Author
Karen W. Makar
Other affiliations: University of Washington, Fred Hutchinson Cancer Research Center
Bio: Karen W. Makar is an academic researcher from Bill & Melinda Gates Foundation. The author has contributed to research in topics: Colorectal cancer & Cancer. The author has an hindex of 32, co-authored 83 publications receiving 4267 citations. Previous affiliations of Karen W. Makar include University of Washington & Fred Hutchinson Cancer Research Center.
Papers
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TL;DR: It is concluded that Dnmt1 and DNA methylation are required for the proper expression of certain genes that define fate and determine function in T cells.
1,133 citations
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Fred Hutchinson Cancer Research Center1, University of Washington2, University of Southern California3, University of North Carolina at Chapel Hill4, National Institutes of Health5, University of Nantes6, German Cancer Research Center7, Kaiser Permanente8, American Cancer Society9, Harvard University10, University of Chicago11, Translational Genomics Research Institute12, Vanderbilt University13, University of Toronto14, New York University15, University of Melbourne16, Ontario Institute for Cancer Research17, Ohio State University18, Yonsei University19, Sun Yat-sen University20, University of Hawaii at Manoa21, Mayo Clinic22, Massey University23, Yeshiva University24, University of Pittsburgh25, University of Utah26, Fudan University27, University of Ottawa28
TL;DR: In a large genome-wide association study, polymorphisms close to nucleic acid binding protein 1 (which encodes a DNA-binding protein involved in DNA repair) with colorectal tumor risk and polymorphisms in laminin gamma 1, cyclin D2, and T-box 3 are associated.
314 citations
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267 citations
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TL;DR: Kirsten Ras (KRAS)-mutated CRC was associated with statistically significantly poorer survival after diagnosis than KRAS-wild-type CRC and patterns were similar for overall survival.
Abstract: KRAS- mutation status in relation to colorectal cancer survival: the joint impact of correlated tumour markers
207 citations
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Fred Hutchinson Cancer Research Center1, University of Washington2, University of Southern California3, University Health Network4, Ottawa Hospital Research Institute5, Ontario Institute for Cancer Research6, Translational Genomics Research Institute7, Harvard University8, University of Chicago9, University of Michigan10, German Cancer Research Center11, Memorial University of Newfoundland12, Ohio State University13, Kaiser Permanente14, New York University15, National Institutes of Health16, University of Pittsburgh17, University of Nantes18, University of Utah19, University of Melbourne20, University of Hawaii at Manoa21, Mayo Clinic22, University of Toronto23
TL;DR: The study suggests a complex nature of the contribution of common genetic variants to risk for colorectal cancer and selected the most statistically significant single nucleotide polymorphisms for replication using ten independent studies.
Abstract: Colorectal cancer is the second leading cause of cancer death in developed countries. Genome-wide association studies (GWAS) have successfully identified novel susceptibility loci for colorectal cancer. To follow up on these findings, and try to identify novel colorectal cancer susceptibility loci, we present results for GWAS of colorectal cancer (2,906 cases, 3,416 controls) that have not previously published main associations. Specifically, we calculated odds ratios and 95% confidence intervals using log-additive models for each study. In order to improve our power to detect novel colorectal cancer susceptibility loci, we performed a meta-analysis combining the results across studies. We selected the most statistically significant single nucleotide polymorphisms (SNPs) for replication using ten independent studies (8,161 cases and 9,101 controls). We again used a meta-analysis to summarize results for the replication studies alone, and for a combined analysis of GWAS and replication studies. We measured ten SNPs previously identified in colorectal cancer susceptibility loci and found eight to be associated with colorectal cancer (p value range 0.02 to 1.8 × 10(-8)). When we excluded studies that have previously published on these SNPs, five SNPs remained significant at p < 0.05 in the combined analysis. No novel susceptibility loci were significant in the replication study after adjustment for multiple testing, and none reached genome-wide significance from a combined analysis of GWAS and replication. We observed marginally significant evidence for a second independent SNP in the BMP2 region at chromosomal location 20p12 (rs4813802; replication p value 0.03; combined p value 7.3 × 10(-5)). In a region on 5p33.15, which includes the coding regions of the TERT-CLPTM1L genes and has been identified in GWAS to be associated with susceptibility to at least seven other cancers, we observed a marginally significant association with rs2853668 (replication p value 0.03; combined p value 1.9 × 10(-4)). Our study suggests a complex nature of the contribution of common genetic variants to risk for colorectal cancer.
200 citations
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TL;DR: This review summarizes the discovery, functions, and relationships among Th cells; the cytokine and signaling requirements for their development; the networks of transcription factors involved in their differentiation; the epigenetic regulation of their key cytokines and transcription factors; and human diseases involving defective CD4 T cell differentiation.
Abstract: CD4 T cells play critical roles in mediating adaptive immunity to a variety of pathogens. They are also involved in autoimmunity, asthma, and allergic responses as well as in tumor immunity. During TCR activation in a particular cytokine milieu, naive CD4 T cells may differentiate into one of several lineages of T helper (Th) cells, including Th1, Th2, Th17, and iTreg, as defined by their pattern of cytokine production and function. In this review, we summarize the discovery, functions, and relationships among Th cells; the cytokine and signaling requirements for their development; the networks of transcription factors involved in their differentiation; the epigenetic regulation of their key cytokines and transcription factors; and human diseases involving defective CD4 T cell differentiation.
2,978 citations
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TL;DR: Recent progress on drug metabolism activity profiles, interindividual variability and regulation of expression, and the functional and clinical impact of genetic variation in drug metabolizing P450s are reviewed.
2,832 citations
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TL;DR: Key concepts in the function of DNA methylation in mammals are discussed, stemming from more than two decades of research, including many recent studies that have elucidated when and whereDNA methylation has a regulatory role in the genome.
Abstract: DNA methylation is among the best studied epigenetic modifications and is essential to mammalian development. Although the methylation status of most CpG dinucleotides in the genome is stably propagated through mitosis, improvements to methods for measuring methylation have identified numerous regions in which it is dynamically regulated. In this Review, we discuss key concepts in the function of DNA methylation in mammals, stemming from more than two decades of research, including many recent studies that have elucidated when and where DNA methylation has a regulatory role in the genome. We include insights from early development, embryonic stem cells and adult lineages, particularly haematopoiesis, to highlight the general features of this modification as it participates in both global and localized epigenetic regulation.
2,550 citations
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TL;DR: The role of DNA methylation in controlling gene expression is illuminated and its links with histone modification and chromatin remodelling are strengthened, and the mechanisms by which it is targeted to specific regions of the genome are understood.
2,418 citations
01 Apr 2012
TL;DR: International experts in cancer prevention analyse global research on diet nutrition physical activity cancer and make public health policy recommendations, the fractions of cancer attributable to potentially modifiable factors are analyzed.
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2,202 citations