0 years of follow-up. 19,365 cancer cases were observed. The most frequent cancers were breast, prostate, lung, colon, and brain cancer. In general, only few associations between the utilization of AD and cancer could be detected. Over four years exposure to AD showed a weak association with increased colon and breast cancer incidence, which could have been caused by bias. As conclusion, no clear evidence of neither beneficial nor harmful association between usage of antidepressant and cancer was found.

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Antidepressants and risk of prostate cancer: a nested case – control study

Cited by 20 publications

References 35 publications

Is norepinephrine an etiological factor in some types of cancer?

Is norepinephrine an etiological factor in some types of cancer?

Effects of desipramine on the cell cycle and apoptosis in Ca3/7 mouse skin squamous carcinoma cells

Incidence of cancer and antidepressant medication: Record linkage study

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