Cancer in schizophrenia: is the risk higher or lower?

Grinshpoon, Alexander; Barchana, Micha; Ponizovsky, Alexander M.; Lipshitz, Irena; Nahon, Daniella; Tal, Orna; Weizman, Abraham; Levav, Itzhak

doi:10.1016/j.schres.2004.06.016

Cited by 140 publications

(129 citation statements)

References 25 publications

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“…We found 23% (adjusted) decreased performance of PSA tests among service users diagnosed with schizophrenia compared to their matched counterparts. In line with previous reports [1][2][3][4][5][6][7][8] we found that the risk of prostate cancer among service users with schizophrenia was lower than matched comparison subjects (in about 61%). According to our hypothesis, the lower rate of PSA tests could suggest that this negative association may reflect more an issue of method than an issue of substance.…”

Section: Discussionsupporting

confidence: 93%

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Lower risk of prostate cancer in schizophrenia: fact or artifact?

2014

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-Background and Objectives: Reduced risk for prostate cancer in persons diagnosed with schizophrenia has been reported repeatedly. While genetic factors and antipsychotic medications were imputed, a methodological hypothesis could be raised: given the reported disparities of health services with regard to service users with schizophrenia these persons may be screened less often compared to schizophrenia-free counterparts resulting in undetected prostate tumors. The study objective was to compare the rates of performance of the prostate specific antigen (PSA) screening test among persons diagnosed with schizophrenia to matched-comparison subjects.Methods: A prospective historical epidemiological study which included service users with and without a diagnosis of schizophrenia (N = 52,131). Linkage was conducted between databases of the nation-wide psychiatric register and Israel's largest health maintenance organization. Annual performance of PSA tests was recorded between the years 2002-2009.Results: Service users with schizophrenia performed the PSA test 23% less than the comparison subjects. However, among service users who were diagnosed with prostate cancer only 44% performed the PSA test during the year prior to diagnosis.Conclusions: In line with our hypothesis, lower rates of PSA screening tests were conducted among service users with schizophrenia. However, the relatively low rate of this test prior to prostate cancer diagnosis ought to be noted.

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Section: Discussionsupporting

confidence: 93%

“…Several studies found a reduced risk for cancer in persons diagnosed with schizophrenia [1][2][3][4][5][6][7] . Among cancer sites the most robust finding was associated with prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

Lower risk of prostate cancer in schizophrenia: fact or artifact?

2014

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“…However, disruption of PI3K signaling also has been implicated in other psychiatric disorders of neurodevelopmental origin, such as schizophrenia (53,54). An altered incidence of various cancers in individuals with schizophrenia is debated (55,56), but reduced cancer incidence is observed consistently in parents and siblings of individuals with schizophrenia compared with the general population (57-59). These data support the plausibility of a genetic impact, through different mutations or common variants, that increases risk for a neurodevelopmental disorder and decreases cancer risk, a hypothesis that can be tested by epidemiological studies and complete sequencing of candidate genes to identify mutations associated with specific disorders.…”

Section: The Basics Of Cnvsmentioning

confidence: 99%

The genetic and neurobiologic compass points toward common signaling dysfunctions in autism spectrum disorders

2009

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Autism spectrum disorder (ASD) is a common neurodevelopmental disorder with high heritability. Here, we discuss data supporting the view that there are at least two distinct genetic etiologies for ASD: rare, private (de novo) single gene mutations that may have a large effect in causing ASD; and inherited, common functional variants of a combination of genes, each having a small to moderate effect in increasing ASD risk. It also is possible that a combination of the two mechanisms may occur in some individuals with ASD. We further discuss evidence from individuals with a number of different neurodevelopmental syndromes, in which there is a high prevalence of ASD, that some private mutations and common variants converge on dysfunctional ERK and PI3K signaling, which negatively impacts neurodevelopmental events regulated by some receptor tyrosine kinases.Autism spectrum disorder (ASD) is a syndrome characterized by a triad of core deficits: disturbances in social behavior, atypical verbal and nonverbal communication, and restricted interests that can be accompanied by repetitive behavior. The clinical diagnosis, which includes individuals with any one of a spectrum of neurodevelopmental conditions (including autism, Rett syndrome, pervasive developmental disorder-not otherwise specified, and Asperger syndrome), is made in 1 of every 150 individuals and is four times more prevalent in boys than girls (1). While ASD is among the most heritable psychiatric disorders defined in the Diagnostic and statistical manual of mental disorders (4th edition) (2), it is not a static or simple disorder with fixed effects on a circumscribed age. Instead, equally fundamental facets of pathology emerge at different points of maturation of the child. Moreover, the disorder does not result in immutable social and cognitive deficits, but rather the core symptoms typically change over time and to different degrees. Co-occurring medical conditions (sleep problems, epilepsy, and gastrointestinal symptoms) and psychiatric disturbances (anxiety, obsessive-compulsive disorder, and aggression) are common and can appear at different ages in children on the spectrum.Contemporary hypotheses of the causes of ASD often include experience-dependent processes through which atypical gene-by-environment (G X E) interactions yield pathophysiology in later emerging systems that underlie social and communication competencies. The later emergence of symptoms is consistent with the concept that developmental differentiation, whether at the cellular, circuit, or systems level, occurs from the bottom up; behavior develops from basic sensory and perceptual systems that feed into higher integration centers (3-5). Impairments in initial basic processes become expressed in ever more complex systems, with the population heterogeneity of the clinical features of ASD expected to increase from infancy to childhood and through adolescence. However, it is not clear whether the factors that contribute to the developmental diversification and phenotypic heterogeneity of...

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“…Due to the established safety of these drugs, combined with their proven ability to cross the BBB, antipsychotic medications are increasingly being tested for efficacy in patients with various cancers, including malignant brain tumors. Furthermore, epidemiological studies with diverse patient populations have reported significantly lower incidences of cancer among patients with schizophrenia compared with the general population (22)(23)(24)(25)(26)(27)(28)(29). These findings support the possibility that antipsychotics may partially ameliorate the risk of cancer development, although molecular elucidations are yet to be accomplished.…”

Section: Anti-neoplastic Effects Of Antipsychoticsmentioning

confidence: 82%

Repurposing antipsychotics as glioblastoma therapeutics: Potentials and challenges

2016

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Abstract. Glioblastoma multiforme (GBM) is the most common and most lethal primary brain tumor, with tragically little therapeutic progress over the last 30 years. Surgery provides a modest benefit, and GBM cells are resistant to radiation and chemotherapy. Despite significant development of the molecularly targeting strategies, the clinical outcome of GBM patients remains dismal. The challenges inherent in developing effective GBM treatments have become increasingly clear, and include resistance to standard treatments, the blood-brain barrier, resistance of GBM stem-like cells, and the genetic complexity and molecular adaptability of GBM. Recent studies have collectively suggested that certain antipsychotics harbor antitumor effects and have potential utilities as anti-GBM therapeutics. In the present review, the anti-tumorigenic effects and putative mechanisms of antipsychotics, and the challenges for the potential use of antipsychotic drugs as anti-GBM therapeutics are reviewed.

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Cancer in schizophrenia: is the risk higher or lower?

Cited by 140 publications

References 25 publications

Lower risk of prostate cancer in schizophrenia: fact or artifact?

Lower risk of prostate cancer in schizophrenia: fact or artifact?

The genetic and neurobiologic compass points toward common signaling dysfunctions in autism spectrum disorders

Repurposing antipsychotics as glioblastoma therapeutics: Potentials and challenges

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