Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cancer occurrence in patients with multiple sclerosis (MS) has been little studied, but associations with brain tumours, breast cancer, Hodgkin lymphoma and nasopharyngeal carcinoma have been suggested. We took advantage of population-based registers of MS and cancer to assess the risk of cancer following diagnosis of MS. Patients registered in the Danish Multiple Sclerosis Register were linked with the Danish Cancer Register to obtain information on cancer occurrence. The ratio of the observed to the number of expected cancers based on population-based incidence rates, i.e., the standardised incidence ratio (SIR), served as measure of the relative cancer risk. A database comprising all Danish women born after April 1, 1935, with information on all live-born children, was used in the analyses of breast cancer to adjust for reproductive factors. Overall 1,037 cancers were observed in 11,817 MS patients during 153,875 person-years of follow-up vs. an expected number of 1,098 (SIR = 0.94 [95% confidence interval CI: (0.89-1.00)]. The risk of brain tumours and Hodgkin lymphoma was not increased. A 16% overall reduced cancer risk in men with MS was explained by reduced numbers of cancers of the digestive, respiratory and genital organs. Though the overall cancer risk was not increased [SIR = 1.01(0.94-1.09), n = 676], female MS patients had an increased risk of breast cancer [SIR = 1.21 (1.05-1.39), n = 193]. Adjusting for parity and age at first child delivery did not change this risk estimate materially. In general MS patients are not at increased risk of cancer. Women with MS, however, seem to have a small excess risk of breast cancer, which cannot be attributed to reduced parity or delayed first child birth.
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PMID:Cancer risk among patients with multiple sclerosis: a population-based register study. 1615 98

Classical theories have conceptualized stress as a reaction to threat to the homeostasis within the organism requiring an adaptive response. However, postulating mechanisms that could link such responses to long-term detrimental health outcomes remains difficult. The allostatic load concept enables us to think about how mediators can be protective in the short run but may have damaging effects when overused and/or not shut off. It further facilitates the formulation of cause-effects cascades to explain the link of dysregulations in stress mediators such as glucocorticoids and catecholamines and increased susceptibility for certain diseases. In the first section, we briefly summarize the theoretical background. We then employ the concept to integrate findings from basic and clinical research on dysregulations of the stress response systems in multiple sclerosis and breast cancer. Based on this model, it seems likely that such dysregulations are implicated in progression and possibly pathogenesis of these diseases. When using allostatic load as a heuristic model, one needs to consider that stress mediators and outcomes are interconnected in a non-linear network.
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PMID:[The concept of allostasis and allostatic load: psychoneuroimmunological findings]. 1627

The detection of gene-gene and gene-environment interactions associated with complex human disease or pharmacogenomic endpoints is a difficult challenge for human geneticists. Unlike rare, Mendelian diseases that are associated with a single gene, most common diseases are caused by the non-linear interaction of numerous genetic and environmental variables. The dimensionality involved in the evaluation of combinations of many such variables quickly diminishes the usefulness of traditional, parametric statistical methods. Multifactor dimensionality reduction (MDR) is a novel and powerful statistical tool for detecting and modelling epistasis. MDR is a non-parametric and model-free approach that has been shown to have reasonable power to detect epistasis in both theoretical and empirical studies. MDR has detected interactions in diseases such as sporadic breast cancer, multiple sclerosis and essential hypertension. As this method is more frequently applied, and was gained acceptance in the study of human disease and pharmacogenomics, it is becoming increasingly important that the implementation of the MDR approach is properly understood. As with all statistical methods, MDR is only powerful and useful when implemented correctly. Concerns regarding dataset structure, configuration parameters and the proper execution of permutation testing in reference to a particular dataset and configuration are essential to the method's effectiveness. The detection, characterisation and interpretation of gene-gene and gene-environment interactions are expected to improve the diagnosis, prevention and treatment of common human diseases. MDR can be a powerful tool in reaching these goals when used appropriately.
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PMID:Multifactor dimensionality reduction: an analysis strategy for modelling and detecting gene-gene interactions in human genetics and pharmacogenomics studies. 1659 76

The human genome contains around 1000 betaretrovirus-like copies, human mouse mammary tumour virus (MMTV)-like (HML) groups 1-10, also referred to as human endogenous retrovirus "HERV-K". Despite many efforts, it is not established whether betaretroviruses, exo- or endogenous, are involved in the etiology of breast cancer, or other cancer diseases, in humans. Quantitative real-time PCR (QPCR) TaqMan-based assays for HML groups 1-7, targeting the conserved reverse transcriptase (RT) and integrase (IN) domains of the pol gene were designed. Plasmids containing the entire pol gene of HML1-7 were used as standards. The RT and IN based QPCRs could detect 10(0)-10(3) copies per PCR reaction of the plasmids. However, not all plasmids gave a signal in both RT and IN QPCRs, probably due to mismatches. Furthermore, RT and IN based HML6 specific QPCRs were developed. They were specific for amplification of transcripts for the whole HML6 group. The methods allow the monitoring in body fluids and tissues of expression of a wide range of betaretrovirus-like sequences. Betaretrovirus-like RNA was studied in normal human tissues and of HML6 in brains of multiple sclerosis (MS) patients. Brain, adrenal gland and testis had a high betaretrovirus-like expression. Multiple sclerosis plaques contained the same HML6 RNA concentration as control tissue. These assays are expected to enhance studies on involvement of betaretroviruses in physiology and disease.
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PMID:Development of real-time PCRs for detection and quantitation of human MMTV-like (HML) sequences HML expression in human tissues. 1671 32

Interdisciplinary psychoneuroimmunological (PNI) research increasingly demonstrates clinically relevant interrelations between psychological stressors and the onset or progression of chronic diseases. Disturbances of the bi-directional interaction between the nervous system, the immune system and the endocrine system have been hypothesized to be implicated in several diseases. Here, we review evidence from psychoneuroimmunology within the theoretical framework of allostatic load to conceptualize some of these associations. Interdisciplinary PNI research investigating the importance of psychological stress for the higher incidence of infections, decreased responses to vaccinations and delayed wound healing is reviewed. Furthermore, the literature supporting similar associations with regard to progression of oncological diseases and autoimmune disorders is reviewed with a focus on breast cancer and multiple sclerosis. The accumulating evidence regarding the importance of neuroendocrine-immune interaction in these diseases may thus lead to novel insights into pathogenetic mechanisms and could contribute to the development of novel preventive and therapeutic strategies.
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PMID:[Psychological stress, immune function and disease development. The psychoneuroimmunologic perspective]. 1686 32

Mitoxantrone is a DNA topoisomerase II poison commonly used for the treatment of hormone-refractory prostate cancer. The risk of secondary leukaemia is well described after mitoxantrone treatment in breast cancer and multiple sclerosis. Recent improvements of systemic chemotherapy increased the median survival in patients becoming resistant to androgen deprivation from 10 to 18 months. As a consequence, chemotherapy-related cumulative toxicities may become a more prominent clinical problem in this patient population. We report here the first case report of secondary leukaemia induced by mitoxantrone in metastatic hormone-refractory prostate cancer. This clinical observation invites us to reconsider the number of administrations to be recommended for mitoxantrone-sensitive metastatic prostate cancer patients.
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PMID:Mitoxantrone-related acute myeloblastic leukaemia in a patient with metastatic hormone-refractory prostate cancer. 1715 10

Nuclear factor-kappaB (NF-kappaB) is responsible for the expression by regulating many genes for immune response, cell adhesion, differentiation, proliferation, angiogenesis and apoptosis. The function of NF-kappaB is inhibited by binding to NF-kappaB inhibitor (IkappaB), and imbalance of NF-kappaB and IkappaB has been associated with development of many diseases, including tumours. In this review, we focus on polymorphisms of the NFKB and NFKBI genes in relation to development of common inflammatory diseases including ulcerative colitis (UC), Crohn's disease (CD), rheumatoid arthritis, systemic lupus erythematosus, psoriatic arthritis, giant cell arthritis, type 1 diabetes, multiple sclerosis, celiac disease, and Parkinson's disease, as well as susceptibility of several cancers, such as oral squamous cell carcinoma, colorectal cancer (CRC), hepatocellular carcinoma, breast cancer and myeloma.
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PMID:NFKB and NFKBI polymorphisms in relation to susceptibility of tumour and other diseases. 1770 19

(1) Cases of acute leukaemia (usually myeloblastic) have been attributed to mitoxantrone. (2) A French epidemiological study showed an increased risk of leukaemia in women treated with mitoxantrone for breast cancer, with a relative risk of about 7. The results of studies conducted elsewhere are similar. (3) The time to onset of leukaemia after mitoxantrone exposure ranges from 8 months to several years. The risk is dose-dependent. The excess risk is particularly high when the cumulative dose is above 13 mg/m2. The prognosis for leukaemia due to mitoxantrone is worse than the prognosis for leukaemia with no known cause. (4) Cases of leukaemia have also been reported after the use of mitoxantrone to treat other cancers and multiple sclerosis. (5) This serious adverse effect must be taken into account when choosing a treatment for patients with a relatively long life expectancy. Patients treated with mitoxantrone should be monitored.
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PMID:Leukaemia due to mitoxantrone. 1772 42

We have genotyped 14,436 nonsynonymous SNPs (nsSNPs) and 897 major histocompatibility complex (MHC) tag SNPs from 1,000 independent cases of ankylosing spondylitis (AS), autoimmune thyroid disease (AITD), multiple sclerosis (MS) and breast cancer (BC). Comparing these data against a common control dataset derived from 1,500 randomly selected healthy British individuals, we report initial association and independent replication in a North American sample of two new loci related to ankylosing spondylitis, ARTS1 and IL23R, and confirmation of the previously reported association of AITD with TSHR and FCRL3. These findings, enabled in part by increased statistical power resulting from the expansion of the control reference group to include individuals from the other disease groups, highlight notable new possibilities for autoimmune regulation and suggest that IL23R may be a common susceptibility factor for the major 'seronegative' diseases.
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PMID:Association scan of 14,500 nonsynonymous SNPs in four diseases identifies autoimmunity variants. 1795 73

Proteasome antibodies were detected by enzyme-linked immunosorbent assay in two of the 45 (4.4%) patients with lung cancer, 0 of the 39 patients with breast cancer and six of the 51 (11.8%) patients with ovarian cancer. Six of the 47 (12.8%) patients with relapsing remitting multiple sclerosis had proteasome antibodies, as well as two of the 100 (2%) blood donors. Significant higher odds ratios compared to the blood donors were found for the patients with ovarian cancer (OR: 6.4; 95% CI: 1.1-68) and multiple sclerosis (OR: 7.1; 95% CI: 1.2-74). There was no association between proteasome antibodies and metastases or onconeural antibodies. The antibodies showed reactivity to 23, 25 and 27 kD proteins of the 20S proteasome using Western blot. The increased prevalence of proteasome antibodies in patients with ovarian cancer or multiple sclerosis may reflect cellular damage and release of intracellular antigens. Whether the antibodies take part in the clearance of released proteasomes and thus participate in the pathogenesis of cancer or autoimmune disease is not known.
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PMID:Proteasome antibodies in patients with cancer or multiple sclerosis. 1826 96


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