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  • 1
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    Molecular classification of cancer: class discovery and class prediction by gene expression monitoring (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-10-16
    Description: Although cancer classification has improved over the past 30 years, there has been no general approach for identifying new cancer classes (class discovery) or for assigning tumors to known classes (class prediction). Here, a generic approach to cancer classification based on gene expression monitoring by DNA microarrays is described and applied to human acute leukemias as a test case. A class discovery procedure automatically discovered the distinction between acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) without previous knowledge of these classes. An automatically derived class predictor was able to determine the class of new leukemia cases. The results demonstrate the feasibility of cancer classification based solely on gene expression monitoring and suggest a general strategy for discovering and predicting cancer classes for other types of cancer, independent of previous biological knowledge.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golub, T R -- Slonim, D K -- Tamayo, P -- Huard, C -- Gaasenbeek, M -- Mesirov, J P -- Coller, H -- Loh, M L -- Downing, J R -- Caligiuri, M A -- Bloomfield, C D -- Lander, E S -- New York, N.Y. -- Science. 1999 Oct 15;286(5439):531-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute/Massachusetts Institute of Technology Center for Genome Research, Cambridge, MA 02139, USA. golub@genome.wi.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10521349" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cell Adhesion/genetics ; Cell Cycle/genetics ; *Gene Expression Profiling ; Homeodomain Proteins/genetics ; Humans ; Leukemia, Myeloid/*classification/drug therapy/*genetics ; Neoplasm Proteins/genetics ; Neoplasms/classification/genetics ; Oligonucleotide Array Sequence Analysis ; Oncogenes ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*classification/drug ; therapy/*genetics ; Predictive Value of Tests ; Reproducibility of Results ; Treatment Outcome
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Identification of RPS14 as a 5q- syndrome gene by RNA interference screen (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-01-19
    Description: Somatic chromosomal deletions in cancer are thought to indicate the location of tumour suppressor genes, by which a complete loss of gene function occurs through biallelic deletion, point mutation or epigenetic silencing, thus fulfilling Knudson's two-hit hypothesis. In many recurrent deletions, however, such biallelic inactivation has not been found. One prominent example is the 5q- syndrome, a subtype of myelodysplastic syndrome characterized by a defect in erythroid differentiation. Here we describe an RNA-mediated interference (RNAi)-based approach to discovery of the 5q- disease gene. We found that partial loss of function of the ribosomal subunit protein RPS14 phenocopies the disease in normal haematopoietic progenitor cells, and also that forced expression of RPS14 rescues the disease phenotype in patient-derived bone marrow cells. In addition, we identified a block in the processing of pre-ribosomal RNA in RPS14-deficient cells that is functionally equivalent to the defect in Diamond-Blackfan anaemia, linking the molecular pathophysiology of the 5q- syndrome to a congenital syndrome causing bone marrow failure. These results indicate that the 5q- syndrome is caused by a defect in ribosomal protein function and suggest that RNAi screening is an effective strategy for identifying causal haploinsufficiency disease genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3771855/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3771855/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebert, Benjamin L -- Pretz, Jennifer -- Bosco, Jocelyn -- Chang, Cindy Y -- Tamayo, Pablo -- Galili, Naomi -- Raza, Azra -- Root, David E -- Attar, Eyal -- Ellis, Steven R -- Golub, Todd R -- R01 HL082945/HL/NHLBI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Jan 17;451(7176):335-9. doi: 10.1038/nature06494.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18202658" target="_blank"〉PubMed〈/a〉
    Keywords: Anemia, Diamond-Blackfan/genetics/physiopathology ; Cell Differentiation ; Cells, Cultured ; Chromosome Deletion ; Chromosomes, Human, Pair 5/*genetics ; Erythroid Cells/cytology/metabolism ; Genetic Linkage/*genetics ; Genetic Predisposition to Disease/*genetics ; Hematopoietic Stem Cells/metabolism ; Humans ; Phenotype ; *RNA Interference ; RNA Precursors/genetics/metabolism ; RNA, Ribosomal/genetics/metabolism ; RNA, Ribosomal, 18S/genetics ; Ribosomal Proteins/deficiency/*genetics/metabolism ; Ribosomes/chemistry/genetics/metabolism ; Syndrome
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    CDK8 is a colorectal cancer oncogene that regulates beta-catenin activity (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-09-17
    Description: Aberrant activation of the canonical WNT/beta-catenin pathway occurs in almost all colorectal cancers and contributes to their growth, invasion and survival. Although dysregulated beta-catenin activity drives colon tumorigenesis, further genetic perturbations are required to elaborate full malignant transformation. To identify genes that both modulate beta-catenin activity and are essential for colon cancer cell proliferation, we conducted two loss-of-function screens in human colon cancer cells and compared genes identified in these screens with an analysis of copy number alterations in colon cancer specimens. One of these genes, CDK8, which encodes a member of the mediator complex, is located at 13q12.13, a region of recurrent copy number gain in a substantial fraction of colon cancers. Here we show that the suppression of CDK8 expression inhibits proliferation in colon cancer cells characterized by high levels of CDK8 and beta-catenin hyperactivity. CDK8 kinase activity was necessary for beta-catenin-driven transformation and for expression of several beta-catenin transcriptional targets. Together these observations suggest that therapeutic interventions targeting CDK8 may confer a clinical benefit in beta-catenin-driven malignancies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587138/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2587138/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Firestein, Ron -- Bass, Adam J -- Kim, So Young -- Dunn, Ian F -- Silver, Serena J -- Guney, Isil -- Freed, Ellen -- Ligon, Azra H -- Vena, Natalie -- Ogino, Shuji -- Chheda, Milan G -- Tamayo, Pablo -- Finn, Stephen -- Shrestha, Yashaswi -- Boehm, Jesse S -- Jain, Supriya -- Bojarski, Emeric -- Mermel, Craig -- Barretina, Jordi -- Chan, Jennifer A -- Baselga, Jose -- Tabernero, Josep -- Root, David E -- Fuchs, Charles S -- Loda, Massimo -- Shivdasani, Ramesh A -- Meyerson, Matthew -- Hahn, William C -- K08 CA134931/CA/NCI NIH HHS/ -- P50CA127003/CA/NCI NIH HHS/ -- R33 CA128625/CA/NCI NIH HHS/ -- R33 CA128625-01A1/CA/NCI NIH HHS/ -- R33CA128625/CA/NCI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Sep 25;455(7212):547-51. doi: 10.1038/nature07179. Epub 2008 Sep 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18794900" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic ; Colorectal Neoplasms/*genetics/*metabolism/pathology ; Cyclin-Dependent Kinase 8 ; Cyclin-Dependent Kinases/deficiency/*genetics/*metabolism ; Gene Dosage ; *Gene Expression Regulation, Neoplastic ; Humans ; Oncogene Proteins/deficiency/genetics/metabolism ; *Oncogenes ; RNA Interference ; Transcription, Genetic ; beta Catenin/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1 (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-10-23
    Description: The proto-oncogene KRAS is mutated in a wide array of human cancers, most of which are aggressive and respond poorly to standard therapies. Although the identification of specific oncogenes has led to the development of clinically effective, molecularly targeted therapies in some cases, KRAS has remained refractory to this approach. A complementary strategy for targeting KRAS is to identify gene products that, when inhibited, result in cell death only in the presence of an oncogenic allele. Here we have used systematic RNA interference to detect synthetic lethal partners of oncogenic KRAS and found that the non-canonical IkappaB kinase TBK1 was selectively essential in cells that contain mutant KRAS. Suppression of TBK1 induced apoptosis specifically in human cancer cell lines that depend on oncogenic KRAS expression. In these cells, TBK1 activated NF-kappaB anti-apoptotic signals involving c-Rel and BCL-XL (also known as BCL2L1) that were essential for survival, providing mechanistic insights into this synthetic lethal interaction. These observations indicate that TBK1 and NF-kappaB signalling are essential in KRAS mutant tumours, and establish a general approach for the rational identification of co-dependent pathways in cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783335/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2783335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barbie, David A -- Tamayo, Pablo -- Boehm, Jesse S -- Kim, So Young -- Moody, Susan E -- Dunn, Ian F -- Schinzel, Anna C -- Sandy, Peter -- Meylan, Etienne -- Scholl, Claudia -- Frohling, Stefan -- Chan, Edmond M -- Sos, Martin L -- Michel, Kathrin -- Mermel, Craig -- Silver, Serena J -- Weir, Barbara A -- Reiling, Jan H -- Sheng, Qing -- Gupta, Piyush B -- Wadlow, Raymond C -- Le, Hanh -- Hoersch, Sebastian -- Wittner, Ben S -- Ramaswamy, Sridhar -- Livingston, David M -- Sabatini, David M -- Meyerson, Matthew -- Thomas, Roman K -- Lander, Eric S -- Mesirov, Jill P -- Root, David E -- Gilliland, D Gary -- Jacks, Tyler -- Hahn, William C -- R01 CA129105/CA/NCI NIH HHS/ -- R01 CA129105-03/CA/NCI NIH HHS/ -- R01 CA130988/CA/NCI NIH HHS/ -- R01 CA130988-01A2/CA/NCI NIH HHS/ -- R33 CA128625/CA/NCI NIH HHS/ -- R33 CA128625-01A1/CA/NCI NIH HHS/ -- R33 CA128625-02/CA/NCI NIH HHS/ -- T32 CA009172/CA/NCI NIH HHS/ -- T32 CA09172-33/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2009 Nov 5;462(7269):108-12. doi: 10.1038/nature08460. Epub 2009 Oct 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115 USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19847166" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Apoptosis ; Cell Line, Tumor ; Cell Survival ; Gene Expression Profiling ; Genes, Lethal ; Genes, ras/*genetics ; Humans ; Lung Neoplasms/genetics/metabolism/pathology ; Neoplasms/genetics/metabolism/pathology ; Oncogene Protein p21(ras)/*genetics/*metabolism ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins c-rel/metabolism ; *RNA Interference ; Signal Transduction ; bcl-X Protein/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Medulloblastoma exome sequencing uncovers subtype-specific somatic mutations (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-07-24
    Description: Medulloblastomas are the most common malignant brain tumours in children. Identifying and understanding the genetic events that drive these tumours is critical for the development of more effective diagnostic, prognostic and therapeutic strategies. Recently, our group and others described distinct molecular subtypes of medulloblastoma on the basis of transcriptional and copy number profiles. Here we use whole-exome hybrid capture and deep sequencing to identify somatic mutations across the coding regions of 92 primary medulloblastoma/normal pairs. Overall, medulloblastomas have low mutation rates consistent with other paediatric tumours, with a median of 0.35 non-silent mutations per megabase. We identified twelve genes mutated at statistically significant frequencies, including previously known mutated genes in medulloblastoma such as CTNNB1, PTCH1, MLL2, SMARCA4 and TP53. Recurrent somatic mutations were newly identified in an RNA helicase gene, DDX3X, often concurrent with CTNNB1 mutations, and in the nuclear co-repressor (N-CoR) complex genes GPS2, BCOR and LDB1. We show that mutant DDX3X potentiates transactivation of a TCF promoter and enhances cell viability in combination with mutant, but not wild-type, beta-catenin. Together, our study reveals the alteration of WNT, hedgehog, histone methyltransferase and now N-CoR pathways across medulloblastomas and within specific subtypes of this disease, and nominates the RNA helicase DDX3X as a component of pathogenic beta-catenin signalling in medulloblastoma.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413789/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3413789/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pugh, Trevor J -- Weeraratne, Shyamal Dilhan -- Archer, Tenley C -- Pomeranz Krummel, Daniel A -- Auclair, Daniel -- Bochicchio, James -- Carneiro, Mauricio O -- Carter, Scott L -- Cibulskis, Kristian -- Erlich, Rachel L -- Greulich, Heidi -- Lawrence, Michael S -- Lennon, Niall J -- McKenna, Aaron -- Meldrim, James -- Ramos, Alex H -- Ross, Michael G -- Russ, Carsten -- Shefler, Erica -- Sivachenko, Andrey -- Sogoloff, Brian -- Stojanov, Petar -- Tamayo, Pablo -- Mesirov, Jill P -- Amani, Vladimir -- Teider, Natalia -- Sengupta, Soma -- Francois, Jessica Pierre -- Northcott, Paul A -- Taylor, Michael D -- Yu, Furong -- Crabtree, Gerald R -- Kautzman, Amanda G -- Gabriel, Stacey B -- Getz, Gad -- Jager, Natalie -- Jones, David T W -- Lichter, Peter -- Pfister, Stefan M -- Roberts, Thomas M -- Meyerson, Matthew -- Pomeroy, Scott L -- Cho, Yoon-Jae -- CA050661/CA/NCI NIH HHS/ -- L40 NS063706/NS/NINDS NIH HHS/ -- P30 HD018655/HD/NICHD NIH HHS/ -- P30 HD18655/HD/NICHD NIH HHS/ -- R01 CA030002/CA/NCI NIH HHS/ -- R01 CA105607/CA/NCI NIH HHS/ -- R01 CA109467/CA/NCI NIH HHS/ -- R01 CA148699/CA/NCI NIH HHS/ -- R01 CA154480/CA/NCI NIH HHS/ -- R01 NS046789/NS/NINDS NIH HHS/ -- R01CA105607/CA/NCI NIH HHS/ -- R01CA109467/CA/NCI NIH HHS/ -- R01CA148699/CA/NCI NIH HHS/ -- R25 NS070682/NS/NINDS NIH HHS/ -- R25NS070682/NS/NINDS NIH HHS/ -- U54 HG003067/HG/NHGRI NIH HHS/ -- U54HG003067/HG/NHGRI NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Aug 2;488(7409):106-10. doi: 10.1038/nature11329.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22820256" target="_blank"〉PubMed〈/a〉
    Keywords: Cerebellar Neoplasms/classification/*genetics ; Child ; DEAD-box RNA Helicases/chemistry/genetics/metabolism ; DNA Helicases/chemistry/genetics ; DNA-Binding Proteins/genetics ; Exome/*genetics ; Genome, Human/*genetics ; Hedgehog Proteins/metabolism ; Histone-Lysine N-Methyltransferase/genetics/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; LIM Domain Proteins/genetics ; Medulloblastoma/classification/*genetics ; Models, Molecular ; Mutation/*genetics ; Neoplasm Proteins/genetics ; Nuclear Proteins/chemistry/genetics ; Promoter Regions, Genetic/genetics ; Protein Structure, Tertiary/genetics ; Proto-Oncogene Proteins/genetics ; Receptors, Cell Surface/genetics ; Repressor Proteins/genetics ; Signal Transduction ; TCF Transcription Factors/metabolism ; Transcription Factors/chemistry/genetics ; Tumor Suppressor Protein p53/genetics ; Wnt Proteins/metabolism ; beta Catenin/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
    Electronic Resource
    Electronic Resource
    Single cluster dynamics for the infinite range O(n) model
    Amsterdam : Elsevier
    Physica A: Statistical Mechanics and its Applications 203 (1994), S. 331-346 
    Details
    ISSN: 0378-4371
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0378-4371(94)90002-7
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  • 7
    Electronic Resource
    Electronic Resource
    Magnetization relaxation to equilibrium on large 2D Swendsen-Wang Ising models
    Amsterdam : Elsevier
    Physica A: Statistical Mechanics and its Applications 201 (1993), S. 543-546 
    Details
    ISSN: 0378-4371
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0378-4371(93)90126-O
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  • 8
    Electronic Resource
    Electronic Resource
    Virtual bond percolation for Ising cluster dynamics
    Amsterdam : Elsevier
    Physica A: Statistical Mechanics and its Applications 193 (1993), S. 314-331 
    Details
    ISSN: 0378-4371
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0378-4371(93)90478-M
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  • 9
    Electronic Resource
    Electronic Resource
    Embedded dynamics for lattice field theory
    Amsterdam : Elsevier
    Nuclear Physics B (Proceedings Supplements) 9 (1989), S. 507-511 
    Details
    ISSN: 0920-5632
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0920-5632(89)90151-5
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  • 10
    Electronic Resource
    Electronic Resource
    Distinct physiological states of Plasmodium falciparum in malaria-infected patients (2007)
    [s.l.] : Nature Publishing Group
    Nature 450 (2007), S. 1091-1095 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Infection with the malaria parasite Plasmodium falciparum leads to widely different clinical conditions in children, ranging from mild flu-like symptoms to coma and death. Despite the immense medical implications, the genetic and molecular basis of this diversity remains largely unknown. ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature06311
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