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Author |
Winklhofer, M. |
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Title |
An Avian Magnetometer |
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Journal Article |
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Year |
2012 |
Publication |
Science |
Abbreviated Journal |
Science |
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Volume |
336 |
Issue |
6084 |
Pages |
991-992 |
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Abstract |
Homing pigeons have remarkable navigational
skills that allow them to
fi nd their way back to the loft when
released from an unfamiliar location hundreds
of miles away. To perform such a feat,
they rely on various cues, such as odors and
Earth’s magnetic fi eld ( 1, 2). Yet, how birds
and other animals obtain magnetic-fi eld information
has been a mystery. On page 1054 of
this issue, Wu and Dickman ( 3) report how
this information is neurally encoded and suggest
a candidate magnetic sensory organ in
the inner ear of the pigeon ( 4). |
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0036-8075 |
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WP6 In vivo |
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CBM.UAM @ ccobaleda @ |
Serial |
188 |
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Enciso-Mora, V.; Hosking, F.J.; Sheridan, E.; Kinsey, S.E.; Lightfoot, T.; Roman, E.; Irving, J.A.; Tomlinson, I.P.; Allan, J.M.; Taylor, M.; Greaves, M.; Houlston, R.S. |
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Title |
Common genetic variation contributes significantly to the risk of childhood B-cell precursor acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2012 |
Publication |
Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K |
Abbreviated Journal |
Leukemia |
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Recent genome-wide association studies (GWAS) have provided the first unambiguous evidence that common genetic variation influences the risk of childhood B-cell precursor acute lymphoblastic leukemia (BCP-ALL), identifying risk single-nucleotide polymorphisms (SNPs) localizing to 7p12.2, 9p21.3, 10q21.2 and 14q11.2. The testing of SNPs individually for an association in GWA studies necessitates the imposition of a very stringent P-value to address the issue of multiple testing. While this reduces false positives, real associations may be missed and therefore any estimate of the total heritability will be negatively biased. Using GWAS data on 823 BCP-ALL cases by considering all typed SNPs simultaneously, we have calculated that 24% of the total variation in BCP-ALL risk is accounted for common genetic variation (95% confidence interval 6-42%). Our findings provide support for a polygenic basis for susceptibility to BCP-ALL and have wider implications for future searches for novel disease-causing risk variants.Leukemia advance online publication, 24 April 2012; doi:10.1038/leu.2012.89. |
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Division of Genetics and Epidemiology, Institute of Cancer Research, Sutton, UK |
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0887-6924 |
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WP6 In vivo |
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PMID:22456626 |
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CBM.UAM @ ccobaleda @ |
Serial |
189 |
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Author |
Pui, C.-H.; Mullighan, C.G.; Evans, W.E.; Relling, M.V. |
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Title |
Pediatric acute lymphoblastic leukemia: where are we going and how do we get there? |
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Journal Article |
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Year |
2012 |
Publication |
Blood |
Abbreviated Journal |
Blood |
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Improved supportive care, more precise risk stratification, and personalized chemotherapy based on the characteristics of leukemic cells and hosts (e.g., pharmacokinetics and pharmacogenetics) have pushed the cure rate of childhood acute lymphoblastic leukemia to near 90%. Further increase in cure rate can be expected from the discovery of additional recurrent molecular lesions, coupled with the development of novel targeted treatment through high-throughput genomics and innovative drug-screening systems. We discuss specific areas of research that promise to further refine current treatment and to improve the cure rate and quality of life of the patients. |
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Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN, United States |
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ISSN |
0006-4971 |
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WP6 In vivo |
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Notes |
PMID:22730540 |
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no |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
190 |
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Author |
Kinlen, L.J. |
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Title |
An examination, with a meta-analysis, of studies of childhood leukaemia in relation to population mixing |
Type |
Journal Article |
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Year |
2012 |
Publication |
British Journal of Cancer |
Abbreviated Journal |
Br J Cancer |
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Volume |
107 |
Issue |
7 |
Pages |
1163-1168 |
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Abstract |
BACKGROUND: Marked influxes of people into rural areas, termed rural population mixing (PM), have been associated with excesses of
childhood leukaemia (CL), consistent with mini-epidemics of a mainly immunising, subclinical infection to which CL is a rare response.
For such situations of rural PM would promote contacts between infected and susceptible individuals, the latter tending to have a
higher than average prevalence in rural or isolated areas. Confusion has arisen from some workers applying the term PM to non-rural
situations lacking known recent change.
METHODS: Available PM studies using the original definition of influxes were examined, a meta-analysis carried out of studies of CL in
relation to exposure to high levels of rural PM, and also a detailed analysis by age group.
RESULTS: The meta-analysis of 17 studies shows a significant CL excess in association with rural PM: overall relative risk (RR) at ages
0–14: 1.57; 95% confidence interval 1.44–1.72; at 0–4 years 1.72 (1.54–1.91). This contrasts with the absence of an excess of CL in
similarly exposed urban areas (RR 1.00; 0.93–1.07), pointing to a high level of immunity there. The mixed results of studies using
other definitions of PM were summarised. The excess associated with rural PM below age 2 years (RR 1.51; 1.17, 1.92) was not
appreciably different from that at later childhood ages.
CONCLUSION: Much of the inconsistency among studies ostensibly about CL and PM reflects the use of definitions other than that
originally proposed. The broad similarity of the CL excess below age 2 with that at older childhood ages is inconsistent with the
Greaves’ delayed infection hypothesis, since any infection underlying the former is difficult to consider as delayed. |
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ISSN |
0007-0920 |
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Area |
WP9 Epidemiology |
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CBM.UAM @ ccobaleda @ |
Serial |
191 |
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Author |
Geng, H.; Brennan, S.; Milne, T.A.; Chen, W.-Y.; Li, Y.; Hurtz, C.; Kweon, S.-M.; Zickl, L.; Shojaee, S.; Neuberg, D.; Huang, C.; Biswas, D.; Xin, Y.; Racevskis, J.; Ketterling, R.P.; Luger, S.M.; Lazarus, H.; Tallman, M.S.; Rowe, J.M.; Litzow, M.R.; Guzman, M.L.; Allis, C.D.; Roeder, R.G.; Muschen, M.; Paietta, E.; Elemento, O.; Melnick, A.M. |
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Title |
Integrative Epigenomic Analysis Identifies Biomarkers and Therapeutic Targets in Adult B-Acute Lymphoblastic Leukemia |
Type |
Journal Article |
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Year |
2012 |
Publication |
Cancer Discovery |
Abbreviated Journal |
Cancer Discov |
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Volume |
2 |
Issue |
11 |
Pages |
1004-1023 |
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Abstract |
Genetic lesions such as BCR-ABL1, E2A-PBX1, and MLL rearrangements (MLLr) are associated with unfavorable outcomes in adult B-cell precursor acute lymphoblastic leukemia (B-ALL). Leukemia oncoproteins may directly or indirectly disrupt cytosine methylation patterning to mediate the malignant phenotype. We postulated that DNA methylation signatures in these aggressive B-ALLs would point toward disease mechanisms and useful biomarkers and therapeutic targets. We therefore conducted DNA methylation and gene expression profiling on a cohort of 215 adult patients with B-ALL enrolled in a single phase III clinical trial (ECOG E2993) and normal control B cells. In BCR-ABL1-positive B-ALLs, aberrant cytosine methylation patterning centered around a cytokine network defined by hypomethylation and overexpression of IL2RA(CD25). The E2993 trial clinical data showed that CD25 expression was strongly associated with a poor outcome in patients with ALL regardless of BCR-ABL1 status, suggesting CD25 as a novel prognostic biomarker for risk stratification in B-ALLs. In E2A-PBX1-positive B-ALLs, aberrant DNA methylation patterning was strongly associated with direct fusion protein binding as shown by the E2A-PBX1 chromatin immunoprecipitation (ChIP) sequencing (ChIP-seq), suggesting that E2A-PBX1 fusion protein directly remodels the epigenome to impose an aggressive B-ALL phenotype. MLLr B-ALL featured prominent cytosine hypomethylation, which was linked with MLL fusion protein binding, H3K79 dimethylation, and transcriptional upregulation, affecting a set of known and newly identified MLL fusion direct targets with oncogenic activity such as FLT3 and BCL6. Notably, BCL6 blockade or loss of function suppressed proliferation and survival of MLLr leukemia cells, suggesting BCL6-targeted therapy as a new therapeutic strategy for MLLr B-ALLs. |
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Address |
1Department of Medicine/Hematology-Oncology Division, 2Institute for Computational Biomedicine, Weill Medical College of Cornell University; 3Laboratory of Chromatin Biology and Epigenetics, 4Laboratory of Biochemistry and Molecular Biology, the Rockefeller University; 5Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York; 6Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, New York; 7Children's Hospital Los Angeles, University of Southern California, Los Angeles; 8Department of Laboratory Medicine, University of California San Francisco, San Francisco, California; 9Dana Farber Cancer Institute, Boston, Massachusetts; 10MRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Headington, Oxford, United Kingdom; 11Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota; 12Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania; 13Department of Hematology and BMT, Rambam Medical Center, Haifa, Israel; 14Department of Medicine, Case Western Reserve University, Cleveland, Ohio; and 15Max Planck Institute for Immunobiology, Freiburg, Germany |
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ISSN |
2159-8274 |
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Notes |
PMID:23107779 |
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Call Number |
CBM.UAM @ ccobaleda @ |
Serial |
214 |
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