Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Children are exposed to pesticides through a number of sources, including residential and agricultural applications. Parental occupational exposure to pesticides is also a concern because exposures occurring during pregnancy and carry-home residues also contribute to children's cumulative burden. A number of epidemiological studies consistently reported increased risks between pesticide exposures and childhood leukemia, brain cancer, neuroblastoma, non-Hodgkin's lymphoma, Wilms' tumor, and Ewing's sarcoma. An extensive review of these studies was published in 1998 (Zahm & Ward, 1998). Fifteen case-control studies, 4 cohort studies, and 2 ecological studies have been published since this review, and 15 of these 21 studies reported statistically significant increased risks between either childhood pesticide exposure or parental occupational exposure and childhood cancer. Therefore, one can confidently state that there is at least some association between pesticide exposure and childhood cancer. However, an unambiguous mechanistic cause-and-effect relationship between pesticide exposure and childhood cancer was not demonstrated in these studies, and modifying factors such as genetic predisposition, rarely considered in the reviewed studies, likely play an important role. While the time window of exposure may be a crucial determinant for biological effects associated with pesticide exposure on children, studies have not contributed definitive information on the most vulnerable period. Accurate exposure assessment remains a challenge; future epidemiological studies need to assess gene-environment interactions and use improved exposure measures, including separate parental interviews, specific pesticide exposure questions, and semiquantitative exposure measures that can be used to confirm information obtained through questionnaires.
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PMID:Pesticides and childhood cancer: an update of Zahm and Ward's 1998 review. 1807 5

Two seminal reviews (IARC, 2002; CDHS, 2002) of possible health effects from power-frequency EMFs reached partly different conclusions from similar epidemiological evidence. These differences have an impact on precautionary policy. We examine the statistical aggregation of results from individual disparate studies. Without consistent exposure metrics, the advantage of meta-analysis to estimate magnitude of effect is lost. However, counting positive and statistically significant results yields important information. This is not a substitute for meta-analysis, but a fall-back when meaningful meta-analysis is not available. Representative results from 33 independent adult leukemia studies tabled by IARC yielded 23.5 positives (p approximately 0.01) and 9 significant-positives (p<10(-7)). From 43 representative results from CDHS, there were 32 positive (p<0.001) and 14 significant-positives (p<10(-12)). There were no significant-negative results in either list. Results for adult brain cancer gave a similar, but less clear, message. Childhood leukemia EMF studies have been sufficiently comparable to allow selective pooled analysis, which was important in classifying carcinogenicity. Aggregating all the studies suggests that results for childhood leukemia are not stronger, numerically, than those for adult leukemia. CDHS did not note the number of significant-positives, but noted the meta-analytic summary and the number of positives, forming a view about the strength of these findings. IARC shows no evidence of considering the aggregation of results other than subjectively. It considered individual studies but this led to a tendency to fragment and dismiss evidence that is intrinsically highly significant. We make recommendations for future reviews.
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PMID:Aggregating disparate epidemiological evidence: comparing two seminal EMF reviews. 1830 19

What do we currently know about the occupational and environmental causes of cancer? As of 2007, the International Agency for Research on Cancer (IARC) identified 415 known or suspected carcinogens. Cancer arises through an extremely complicated web of multiple causes, and we will likely never know the full range of agents or combinations of agents. We do know that preventing exposure to individual carcinogens prevents the disease. Declines in cancer rates-such as the drop in male lung cancer cases from the reduction in tobacco smoking or the drop in bladder cancer among cohorts of dye workers from the elimination of exposure to specific aromatic amines-provides evidence that preventing cancer is possible when we act on what we know. Although the overall age-adjusted cancer incidence rates in the United States among both men and women have declined in the last decade, the rates of several types of cancers are on the rise; some of which are linked to environmental and occupational exposures. This report chronicles the most recent epidemiologic evidence linking occupational and environmental exposures with cancer. Peer-reviewed scientific studies published from January 2005 to June 2007 were reviewed, supplementing our state-of-the-evidence report published in September 2005. Despite weaknesses in certain individual studies, we consider the evidence linking the increased risk of several types of cancer with specific exposures somewhat strengthened by recent publications, among them brain cancer from exposure to non-ionizing radiation, particularly radiofrequency fields emitted by mobile telephones; breast cancer from exposure to the pesticide dichlorodiphenyltrichloroethane (DDT) before puberty; leukemia from exposure to 1,3-butadiene; lung cancer from exposure to air pollution; non-Hodgkin's lymphoma (NHL) from exposure to pesticides and solvents; and prostate cancer from exposure to pesticides, polyaromatic hydrocarbons (PAHs), and metal working fluids or mineral oils. In addition to NHL and prostate cancer, early findings from the National Institutes of Health Agricultural Health Study suggest that several additional cancers may be linked to a variety of pesticides. Our report also briefly describes the toxicological evidence related to the carcinogenic effect of specific chemicals and mechanisms that are difficult to study in humans, namely exposures to bis-phenol A and epigenetic, trans-generational effects. To underscore the multi-factorial, multi-stage nature of cancer, we also present a technical description of cancer causation summarizing current knowledge in molecular biology. We argue for a new cancer prevention paradigm, one based on an understanding that cancer is ultimately caused by multiple interacting factors rather than a paradigm based on dubious attributable fractions. This new cancer prevention paradigm demands that we limit exposure to avoidable environmental and occupational carcinogens, in combination with additional important risk factors like diet and lifestyle. The research literature related to environmental and occupational causes of cancer is constantly growing, and future updates will be carried out in light of new biological understanding of the mechanisms and new methods for studying exposures in human populations. The current state of knowledge is sufficient to compel us to act on what we know. We repeat the call of ecologist Sandra Steingraber: "From the right to know and the duty to inquire flows the obligation to act."
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PMID:Environmental and occupational causes of cancer: new evidence 2005-2007. 1855 96

Arsenic in drinking water is an established cause of lung, bladder, and skin cancers in adults and may also cause adult kidney and liver cancers. Some evidence for these effects originated from region II of Chile, which had a period of elevated arsenic levels in drinking water, in particular from 1958 to 1970. This unique exposure scenario provides a rare opportunity to investigate the effects of early-life arsenic exposure on childhood mortality; to our knowledge, this is the first study of childhood cancer mortality and high concentrations of arsenic in drinking water. In this article, we compare cancer mortality rates under the age of 20 in region II during 1950 to 2000 with those of unexposed region V, dividing subjects into those born before, during, or after the peak exposure period. Mortality from the most common childhood cancers, leukemia and brain cancer, was not increased in the exposed population. However, we found that childhood liver cancer mortality occurred at higher rates than expected. For those exposed as young children, liver cancer mortality between ages 0 and 19 was especially high: the relative risk (RR) for males born during this period was 8.9 [95% confidence interval (95% CI), 1.7-45.8; P = 0.009]; for females, the corresponding RR was 14.1 (95% CI, 1.6-126; P = 0.018); and for males and females pooled, the RR was 10.6 (95% CI, 2.9-39.2; P < 0.001). These findings suggest that exposure to arsenic in drinking water during early childhood may result in an increase in childhood liver cancer mortality.
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PMID:Increased childhood liver cancer mortality and arsenic in drinking water in northern Chile. 1870 88

Brain tumours are a diverse group of neoplasms that continue to present a formidable challenge in our attempt to achieve curable intervention. Our conceptual framework of human brain cancer has been redrawn in the current decade. There is a gathering acceptance that brain tumour formation is a phenotypic outcome of dysregulated neurogenesis, with tumours viewed as abnormally differentiated neural tissue. In relation, there is accumulating evidence that brain tumours, similar to leukaemia and many solid tumours, are organized as a developmental hierarchy which is maintained by a small fraction of cells endowed with many shared properties of tissue stem cells. Proof that neurogenesis persists throughout adult life, compliments this concept. Although the cancer cell of origin is unclear, the proliferative zones that harbour stem cells in the embryonic, post-natal and adult brain are attractive candidates within which tumour-initiation may ensue. Dysregulated, unlimited proliferation and an ability to bypass senescence are acquired capabilities of cancerous cells. These abilities in part require the establishment of a telomere maintenance mechanism for counteracting the shortening of chromosomal termini. A strategy based upon the synthesis of telomeric repeat sequences by the ribonucleoprotein telomerase, is prevalent in approximately 90% of human tumours studied, including the majority of brain tumours. This review will provide a developmental perspective with respect to normal (neurogenesis) and aberrant (tumourigenesis) cellular turnover, differentiation and function. Within this context our current knowledge of brain tumour telomere/telomerase biology will be discussed with respect to both its developmental and therapeutic relevance to the hierarchical model of brain tumourigenesis presented by the cancer stem cell paradigm.
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PMID:Cellular immortality in brain tumours: an integration of the cancer stem cell paradigm. 1941 2

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

To better understand premature mortality due to cancer, we estimated years of life lost (YLL) and average years of life lost (AYLL) due to cancer for the years 1995 and 2005, based on data from the Vital Statistic of Japan. In men, we identified a total of 159,623 cancer deaths in 1995 and 196,603 in 2005. Total YLL were 2,342,560.4 and 2,724,066.0 years, respectively. Averaged for all cancers, people died 14.7 years earlier than life expectancy in 1995 and 13.9 years in 2005. AYLL was longest for brain cancer deaths, at 26.3 years earlier than expected in 1995 and 22.8 years in 2005, followed by leukemia. In women, a total of 103,399 cancer deaths occurred in 1995 and 129,338 in 2005. Total YLL were 1,818,960.4 years in 1995 and 2,160,706.5 years in 2005, corresponding to AYLL for all cancer combined of 17.6 and 16.7 years. The AYLL of brain cancer deaths was also the longest, at 29.4 years in 1995 and 27.8 in 2005, followed by leukemia and female sex-related cancers. Results showed that cancer of the stomach, colorectum, liver and lung were the most frequent cancers in both sexes in both 1995 and 2005 and responsible for a remarkable number of YLL. Further, AYLL was greatest for brain cancer and leukemia in both sexes and for sex-related cancers in women, namely breast, cervix and ovarian cancer.
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PMID:Premature mortality due to cancer in Japan, 1995 and 2005. 1988 11

Everyone is exposed to electromagnetic fields (EMFs) from electricity (extremely low frequency, ELF), communication frequencies, and wireless devices (radiofrequency, RF). Concern of health hazards from EMFs has increased as the use of cell phones and other wireless devices has grown in all segments of society, especially among children. While there has been strong evidence for an association between leukemia and residential or occupational exposure to ELF EMFs for many years, the standards in existence are not sufficiently stringent to protect from an increased risk of cancer. For RF EMFs, standards are set at levels designed to avoid tissue heating, in spite of convincing evidence of adverse biological effects at intensities too low to cause significant heating. Recent studies demonstrate elevations in rates of brain cancer and acoustic neuroma only on the side of the head where individuals used their cell phone. Individuals who begin exposure at younger ages are more vulnerable. These data indicate that the existing standards for radiofrequency exposure are not adequate. While there are many unanswered questions, the cost of doing nothing will result in an increasing number of people, many of them young, developing cancer.
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PMID:Electromagnetic fields and cancer: the cost of doing nothing. 2042 63

Emissions from petrochemical industries may contain suspected or established carcinogens. As increased incidence of cancer in residential areas close to petrochemical industries has been reported in the literature, we conducted a study of cancer incidence in Stenungsund, Sweden, where petrochemical industries were established in the mid 1960s. A number of cancer cases in the central parts of Stenungsund were collected from the regional cancer registry for each year between 1974 and 2005. In addition to the total number of cases, the numbers of leukemia, lymphoma, liver cancer, lung cancer, and brain cancer were also collected. Expected numbers for each year were calculated based on age- and sex-specific incidence rates in reference areas. Levels of carcinogenic volatile hydrocarbons (VOC) were estimated from measurements and emission data. A dispersion model was used to classify Stenungsund into a "low" and "high" ethylene level area. Standardized Incidence Ratio (SIR) for all cancer for the entire period was 1.02 (95% CI 0.97-1.08). The occurrence of leukemia, lymphoma, and cancer in the central nervous system was slightly lower than expected for the entire period. SIR for lung cancer was 1.37 (95% CI 1.10-1.69), and SIR for liver cancer was 1.50 (0.82-2.53). VOC levels were low. Taking estimated exposure and demographic factors into account, our assessment is that occurrence of cancer was not affected by industrial emissions in any of the studied sites.
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PMID:Cancer incidence in a petrochemical industry area in Sweden. 2061 81

Tremendous progress in nanotechnology has lead to the development of nanometer-sized objects as medical implants or devices. Many of these nanodevices have recently been tested in many cancer diagnostic and therapeutic applications, such as leukemia, melanoma, breast tumor, prostate tumor, and brain cancer. Despite the increasing importance of nanotechnology in cancer, the potential of these nanodevices in diagnosing and treating intraocular cancers has not been systematically evaluated. This review summarizes the significant advancements and potential areas for development in the field of nanotechnology-based intraocular drug delivery and imaging.
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PMID:NANOTECHNOLOGY IN THE TREATMENT AND DETECTION OF INTRAOCULAR CANCERS. 2066 48


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