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  • 1
    Language: English
    In: Radiation research, 2015-09, Vol.184 (3), p.235-248
    Description: Although radiation therapy is an important cancer treatment modality, patients may experience adverse effects. The use of a radiation-effect modulator may help improve the outcome and health-related quality of life (HRQOL) of patients undergoing radiation therapy either by enhancing tumor cell killing or by protecting normal tissues. Historically, the successful translation of radiation-effect modulators to the clinic has been hindered due to the lack of focused collaboration between academia, pharmaceutical companies and the clinic, along with limited availability of support for such ventures. The U.S. Government has been developing medical countermeasures against accidental and intentional radiation exposures to mitigate the risk and/or severity of acute radiation syndrome (ARS) and the delayed effects of acute radiation exposures (DEARE), and there is now a drug development pipeline established. Some of these medical countermeasures could potentially be repurposed for improving the outcome of radiation therapy and HRQOL of cancer patients. With the objective of developing radiation-effect modulators to improve radiotherapy, the Small Business Innovation Research (SBIR) Development Center at the National Cancer Institute (NCI), supported by the Radiation Research Program (RRP), provided funding to companies from 2011 to 2014 through the SBIR contracts mechanism. Although radiation-effect modulators collectively refer to radioprotectors, radiomitigators and radiosensitizers, the focus of this article is on radioprotection and mitigation of radiation injury. This specific SBIR contract opportunity strengthened existing partnerships and facilitated new collaborations between academia and industry. In this commentary, we assess the impact of this funding opportunity, outline the review process, highlight the organ/site-specific disease needs in the clinic for the development of radiation-effect modulators, provide a general understanding of a framework for gathering preclinical and clinical evidence to obtain regulatory approval and provide a basis for broader venture capital needs and support from pharmaceutical companies to fully capitalize on the advances made thus far in this field.
    Subject(s): Cancer ; COMMENTARY ; Countermeasures ; Genetic Therapy ; Genistein - therapeutic use ; Humans ; Medical ; Megakaryocyte Progenitor Cells - physiology ; Modulators ; Neoplasms - psychology ; Neoplasms - radiotherapy ; Patients ; Peptide Fragments - therapeutic use ; Quality of Life ; Radiation effects ; Radiation Protection ; Radiation therapy ; Radiotherapy - adverse effects ; Small Business ; Space life sciences ; Thrombin - therapeutic use ; Toll-Like Receptor 5 - agonists ; Translations
    ISSN: 0033-7587
    E-ISSN: 1938-5404
    Source: JSTOR Life Sciences
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  • 2
    Language: English
    In: Radiation oncology (London, England), 2012-03-27, Vol.7 (1), p.48-48
    Description: The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is activated in tumor cells and promotes tumor cell survival after radiation-induced DNA damage. Because the pathway may not be completely inhibited after blockade of PI3K itself, due to feedback through mammalian target of rapamycin (mTOR), more effective inhibition might be expected by targeting both PI3K and mTOR inhibition. We investigated the effect of two dual PI3K/mTOR (both mTORC1 and mTORC2) inhibitors, NVP-BEZ235 and NVP-BGT226, on SQ20B laryngeal and FaDu hypopharyngeal cancer cells characterised by EGFR overexpression, on T24 bladder tumor cell lines with H-Ras mutation and on endothelial cells. Analysis of target protein phosphorylation, clonogenic survival, number of residual γH2AX foci, cell cycle and apoptosis after radiation was performed in both tumor and endothelial cells. In vitro angiogenesis assays were conducted as well. Both compounds effectively inhibited phosphorylation of Akt, mTOR and S6 target proteins and reduced clonogenic survival in irradiated tumor cells. Persistence of DNA damage, as evidenced by increased number of γH2AX foci, was detected after irradiation in the presence of PI3K/mTOR inhibition, together with enhanced G2 cell cycle delay. Treatment with one of the inhibitors, NVP-BEZ235, also resulted in decreased clonogenicity after irradiation of tumor cells under hypoxic conditions. In addition, NVP-BEZ235 blocked VEGF- and IR-induced Akt phosphorylation and increased radiation killing in human umbilical venous endothelial cells (HUVEC) and human dermal microvascular dermal cells (HDMVC). NVP-BEZ235 inhibited VEGF-induced cell migration and capillary tube formation in vitro and enhanced the antivascular effect of irradiation. Treatment with NVP-BEZ235 moderately increased apoptosis in SQ20B and HUVEC cells but not in FaDu cells, and increased necrosis in both tumor and endothelial all cells tumor. The results of this study demonstrate that PI3K/mTOR inhibitors can enhance radiation-induced killing in tumor and endothelial cells and may be of benefit when combined with radiotherapy.
    Subject(s): Analysis ; Cancer ; Cancer cells ; Cell Line, Tumor ; Endothelial cells ; Endothelial Cells - drug effects ; Enzyme inhibitors ; Enzymes ; Human Umbilical Vein Endothelial Cells - drug effects ; Humans ; Imidazoles - pharmacology ; Kinases ; Medical research ; mTOR ; Mutation ; Phosphoinositide-3 Kinase Inhibitors ; Physiological aspects ; PI3K ; Quinolines - pharmacology ; Radiation-Sensitizing Agents - pharmacology ; Radiosensitization ; Radiotherapy ; Rodents ; TOR Serine-Threonine Kinases - antagonists & inhibitors ; Vascular endothelial growth factor ; VEGF
    ISSN: 1748-717X
    E-ISSN: 1748-717X
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 3
    Language: English
    In: Clinical cancer research, 2016-07-01, Vol.22 (13), p.3138-3147
    Description: There is an urgent need to improve reproducibility and translatability of preclinical data to fully exploit opportunities for molecular therapeutics involving radiation and radiochemotherapy. For in vitro research, the clonogenic assay remains the current state-of-the-art of preclinical assays, whereas newer moderate and high-throughput assays offer the potential for rapid initial screening. Studies of radiation response modification by molecularly targeted agents can be improved using more physiologic 3D culture models. Elucidating effects on the cancer stem cells (CSC, and CSC-like) and developing biomarkers for defining targets and measuring responses are also important. In vivo studies are necessary to confirm in vitro findings, further define mechanism of action, and address immunomodulation and treatment-induced modification of the microenvironment. Newer in vivo models include genetically engineered and patient-derived xenograft mouse models and spontaneously occurring cancers in domesticated animals. Selection of appropriate endpoints is important for in vivo studies; for example, regrowth delay measures bulk tumor killing, whereas local tumor control assesses effects on CSCs. The reliability of individual assays requires standardization of procedures and cross-laboratory validation. Radiation modifiers must be tested as part of clinical standard of care, which includes radiochemotherapy for most tumors. Radiation models are compatible with but also differ from those used for drug screening. Furthermore, the mechanism of a drug as a chemotherapeutic agent may be different from its interaction with radiation and/or radiochemotherapy. This provides an opportunity to expand the use of molecular-targeted agents. Clin Cancer Res; 22(13); 3138-47. ©2016 AACR.
    Subject(s): Animals ; Antineoplastic Agents - pharmacology ; Cell Line, Tumor ; Disease Models, Animal ; Drug Evaluation, Preclinical - methods ; HeLa Cells ; Humans ; Mice ; Molecular Targeted Therapy - methods ; Neoplasms - pathology ; Neoplasms - therapy ; Neoplastic Stem Cells - drug effects ; Radiation Tolerance - drug effects ; Radiation-Sensitizing Agents - pharmacology ; Reproducibility of Results ; Xenograft Model Antitumor Assays - methods
    ISSN: 1078-0432
    E-ISSN: 1557-3265
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
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  • 4
    Language: English
    In: Nature communications, 2014-06-09, Vol.5 (1), p.4091-4091
    Description: DNA double-strand break (DSB) repair is a highly regulated process performed predominantly by non-homologous end joining (NHEJ) or homologous recombination (HR) pathways. How these pathways are coordinated in the context of chromatin is unclear. Here we uncover a role for histone H3K36 modification in regulating DSB repair pathway choice in fission yeast. We find Set2-dependent H3K36 methylation reduces chromatin accessibility, reduces resection and promotes NHEJ, while antagonistic Gcn5-dependent H3K36 acetylation increases chromatin accessibility, increases resection and promotes HR. Accordingly, loss of Set2 increases H3K36Ac, chromatin accessibility and resection, while Gcn5 loss results in the opposite phenotypes following DSB induction. Further, H3K36 modification is cell cycle regulated with Set2-dependent H3K36 methylation peaking in G1 when NHEJ occurs, while Gcn5-dependent H3K36 acetylation peaks in S/G2 when HR prevails. These findings support an H3K36 chromatin switch in regulating DSB repair pathway choice.
    Subject(s): Acetylation ; Acetyltransferases - metabolism ; Chromatin - metabolism ; DNA End-Joining Repair ; DNA Repair ; DNA, Fungal - metabolism ; Histone-Lysine N-Methyltransferase - metabolism ; Histones - metabolism ; Methylation ; Recombinational DNA Repair ; Schizosaccharomyces - genetics ; Schizosaccharomyces - metabolism ; Schizosaccharomyces pombe Proteins - metabolism
    ISSN: 2041-1723
    E-ISSN: 2041-1723
    Source: Nature Open Access
    Source: PubMed Central
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  • 5
    Language: English
    In: Cancer research (Chicago, Ill.), 2009, Vol.69 (15), p.6347-6354
    Description: Many inhibitors of the epidermal growth factor receptor (EGFR)-RAS-phosphatidylinositol 3-kinase (PI3K)-AKT signaling pathway are in clinical use or under development for cancer therapy. Here, we show that treatment of mice bearing human tumor xenografts with inhibitors that block EGFR, RAS, PI3K, or AKT resulted in prolonged and durable enhancement of tumor vascular flow, perfusion, and decreased tumor hypoxia. The vessels in the treated tumors had decreased tortuosity and increased internodal length accounting for the functional alterations. Inhibition of tumor growth cannot account for these results, as the drugs were given at doses that did not alter tumor growth. The tumor cell itself was an essential target, as HT1080 tumors that lack EGFR did not respond to an EGFR inhibitor but did respond with vascular alterations to RAS or PI3K inhibition. We extended these observations to spontaneously arising tumors in MMTV-neu mice. These tumors also responded to PI3K inhibition with decreased tumor hypoxia, increased vascular flow, and morphologic alterations of their vessels, including increased vascular maturity and acquisition of pericyte markers. These changes are similar to the vascular normalization that has been described after the antiangiogenic treatment of xenografts. One difficulty in the use of vascular normalization as a therapeutic strategy has been its limited duration. In contrast, blocking tumor cell RAS-PI3K-AKT signaling led to persistent vascular changes that might be incorporated into clinical strategies based on improvement of vascular flow or decreased hypoxia. These results indicate that vascular alterations must be considered as a consequence of signaling inhibition in cancer therapy.
    Subject(s): AKT ; Animals ; Antineoplastic agents ; Biological and medical sciences ; Cell Hypoxia - physiology ; Cell Line, Tumor ; EGFR ; Enzyme Inhibitors - pharmacology ; Female ; Fibrosarcoma - blood supply ; Fibrosarcoma - drug therapy ; Fibrosarcoma - metabolism ; Humans ; hypoxia ; Medical sciences ; Mice ; Mice, SCID ; Mice, Transgenic ; Neovascularization, Pathologic - drug therapy ; Neovascularization, Pathologic - metabolism ; Oxygen - metabolism ; Pharmacology. Drug treatments ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - metabolism ; PI3 Kinase ; Proto-Oncogene Proteins c-akt - antagonists & inhibitors ; Proto-Oncogene Proteins c-akt - metabolism ; RAS ; ras Proteins - antagonists & inhibitors ; ras Proteins - metabolism ; Receptor, Epidermal Growth Factor - antagonists & inhibitors ; Receptor, Epidermal Growth Factor - metabolism ; Signal Transduction - drug effects ; Signaling inhibition ; tumor vasculature ; Tumors ; Xenograft Model Antitumor Assays
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
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  • 6
    Language: English
    In: Cancer research (Chicago, Ill.), 2012, Vol.72 (1), p.239-248
    Description: The aberrant vascular architecture of solid tumors results in hypoxia that limits the efficacy of radiotherapy. Vascular normalization using antiangiogenic agents has been proposed as a means to improve radiation therapy by enhancing tumor oxygenation, but only short-lived effects for this strategy have been reported so far. Here, we show that NVP-BEZ235, a dual inhibitor of phosphoinositide-3-kinase (PI3K) and mTOR, can improve tumor oxygenation and vascular structure over a prolonged period that achieves the aim of effective vascular normalization. Because PI3K inhibition can radiosensitize tumor cells themselves, our experimental design explicitly distinguished effects on the blood vasculature versus tumor cells. Drug administration coincident with radiation enhanced the delay in tumor growth without changing tumor oxygenation, establishing that radiosensitization is a component of the response. However, the enhanced growth delay was substantially greater after induction of vascular normalization, meaning that this treatment enhanced the tumoral radioresponse. Importantly, changes in vascular morphology persisted throughout the entire course of the experiment. Our findings indicated that targeting the PI3K/mTOR pathway can modulate the tumor microenvironment to induce a prolonged normalization of blood vessels. The substantial therapeutic gain observed after combination of NVP-BEZ235 with irradiation has conceptual implications for cancer therapy and could be of broad translational importance.
    Subject(s): Animals ; Antineoplastic agents ; Biological and medical sciences ; Dose-Response Relationship, Drug ; Humans ; Medical sciences ; Mice ; Neoplasms, Experimental - blood supply ; Neoplasms, Experimental - radiotherapy ; Neovascularization, Pathologic ; Pharmacology. Drug treatments ; Phosphoinositide-3 Kinase Inhibitors ; Radiation Tolerance ; TOR Serine-Threonine Kinases - antagonists & inhibitors ; Tumors ; Xenograft Model Antitumor Assays
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
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  • 7
    Language: English
    In: PloS one, 2009-08-28, Vol.4 (8), p.e6816
    Description: MicroRNAs (miRNAs) have been implicated in cancer initiation and progression via their ability to affect expression of genes and proteins that regulate cell proliferation and/or cell death. Transcription of the three miRNA miR-34 family members was recently found to be directly regulated by p53. Among the target proteins regulated by miR-34 are Notch pathway proteins and Bcl-2, suggesting the possibility of a role for miR-34 in the maintenance and survival of cancer stem cells. We examined the roles of miR-34 in p53-mutant human pancreatic cancer cell lines MiaPaCa2 and BxPC3, and the potential link to pancreatic cancer stem cells. Restoration of miR-34 expression in the pancreatic cancer cells by either transfection of miR-34 mimics or infection with lentiviral miR-34-MIF downregulated Bcl-2 and Notch1/2. miR-34 restoration significantly inhibited clonogenic cell growth and invasion, induced apoptosis and G1 and G2/M arrest in cell cycle, and sensitized the cells to chemotherapy and radiation. We identified that CD44+/CD133+ MiaPaCa2 cells are enriched with tumorsphere-forming and tumor-initiating cells or cancer stem/progenitor cells with high levels of Notch/Bcl-2 and loss of miR-34. More significantly, miR-34 restoration led to an 87% reduction of the tumor-initiating cell population, accompanied by significant inhibition of tumorsphere growth in vitro and tumor formation in vivo. Our results demonstrate that miR-34 may restore, at least in part, the tumor suppressing function of the p53 in p53-deficient human pancreatic cancer cells. Our data support the view that miR-34 may be involved in pancreatic cancer stem cell self-renewal, potentially via the direct modulation of downstream targets Bcl-2 and Notch, implying that miR-34 may play an important role in pancreatic cancer stem cell self-renewal and/or cell fate determination. Restoration of miR-34 may hold significant promise as a novel molecular therapy for human pancreatic cancer with loss of p53-miR34, potentially via inhibiting pancreatic cancer stem cells.
    Subject(s): 3' Untranslated Regions ; AC133 Antigen ; Androgens ; Animals ; Antigens, CD - immunology ; Apoptosis ; Base Sequence ; Bcl-2 protein ; Brain cancer ; Breast cancer ; Cancer ; CD44 antigen ; Cell Biology ; Cell Cycle ; Cell death ; Cell Division ; Cell fate ; Cell growth ; Cell proliferation ; Cell survival ; Cells (biology) ; Cellular Death and Stress Responses ; Chemotherapy ; Development and progression ; DNA Primers ; Female ; Gastroenterology and Hepatology ; Gastrointestinal Cancers ; Gene Expression ; Genetic transcription ; Glycoproteins - immunology ; Hospitals ; Humans ; Hyaluronan Receptors - immunology ; Inhibition ; Internal medicine ; Laboratories ; Metastasis ; Mice ; Mice, Nude ; MicroRNA ; MicroRNAs ; MicroRNAs - physiology ; miRNA ; Notch protein ; Oncology ; p53 Protein ; Pancreatic cancer ; Pancreatic Neoplasms - immunology ; Pancreatic Neoplasms - pathology ; Pathology ; Pathophysiology ; Peptides - immunology ; Prostate cancer ; Proteins ; Radiation ; Restoration ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonucleic acid ; RNA ; Stem cells ; Transcription ; Transfection ; Tumor cell lines ; Tumor proteins ; Tumors
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 8
    Language: English
    In: PloS one, 2011, Vol.6 (10), p.e25915-e25915
    Description: Once thought to be a part of the 'dark matter' of the genome, long non-coding RNAs (lncRNAs) are emerging as an integral functional component of the mammalian transcriptome. LncRNAs are a novel class of mRNA-like transcripts which, despite no known protein-coding potential, demonstrate a wide range of structural and functional roles in cellular biology. However, the magnitude of the contribution of lncRNA expression to normal human tissues and cancers has not been investigated in a comprehensive manner. In this study, we compiled 272 human serial analysis of gene expression (SAGE) libraries to delineate lncRNA transcription patterns across a broad spectrum of normal human tissues and cancers. Using a novel lncRNA discovery pipeline we parsed over 24 million SAGE tags and report lncRNA expression profiles across a panel of 26 different normal human tissues and 19 human cancers. Our findings show extensive, tissue-specific lncRNA expression in normal tissues and highly aberrant lncRNA expression in human cancers. Here, we present a first generation atlas for lncRNA profiling in cancer.
    Subject(s): Aberration ; Analysis ; Biology ; Cancer ; Cellular structure ; Chromosomes, Human - genetics ; Dark matter ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Library ; Genes ; Genetic transcription ; Genome, Human - genetics ; Genomes ; Genomics ; Human tissues ; Humans ; Interdisciplinary aspects ; Laboratories ; Leukemia ; Lymphomas ; Medicine ; Metastasis ; Mutation ; Neoplasms - genetics ; Non-coding RNA ; Oncology ; Organ Specificity - genetics ; Pathology ; Pediatrics ; Proteins ; Ribonucleic acid ; RNA ; RNA, Untranslated - genetics ; RNA, Untranslated - metabolism ; Serial analysis of gene expression ; Structure-function relationships ; Tissues ; Transcription ; Transcriptome ; Tumors
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 9
    Language: English
    In: Oncogene, 2004-06-03, Vol.23 (26), p.4594-4602
    Description: Amplification and mutation of the epidermal growth factor receptor (EGFR) are common features of malignant gliomas. The most frequent mutation seen in these tumors involves deletion of exon 2-7 resulting in a constitutively active form of the receptor (EGFRvIII, or deltaEGFR). Since EGFRvIII is found primarily in gliomas and has not been reported in sarcomas, we compared the effects of this altered receptor in immortalized primary astrocytes and fibroblasts. While EGFRvIII displayed ligand-independent autophosphorylation in both cell types, downstream signaling differed. While EGFRvIII increased the proliferative capacity of both astrocytes and fibroblasts consistent with activation of ERK in these cells, EGFRvIII activated AKT only in the immortalized astrocytes. EGFRvIII expression in astrocytes also led to increased radioresistance in that cell type. Furthermore, specific inhibition of phosphotidylinositol-3 kinase (PI-3K) with LY294002 reverted the radioresistant phenotype in the immortalized astrocytes. Thus, selective activation of PI-3K/AKT in astrocytes expressing EGFRvIII appears to be responsible for the observed increase in radioresistance. EGFRvIII's differential ability to activate the PI-3K downstream signal may explain why this mutant receptor is such a prominent lesion in malignant gliomas but less often seen in other tumor types, even those where EGFR signaling has a prominent role.
    Subject(s): 1-Phosphatidylinositol 3-kinase ; AKT protein ; Astrocytes ; Astrocytes - metabolism ; Astrocytes - pathology ; Astrocytes - radiation effects ; Biological and medical sciences ; Cell Division - physiology ; Cell Line, Transformed ; Cell physiology ; Cell receptors ; Cell structures and functions ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Central Nervous System Neoplasms - metabolism ; Chromones ; Enzyme Activation ; Epidermal growth factor ; Epidermal growth factor receptors ; Extracellular signal-regulated kinase ; Fibroblasts ; Fibroblasts - metabolism ; Fibroblasts - radiation effects ; Fundamental and applied biological sciences. Psychology ; Gene deletion ; Glioma - metabolism ; Humans ; Medical sciences ; Miscellaneous ; Mitogen-Activated Protein Kinases - metabolism ; Molecular and cellular biology ; Morpholines ; Mutants ; Mutation ; Neurology ; Phenotypes ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-akt ; Radiation Tolerance - physiology ; Radioresistance ; Receptor, Epidermal Growth Factor - genetics ; Receptor, Epidermal Growth Factor - metabolism ; Reference Values ; Signal Transduction ; Tumors ; Tumors of the nervous system. Phacomatoses
    ISSN: 0950-9232
    E-ISSN: 1476-5594
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
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  • 10
    Language: English
    In: Cancer research (Chicago, Ill.), 2010, Vol.70 (6), p.2141-2145
    Description: The tumor microenvironment is a key factor in cancer treatment response. Recent work has shown that changes in the tumor vasculature can be achieved by inhibiting tumor cell signaling, resulting in enhanced tumor oxygenation. These changes could promote responses to both chemo- and radiation therapy.
    Subject(s): Antineoplastic agents ; Biological and medical sciences ; Humans ; Medical sciences ; Neoplasms - blood supply ; Neoplasms - metabolism ; Neoplasms - pathology ; Neoplasms - therapy ; Neovascularization, Pathologic - metabolism ; Neovascularization, Pathologic - therapy ; Oxygen - metabolism ; Pharmacology. Drug treatments ; Signal Transduction ; Tumors
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: HighWire Press (Free Journals)
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
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