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  1. AU="Albacker, L"
  2. AU="Rupp, Adam"
  3. AU=Chia Helena N
  4. AU="Agostini, Ludovico"
  5. AU="Vieira, Dorice"
  6. AU="Sharma, Arya M"
  7. AU="Lieve E. H. van der Donk"
  8. AU="Großer, Matthias"
  9. AU="Ong, Edison"
  10. AU=Lavery James V
  11. AU=Moss Arthur J
  12. AU="Ni, Dongchun"
  13. AU="Yang, Yanfan"
  14. AU="Shona Manning"
  15. AU=Charters Pia F P AU=Charters Pia F P
  16. AU="Adumuah, Naa N"
  17. AU="Rodrigues, Jonathan Carl Luis"
  18. AU=Seidel Bastian M
  19. AU="Duan Weimin"
  20. AU=Ioanas M
  21. AU="Nancy Zambon"
  22. AU="Kumawat, Sunita"
  23. AU=Bogliacino Francesco
  24. AU="Setter, Peter"
  25. AU=Shikata Chihiro
  26. AU="Jordan P. Metcalf"
  27. AU=Peri?i? Nanut Milica AU=Peri?i? Nanut Milica
  28. AU="Pramod, Ganapathiraju"
  29. AU="Fu, Chu-Jun"
  30. AU="Nejad, Harry G."
  31. AU="Zhang, Q E"
  32. AU="Oppenheim, Madeline"

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  1. Artikel ; Online: Real-world prevalence across 159 872 patients with cancer supports the clinical utility of TMB-H to define metastatic solid tumors for treatment with pembrolizumab.

    Fabrizio, D / Cristescu, R / Albacker, L / Snyder, A / Ward, A / Lunceford, J / Aurora-Garg, D / Jin, F / Hopkins, J / Rubin, E / Hegde, P

    Annals of oncology : official journal of the European Society for Medical Oncology

    2021  Band 32, Heft 9, Seite(n) 1193–1194

    Mesh-Begriff(e) Antibodies, Monoclonal, Humanized ; Humans ; Neoplasms/drug therapy ; Neoplasms/epidemiology ; Prevalence
    Chemische Substanzen Antibodies, Monoclonal, Humanized ; pembrolizumab (DPT0O3T46P)
    Sprache Englisch
    Erscheinungsdatum 2021-05-31
    Erscheinungsland England
    Dokumenttyp Letter ; Comment
    ZDB-ID 1025984-3
    ISSN 1569-8041 ; 0923-7534
    ISSN (online) 1569-8041
    ISSN 0923-7534
    DOI 10.1016/j.annonc.2021.05.805
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Phosphatidylinositol 3-kinase pathway genomic alterations in 60,991 diverse solid tumors informs targeted therapy opportunities.

    Millis, Sherri Z / Jardim, Denis L / Albacker, Lee / Ross, Jeffrey S / Miller, Vincent A / Ali, Siraj M / Kurzrock, Razelle

    Cancer

    2018  Band 125, Heft 7, Seite(n) 1185–1199

    Abstract: Background: The phosphatidylinositol 3-kinase (PI3K) pathway is frequently altered in cancer. This report describes the landscape of PI3K alterations in solid tumors as well as co-alterations serving as potential resistance/attenuation mechanisms.: ... ...

    Abstract Background: The phosphatidylinositol 3-kinase (PI3K) pathway is frequently altered in cancer. This report describes the landscape of PI3K alterations in solid tumors as well as co-alterations serving as potential resistance/attenuation mechanisms.
    Methods: Consecutive samples were analyzed in a commercial Clinical Laboratory Improvement Amendment-certified laboratory using comprehensive genomic profiling performed by next-generation sequencing (315 genes). The co-alterations evaluated included the Erb-B2 receptor tyrosine kinase 2 (ERBB2), ERBB3, ERBB4, RAS, MET proto-oncogene tyrosine kinase (MET), and mitogen-activated protein kinase kinase (MAP2K) genes as well as tumor protein 53 (TP53), estrogen receptor 1 (ESR1), and androgen receptor (AR).
    Results: Alterations in any of 18 PI3K-pathway associated genes were identified in 44% of 60,991 tumors. Although single base and insertions/deletions (indels) were the most frequent alterations, copy number changes and rearrangements were identified in 11% and 0.9% of patients, respectively. Overall, the most frequently altered genes were PIK3 catalytic subunit α (PIK3CA) (13%), phosphatase and tensin homolog (PTEN) (9%), and serine/threonine kinase 11 (STK11) (5%). Tumor types that frequently harbored at least 1 PI3K alteration were uterine (77%), cervical (62%), anal (59%), and breast (58%) cancers. Alterations also were discerned frequently in tumors with carcinosarcoma (89%) and squamous cell carcinoma (62%) histologies. Tumors with a greater likelihood of co-occurring PI3K pathway and MAPK pathway alterations included colorectal cancers (odds ratio [OR], 1.64; P < .001), mesotheliomas (OR, 2.67; P = .024), anal cancers (OR, 1.98; P = .03), and nonsquamous head and neck cancers (OR, 2.03; P = .019). The co-occurrence of ESR1 and/or AR alterations with PI3K alterations was statistically significant in bladder, colorectal, uterine, prostate, and unknown primary cancers.
    Conclusions: Comprehensive genomic profiling reveals altered PI3K-related genes in 44% of solid malignancies, including rare disease and histology types. The frequency of alterations and the co-occurrence of resistance pathways vary by tumor type, directly affecting opportunities for targeted therapy.
    Mesh-Begriff(e) Class I Phosphatidylinositol 3-Kinases/genetics ; Estrogen Receptor alpha/genetics ; F-Box-WD Repeat-Containing Protein 7/genetics ; Female ; Genes, erbB/genetics ; Humans ; Male ; Mitogen-Activated Protein Kinase Kinases/genetics ; Molecular Targeted Therapy ; Neoplasms/genetics ; Neoplasms/pathology ; Odds Ratio ; PTEN Phosphohydrolase/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Protein-Serine-Threonine Kinases/genetics ; Proto-Oncogene Proteins c-met/genetics ; Receptors, Androgen/genetics ; Signal Transduction/genetics ; Tumor Suppressor Protein p53/genetics ; ras Proteins/genetics
    Chemische Substanzen AR protein, human ; ESR1 protein, human ; Estrogen Receptor alpha ; F-Box-WD Repeat-Containing Protein 7 ; FBXW7 protein, human ; Receptors, Androgen ; TP53 protein, human ; Tumor Suppressor Protein p53 ; STK11 protein, human (EC 2.7.1.-) ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CA protein, human (EC 2.7.1.137) ; MET protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67) ; ras Proteins (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2018-12-24
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1429-1
    ISSN 1097-0142 ; 0008-543X ; 1934-662X
    ISSN (online) 1097-0142
    ISSN 0008-543X ; 1934-662X
    DOI 10.1002/cncr.31921
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Checkpoint inhibitor is active against large cell neuroendocrine carcinoma with high tumor mutation burden.

    Wang, Victoria E / Urisman, Anatoly / Albacker, Lee / Ali, Siraj / Miller, Vincent / Aggarwal, Rahul / Jablons, David

    Journal for immunotherapy of cancer

    2017  Band 5, Heft 1, Seite(n) 75

    Abstract: Background: Large cell neuroendocrine tumor (LCNEC) of the lung is a rare and aggressive tumor similar to small cell lung cancer (SCLC). Thus, it is often treated similarly to SCLC in the front-line setting with a platinum doublet. However, treatment ... ...

    Abstract Background: Large cell neuroendocrine tumor (LCNEC) of the lung is a rare and aggressive tumor similar to small cell lung cancer (SCLC). Thus, it is often treated similarly to SCLC in the front-line setting with a platinum doublet. However, treatment for patients beyond the first line remains undefined.
    Case presentation: We report the case of a patient with stage IB LCNEC (PD-L1 negative but positive for PD-L1 amplification and tumor mutation burden high) who progressed after adjuvant chemotherapy after surgery and subsequent therapy with an antibody drug conjugate targeting a neuroendocrine-specific cell surface marker but achieved a significant and durable response with pembrolizumab, a humanized IgG4 monoclonal anti-PD-1 antibody.
    Conclusions: Immunotherapy with checkpoint inhibitors is an effective treatment option for patients with metastatic LCNEC, even if PD-L1 expression is negative.
    Sprache Englisch
    Erscheinungsdatum 2017-09-19
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2719863-7
    ISSN 2051-1426 ; 2051-1426
    ISSN (online) 2051-1426
    ISSN 2051-1426
    DOI 10.1186/s40425-017-0281-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Erratum to "Emergence of novel and dominant acquired EGFR solvent-front mutations at Gly796 (G796S/R) together with C797S/G and L792F/H mutations in one EGFR (L858R/T790M) NSCLC patient who progressed on osimertinib" [Lung Cancer, 108 (June 2017) 228-231].

    Ou, Sai-Hong Ignatius / Cui, Jean / Schrock, Alexa B / Goldberg, Michael E / Zhu, Viola W / Albacker, Lee / Stephens, Philip J / Miller, Vincent A / Ali, Siraj M

    Lung cancer (Amsterdam, Netherlands)

    2019  Band 138, Seite(n) 141

    Sprache Englisch
    Erscheinungsdatum 2019-08-22
    Erscheinungsland Ireland
    Dokumenttyp Published Erratum
    ZDB-ID 632771-0
    ISSN 1872-8332 ; 0169-5002
    ISSN (online) 1872-8332
    ISSN 0169-5002
    DOI 10.1016/j.lungcan.2019.08.013
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  5. Artikel ; Online: Emergence of novel and dominant acquired EGFR solvent-front mutations at Gly796 (G796S/R) together with C797S/R and L792F/H mutations in one EGFR (L858R/T790M) NSCLC patient who progressed on osimertinib.

    Ou, Sai-Hong Ignatius / Cui, Jean / Schrock, Alexa B / Goldberg, Michael E / Zhu, Viola W / Albacker, Lee / Stephens, Philip J / Miller, Vincent A / Ali, Siraj M

    Lung cancer (Amsterdam, Netherlands)

    2017  Band 108, Seite(n) 228–231

    Abstract: Acquired epidermal growth factor receptor (EGFR) resistance mutations to osimertinib are common, including the EGFR C797S that abolishes the covalent binding of osimertinib to EGFR. Here we report the emergence of novel EGFR solvent front mutations at ... ...

    Abstract Acquired epidermal growth factor receptor (EGFR) resistance mutations to osimertinib are common, including the EGFR C797S that abolishes the covalent binding of osimertinib to EGFR. Here we report the emergence of novel EGFR solvent front mutations at Gly796 (G796S/R) in addition to a hinge pocket L792F/H mutations, and C797S/G all in cis with T790M in a single patient on progression on osimertinib as detected by plasma circulating tumor DNA (ctDNA) assay in the course of clinical care. A 69-year-old Caucasian female former light-smoker presented with stage IV EGFR L858R positive adenocarcinoma who developed EGFR T790M mutation after 8 month treatment of erlotinib. The patient was initiated on osimertinib with disease shrinkage after 2 months, but tumor regrowth was observed after 5 months of osimertinib treatment. Assay of plasma ctDNA at this time revealed these different secondary resistance mutations all in trans with each other including distinct mutations at the same codon producing different amino acid changes: G796S/R (mutant allele frequency [MAF]; 14.4%), C797S/G (MAF: 2.26%), L792F/H (MAF: 0.36%), and V802F (MAF: 0.40%), in addition to the pre-existing L858R (MAF:17.9%) and T790M (MAF:18.2%) but all in cis with T790M. The G796S/R mutations are homologous with known reported solvent front mutations in ALK G1202R, ROS1 G2032R, TrkA G595R and TrkC G623R, all of which are associated with acquired resistance to type I TKIs. In silico modeling revealed mutation at G796 interferes with osimertinib binding to the EGFR kinase domain at the phenyl aromatic ring position as this residue forms a narrow "hydrophobic sandwich" with L718, while L792F/H mutation interferes with osimertinib binding at the methoxyl group on the phenyl ring. Multiple resistance mutations at differing allele frequencies including novel EGFR solvent front mutations can emerge in a single patient with progression on osimertinib potentially due to tumor hetereogeneity and definitely present a significant therapeutic and drug development challenge.
    Mesh-Begriff(e) Acrylamides ; Aged ; Alleles ; Amino Acid Substitution ; Aniline Compounds ; Animals ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/therapeutic use ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Disease Models, Animal ; ErbB Receptors/chemistry ; ErbB Receptors/genetics ; Female ; Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Models, Molecular ; Molecular Conformation ; Mutation ; Neoplasm Staging ; Piperazines/chemistry ; Piperazines/therapeutic use ; Protein Binding ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/therapeutic use
    Chemische Substanzen Acrylamides ; Aniline Compounds ; Antineoplastic Agents ; Piperazines ; Protein Kinase Inhibitors ; osimertinib (3C06JJ0Z2O) ; ErbB Receptors (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2017-04-12
    Erscheinungsland Ireland
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 632771-0
    ISSN 1872-8332 ; 0169-5002
    ISSN (online) 1872-8332
    ISSN 0169-5002
    DOI 10.1016/j.lungcan.2017.04.003
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  6. Artikel ; Online: Comprehensive Genomic Profiling Facilitates Implementation of the National Comprehensive Cancer Network Guidelines for Lung Cancer Biomarker Testing and Identifies Patients Who May Benefit From Enrollment in Mechanism-Driven Clinical Trials.

    Suh, James H / Johnson, Adrienne / Albacker, Lee / Wang, Kai / Chmielecki, Juliann / Frampton, Garrett / Gay, Laurie / Elvin, Julia A / Vergilio, Jo-Anne / Ali, Siraj / Miller, Vincent A / Stephens, Philip J / Ross, Jeffrey S

    The oncologist

    2016  Band 21, Heft 6, Seite(n) 684–691

    Abstract: Background: The National Comprehensive Cancer Network (NCCN) guidelines for patients with metastatic non-small cell lung cancer (NSCLC) recommend testing for EGFR, BRAF, ERBB2, and MET mutations; ALK, ROS1, and RET rearrangements; and MET amplification. ...

    Abstract Background: The National Comprehensive Cancer Network (NCCN) guidelines for patients with metastatic non-small cell lung cancer (NSCLC) recommend testing for EGFR, BRAF, ERBB2, and MET mutations; ALK, ROS1, and RET rearrangements; and MET amplification. We investigated the feasibility and utility of comprehensive genomic profiling (CGP), a hybrid capture-based next-generation sequencing (NGS) test, in clinical practice.
    Methods: CGP was performed to a mean coverage depth of 576× on 6,832 consecutive cases of NSCLC (2012-2015). Genomic alterations (GAs) (point mutations, small indels, copy number changes, and rearrangements) involving EGFR, ALK, BRAF, ERBB2, MET, ROS1, RET, and KRAS were recorded. We also evaluated lung adenocarcinoma (AD) cases without GAs, involving these eight genes.
    Results: The median age of the patients was 64 years (range: 13-88 years) and 53% were female. Among the patients studied, 4,876 (71%) harbored at least one GA involving EGFR (20%), ALK (4.1%), BRAF (5.7%), ERBB2 (6.0%), MET (5.6%), ROS1 (1.5%), RET (2.4%), or KRAS (32%). In the remaining cohort of lung AD without these known drivers, 273 cancer-related genes were altered in at least 0.1% of cases, including STK11 (21%), NF1 (13%), MYC (9.8%), RICTOR (6.4%), PIK3CA (5.4%), CDK4 (4.3%), CCND1 (4.0%), BRCA2 (2.5%), NRAS (2.3%), BRCA1 (1.7%), MAP2K1 (1.2%), HRAS (0.7%), NTRK1 (0.7%), and NTRK3 (0.2%).
    Conclusion: CGP is practical and facilitates implementation of the NCCN guidelines for NSCLC by enabling simultaneous detection of GAs involving all seven driver oncogenes and KRAS. Furthermore, without additional tissue use or cost, CGP identifies patients with "pan-negative" lung AD who may benefit from enrollment in mechanism-driven clinical trials.
    Implications for practice: National Comprehensive Cancer Network guidelines for patients with metastatic non-small cell lung cancer (NSCLC) recommend testing for several genomic alterations (GAs). The feasibility and utility of comprehensive genomic profiling were studied in NSCLC and in lung adenocarcinoma (AD) without GAs. Of patients with NSCLC, 71% harbored at least one GA to a gene listed in the guidelines or KRAS; 273 cancer-related genes were altered in at least 0.1% of the AD cases. Although logistical and administrative hurdles limit the widespread use of next-generation sequencing, the data confirm the feasibility and potential utility of comprehensive genomic profiling in clinical practice.
    Mesh-Begriff(e) Adenocarcinoma/genetics ; Adenocarcinoma of Lung ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biomarkers, Tumor ; Carcinoma, Non-Small-Cell Lung/genetics ; Clinical Trials as Topic ; ErbB Receptors/genetics ; Gene Expression Profiling ; High-Throughput Nucleotide Sequencing ; Humans ; Lung Neoplasms/genetics ; Middle Aged ; Mutation ; Patient Participation ; Young Adult
    Chemische Substanzen Biomarkers, Tumor ; ErbB Receptors (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2016-05-05
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1409038-7
    ISSN 1549-490X ; 1083-7159
    ISSN (online) 1549-490X
    ISSN 1083-7159
    DOI 10.1634/theoncologist.2016-0030
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel: CD28-dependent HIV-1 transcription is associated with Vav, Rac, and NF-kappa B activation.

    Cook, Julie A / Albacker, Lee / August, Avery / Henderson, Andrew J

    The Journal of biological chemistry

    2003  Band 278, Heft 37, Seite(n) 35812–35818

    Abstract: Activation of HIV-1-infected T cells through the T cell receptor and costimulatory molecule CD28 induces proviral transcription; however, the mechanism behind this enhanced virus expression is unknown. Jurkat T cells and primary CD4+ T cells expressing a ...

    Abstract Activation of HIV-1-infected T cells through the T cell receptor and costimulatory molecule CD28 induces proviral transcription; however, the mechanism behind this enhanced virus expression is unknown. Jurkat T cells and primary CD4+ T cells expressing a CD8 alpha/CD28 chimeric receptor containing a mutation at tyrosine 200 in the cytoplasmic tail were unable to fully induce HIV-1 proviral transcription in response to CD8 alpha/28 receptor cross-linking in comparison to CD28 costimulation. The loss of transactivation seen with the mutant chimeric receptor correlated with a decrease in Vav tyrosine phosphorylation. CD28-dependent activation of HIV-1 transcription also required the GTPase activity of Rac1, which was not activated during costimulation with the mutated receptor. Furthermore, the mutated receptor was unable to induce NF-kappa B DNA binding or transactivation, as demonstrated by electromobility shift assays and HIV-1 long terminal repeat and NF-kappa B-dependent reporter constructs. These studies show that signaling events initiated by tyrosine 200 of CD28 are required for efficient expression of HIV-1 transcription in activated T cells.
    Mesh-Begriff(e) Antigens, CD/physiology ; CD28 Antigens/physiology ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/physiology ; CD4-Positive T-Lymphocytes/virology ; HIV-1/genetics ; Humans ; Jurkat Cells ; NF-kappa B/metabolism ; Oncogene Proteins/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-vav ; Recombinant Fusion Proteins/metabolism ; Transcription Factor AP-1/metabolism ; Transcription, Genetic ; Tyrosine ; rac1 GTP-Binding Protein/metabolism
    Chemische Substanzen Antigens, CD ; CD28 Antigens ; NF-kappa B ; Oncogene Proteins ; Proto-Oncogene Proteins c-vav ; Recombinant Fusion Proteins ; Transcription Factor AP-1 ; VAV1 protein, human ; Tyrosine (42HK56048U) ; rac1 GTP-Binding Protein (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2003-07-03
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M302878200
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: TIM-4, expressed by medullary macrophages, regulates respiratory tolerance by mediating phagocytosis of antigen-specific T cells.

    Albacker, L A / Yu, S / Bedoret, D / Lee, W-L / Umetsu, S E / Monahan, S / Freeman, G J / Umetsu, D T / DeKruyff, R H

    Mucosal immunology

    2012  Band 6, Heft 3, Seite(n) 580–590

    Abstract: Respiratory exposure to antigen induces T cell tolerance via several overlapping mechanisms that limit the immune response. While the mechanisms involved in the development of Treg cells have received much attention, those that result in T cell deletion ... ...

    Abstract Respiratory exposure to antigen induces T cell tolerance via several overlapping mechanisms that limit the immune response. While the mechanisms involved in the development of Treg cells have received much attention, those that result in T cell deletion are largely unknown. Herein, we show that F4/80(+) lymph node medullary macrophages expressing TIM-4, a phosphatidylserine receptor, remove antigen-specific T cells during respiratory tolerance, thereby reducing secondary T cell responses. Blockade of TIM-4 inhibited the phagocytosis of antigen-specific T cells by TIM-4 expressing lymph node medullary macrophages, resulting in an increase in the number of antigen-specific T cells and the abrogation of respiratory tolerance. Moreover, specific depletion of medullary macrophages inhibited the induction of respiratory tolerance, highlighting the key role of TIM-4 and medullary macrophages in tolerance. Therefore, TIM-4-mediated clearance of antigen specific T cells represents an important previously unrecognized mechanism regulating respiratory tolerance.
    Mesh-Begriff(e) Administration, Intranasal ; Adoptive Transfer ; Animals ; Antibodies, Blocking/administration & dosage ; Antigens/immunology ; Antigens, Differentiation/metabolism ; Cells, Cultured ; Immune Tolerance ; Lymph Nodes/pathology ; Macrophages/immunology ; Membrane Proteins/immunology ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred BALB C ; Ovalbumin/immunology ; Phagocytosis/immunology ; Respiratory Hypersensitivity/immunology ; T-Lymphocytes/immunology
    Chemische Substanzen Antibodies, Blocking ; Antigens ; Antigens, Differentiation ; Membrane Proteins ; TIM-4 protein, mouse ; monocyte-macrophage differentiation antigen ; Ovalbumin (9006-59-1)
    Sprache Englisch
    Erscheinungsdatum 2012-11-14
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2411370-0
    ISSN 1935-3456 ; 1933-0219
    ISSN (online) 1935-3456
    ISSN 1933-0219
    DOI 10.1038/mi.2012.100
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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