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Query: UMLS:C0006142 (breast cancer)
 160,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In recent years, evidence has emerged supporting the hypothesis that cancer is a stem cell disease. The cancer stem cell field was led by the discovery of leukemia stem cells (Tan, B.T., Park, C.Y., Ailles, L.E., and Weissman, I.L. (2006) The cancer stem cell hypothesis: a work in progress. Laboratory Investigation. 86, 1203-1207), and within the past few years cancer stem cells have been isolated from a number of solid tumor including those of breast and brain cancer among others (Al-Hajj M., Wicha M.S., Benito-Hernandez A., Morrison, S.J., and Clarke, M.F. (2003) Prospective identification of tumorigenic breast cancer cells. Proc. Natl. Acad. Sci. USA 100, 3983-3988; Singh, S.K., Clarke, I.D., Terasaki, M., Bonn, V.E., Hawkins, C., Squire, J., and Dirks, P.B. (2003) Identification of a Cancer Stem Cell in Human Brain Tumors. Cancer Research. 63, 5821-5828). Cancer stem cells exhibit far different properties than established cells lines such as relative quiescence, multidrug resistance, and multipotency (Clarke, M.F., Dick, J.E., Dirks, P.B., Eaves, C.J., Jamieson, C.H.M., Jones, D.L., Visvader, J., Weissman, I.L., and Wahl, G.M. (2006) Cancer Stem Cells-Perspectives on Current Status and Future Directions: AACR Workshop on Cancer Stem Cells. Cancer Research. 66, 9339-9344). In addition, our laboratory has demonstrated that breast cancer stem cells exhibit a strong metastatic phenotype when passaged in mice. Since stem cells exhibit these somewhat unique properties, it will be important for endocrinologists to evaluate hormonal action in these precursor cells for a more thorough understanding of cancer biology and development of more effective treatment modalities. A relatively easy and low cost method was developed to isolate breast cancer stem cells from primary needle biopsies taken from patients diagnosed with primary invasive ductal carcinoma during the routine care of patients with consent and IRB approval. Fresh needle biopsies (2-3 biopsies at 2 cm in length) were enzymatically dissociated in a collagenase (300 U/ml)/hyaluronidase (100 U/ml) solution followed by sequential filtration. Single cell suspensions were cultured on ultra low attachment plastic flasks in defined medium and formed non-adherent tumorspheres. The tumorspheres exhibited surface marker expression of CD44(+)/CD24(low/-)/ESA(+), previously defined as a "breast cancer stem cell" phenotype by Al Hajj et al. (Al-Hajj M., Wicha M.S., Benito-Hernandez A., Morrison, S.J., and Clarke, M.F. (2003) Prospective identification of tumorigenic breast cancer cells.
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PMID:Breast tumor-initiating cells isolated from patient core biopsies for study of hormone action. 1976 16

Aircrew members are exposed to cosmic radiation and other specific occupational factors. In a previous analysis of a large cohort of German aircrew, no increase in cancer mortality or dose-related effects was observed. In the present study, the follow-up of this cohort of 6,017 cockpit and 20,757 cabin crew members was extended by 6 years to 2003. Among male cockpit crew, the resulting all-cancer standardized mortality ratio (SMR) (n = 127) is 0.6 (95% CI 0.5-0.8), while for brain tumors it is 2.1 (95% CI 1.0-3.9). The cancer risk is significantly raised (RR = 2.2, 95% CI 1.2-4.1) among cockpit crew members employed 30 years or more compared to those employed less than 10 years. Among both female and male cabin crew, the all-cancer SMR and that for most individual cancers are close to 1. The SMR for breast cancer among female crew is 1.2 (95% CI 0.8-1.8). Non-Hodgkin's Lymphoma among male cabin crew is increased (SMR 4.2; 95% CI 1.3-10.8). However, cancers associated with radiation exposure are not raised in the cohort. It is concluded that among cockpit crew cancer mortality is low, particularly for lung cancer. The positive trend of all cancer with duration of employment persists. The increased brain cancer SMR among cockpit crew requires replication in other cohorts. For cabin crew, cancer mortality is generally close to population rates. Cosmic radiation dose estimates will allow more detailed assessments, as will a pooling of updated aircrew studies currently in planning.
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PMID:Cancer mortality among German aircrew: second follow-up. 1984 29

The population-based Aden Cancer Registry (ACR) started its activities in 1997. The objective of the registry is to establish a reliable magnitude of cancer in the area covered and the first report was published in 2003. The present article describes data from the second report of cancer incidence over a five year period (2002-2006). Internationally accepted standardized cancer registration methodologies described by IACR and IARC were used. CanReg-4 using ICDO-3 and ICD-10 were applied in the data processing and analysis. Results showed no difference in the overall incidence between the males and females (ratio was 0.83:1) and age standardized rate s(ASR) per 100,000 inhabitants were 30.2 and 31.1. The five most common cancers were breast cancer, leukemia, non-Hodgkin's lymphomas (NH lymphoma), brain cancer and Hodgkin's disease (16.6%, 12.6%, 7.8%, 5.2% and 4.4%, respectively). Among males, leukemia was the first followed by NH lymphoma, Hodgkin's disease, brain and liver. In females, breast was the first, then leukemia, NH lymphoma, thyroid and brain cancer. The highest ASR for males (145 per 100,00 inhabitants) was observed at age 70-74 years whereas for females, two peaks (each 105 per 100,000 inhabitants) were equally noticed at age 60-64 and 70-74 years. Generally, females showed equal or higher incidence compared to males until age 55-59 where males reported higher incidence. The overall pattern of cancer incidence in this report is not much different from that in the previous report. Furthermore, the report generally indicates that the pattern of the most common registered cancer bears some similarities with the adjacent Gulf Cooperation Council States with which we share many characteristics, despite differences that warrant further investigation.
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PMID:Five years cancer incidence in Aden Cancer Registry, Yemen (2002-2006). 2084 42

This paper describes an effort to estimate variations in cognitive effort among cancer survivors experiencing treatment related cognitive decline. EEG-based cognitive state sensing algorithms were validated in the context of an experiment with 5 brain cancer and 5 breast cancer survivors. Workload was manipulated by varying text complexity and time pressure. Analysis indicates that EEG-based cognitive state sensing algorithms were able to distinguish between high and low cognitive workload with an average classification accuracy of 0.84. Results suggest that 5 to 10 channels of EEG can provide enough information to achieve classification accuracies exceeding 0.80. The highest density of informative sites were over the left temporal and mid to inferior frontal regions in the left hemisphere - regions that play a major role in language.
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PMID:Towards an index of cognitive efficacy EEG-based estimation of cognitive load among individuals experiencing cancer-related cognitive decline. 2109 15

Glycolipids are compounds containing one or more monosaccharide residues bound by a glycosidic linkage to a hydrophobic moiety. Because of their expression patterns and the intracellular localization patterns, glycolipids, including stage-specific embryonic antigens (SSEA-3, SSEA-4, and possibly SSEA-1) and gangliosides (e.g., GD3, GD2, and A2B5 antigens), have been used as marker molecules of stem cells. In this review, I will introduce glycolipids expressed in pluripotent stem cells (embryonic stem cells, induced pluripotent stem cells, very small embryonic-like stem cells, amniotic stem cells, and multilineage-differentiating stress enduring cells), multipotent stem cells (neural stem cells, mesenchymal stem cells, fetal liver multipotent progenitor cells, and hematopoietic stem cells), and cancer stem cells (brain cancer stem cells and breast cancer stem cells), and discuss their availability as biomarkers for identifying and isolating stem cells.
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PMID:Stem cell glycolipids. 2116 92

Dichloromethane (methylene chloride) is a widely used chlorinated solvent. We review the available epidemiology studies (five cohort studies, 13 case-control studies, including seven of hematopoietic cancers), focusing on specific cancer sites. There was little indication of an increased risk of lung cancer in the cohort studies (standardized mortality ratios ranging from 0.46 to 1.21). These cohorts are relatively small, and variable effects (e.g., point estimates ranging from 0.5 to 2.0) were seen for the rarer forms of cancers such as brain cancer and specific hematopoietic cancers. Three large population-based case-control studies of incident non-Hodgkin lymphoma in Europe and the United States observed odds ratios between 1.5 and 2.2 with dichloromethane exposure (ever exposed or highest category of exposure), with higher risk seen in specific subsets of disease. More limited indications of associations with brain cancer, breast cancer, and liver and biliary cancer were also seen in this collection of studies. Existing cohort studies, given their size and uneven exposure information, are unlikely to resolve questions of cancer risks and dichloromethane exposure. More promising approaches are population-based case-control studies of incident disease, and the combination of data from such studies, with robust exposure assessments that include detailed occupational information and exposure assignment based on industry-wide surveys or direct exposure measurements.
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PMID:Insights from epidemiology into dichloromethane and cancer risk. 2190 13

Many biological and clinical outcomes are based not on single proteins, but on modules of proteins embedded in protein networks. A fundamental question is how the proteins within each module contribute to the overall module activity. Here, we study the modules underlying three representative biological programs related to tissue development, breast cancer metastasis, or progression of brain cancer, respectively. For each case we apply a new method, called Network-Guided Forests, to identify predictive modules together with logic functions which tie the activity of each module to the activity of its component genes. The resulting modules implement a diverse repertoire of decision logic which cannot be captured using the simple approximations suggested in previous work such as gene summation or subtraction. We show that in cancer, certain combinations of oncogenes and tumor suppressors exert competing forces on the system, suggesting that medical genetics should move beyond cataloguing individual cancer genes to cataloguing their combinatorial logic.
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PMID:Protein networks as logic functions in development and cancer. 2198 Feb 75

One of the main topics of the annual meeting of the American Society for Clinical Oncology in 2011 were the results presented on breast cancer chemotherapy and concomitant administration of the oral antidiabetic metformin. The overall agreement was that current evidence is just enough to dramatically change the clinical practice of oncology, and in our case, brain cancer treatment, and that further research is needed to address the relationship between diabetes, metabolism, insulin analogues and neoplasia. Still, it is very interesting to explore the potentially beneficial effects of metformin in glioma chemo/immunotherapy and wait for results in the clinic. In the current paper we present the cell and molecular aspects of the metabolic syndrome, metformin administration and cancer chemotherapy, with a special emphasis in neuro-oncology, since brain tumors are usually devastating diseases with an extremely high mortality within two years of diagnosis even when surgical, radiotherapeutic and chemotherapeutic interventions are applied.
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PMID:Antidiabetic pharmacology: a link between metabolic syndrome and neuro-oncology? 2200 41

Background Contact allergy is a prevalent disorder. It is estimated that about 20% of the general population are allergic to one or more of the chemicals that constitute the European baseline patch test panel. While many studies have investigated associations between type I allergic disorders and cancer, few have looked into the association between cancer and contact allergy, a type IV allergy. By linking two clinical databases, the authors investigate the possible association between contact allergy and cancer. Methods Record linkage of two different registers was performed: (1) a tertiary hospital register of dermatitis patients patch tested for contact allergy and (2) a nationwide cancer register (the Danish Cancer Register). After linking the two registers, only cancer subtypes with 40 or more patients registered were included in the analysis. The final associations were evaluated by logistic regression analysis. Results An inverse association between contact allergy and non-melanoma skin- and breast cancer, respectively, was identified in both sexes, and an inverse trend for brain cancer was found in women with contact allergy. Additionally, a positive association between contact allergy and bladder cancer was found. Conclusion The inverse associations support the immunosurveillance hypothesis (ie, individuals with an allergy are less likely to get cancer due to a triggered immune system), while the positive association with bladder cancer could be due to accumulations of chemical metabolites in the bladder. The authors' findings add to the limited knowledge about contact allergy and the risk of cancer.
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PMID:Association between cancer and contact allergy: a linkage study. 2202 56

The epidermal growth factor receptor (EGFR) is a member of the EGFR family of receptor tyrosine kinases (RTKs). EGFR activation via ligand binding results in signaling through various pathways ultimately resulting in cellular proliferation, survival, angiogenesis, invasion, and metastasis. Aberrant expression or activity of EGFR has been strongly linked to the etiology of several human epithelial cancers including but not limited to head and neck squamous cell carcinoma (HNSCC), non-small cell lung cancer (NSCLC), colorectal cancer (CRC), breast cancer, pancreatic cancer, and brain cancer. Thus intense efforts have been made to inhibit the activity of EGFR by designing antibodies against the ligand binding domains (cetuximab and panitumumab) or small molecules against the tyrosine kinase domain (erlotinib, gefitinib, and lapatinib). Although targeting membrane-bound EGFR has shown benefit, a new and emerging role for EGFR is now being elucidated. In this review we will summarize the current knowledge of the nuclear EGFR signaling network, including how it is trafficked to the nucleus, the functions it serves in the nucleus, and how these functions impact cancer progression, survival, and response to chemotherapeutics.
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PMID:The nuclear epidermal growth factor receptor signaling network and its role in cancer. 2212 13


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