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Article ; Online: Radiation Damage by Heavy Ions in Silicon and Silicon Carbide Detectors.

Altana, Carmen / Calcagno, Lucia / Ciampi, Caterina / La Via, Francesco / Lanzalone, Gaetano / Muoio, Annamaria / Pasquali, Gabriele / Pellegrino, Domenico / Puglia, Sebastiana / Rapisarda, Giuseppe / Tudisco, Salvatore

Sensors (Basel, Switzerland)

2023 Volume 23, Issue 14

Abstract: While silicon has been a steadfast semiconductor material for the past 50 years, it is now facing competition from other materials, especially for detector design. In that respect, due to its high resistance to radiation damage, silicon carbide is one of ...

Abstract	While silicon has been a steadfast semiconductor material for the past 50 years, it is now facing competition from other materials, especially for detector design. In that respect, due to its high resistance to radiation damage, silicon carbide is one of the most promising materials. In this work, we discuss the radiation damage studies of a new, large area, p-n junction silicon carbide device developed by the SiCILIA collaboration. We have studied the general performances of several devices, as a function of fluence, irradiated in different experimental conditions with different beams. A standard p-n junction silicon detector was also irradiated for comparison. The new detectors manifest excellent performance in terms of stability of the main parameters, linearity, defect distribution, charge collection efficiency, energy resolution, leakage current, etc. Experimental results evidence a radiation resistance of SiC devices more than two order of magnitude higher than Si devices. The new construction technology applied to silicon carbide material has made it possible to create very robust devices with excellent performance. These devices will soon be available for all those scientific projects where a high resistance to radiation damage is required.
Language	English
Publishing date	2023-07-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2052857-7
ISSN	1424-8220 ; 1424-8220
ISSN (online)	1424-8220
ISSN	1424-8220
DOI	10.3390/s23146522
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Article ; Online: ATR inhibition reverses the resistance of homologous recombination deficient MGMT

El Touny, Lara H / Hose, Curtis / Connelly, John / Harris, Erik / Monks, Anne / Dull, Angie B / Wilsker, Deborah F / Hollingshead, Melinda G / Gottholm-Ahalt, Michelle / Alcoser, Sergio Y / Mullendore, Michael E / Parchment, Ralph E / Doroshow, James H / Teicher, Beverly A / Rapisarda, Annamaria

Oncotarget

2021 Volume 12, Issue 21, Page(s) 2114–2130

Abstract: The therapeutic efficacy of temozolomide (TMZ) is hindered by inherent and acquired resistance. Biomarkers such as MGMT expression and MMR proficiency are used as predictors of response. However, not all ... ...

Abstract	The therapeutic efficacy of temozolomide (TMZ) is hindered by inherent and acquired resistance. Biomarkers such as MGMT expression and MMR proficiency are used as predictors of response. However, not all MGMT
Language	English
Publishing date	2021-10-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.28090
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Article ; Online: Role of the VEGF/VEGFR axis in cancer biology and therapy.

Rapisarda, Annamaria / Melillo, Giovanni

Advances in cancer research

2012 Volume 114, Page(s) 237–267

Abstract: New vessel formation (angiogenesis) is an essential physiological process for embryologic development, normal growth, and tissue repair. Angiogenesis is tightly regulated at the molecular level; however, this process is dysregulated in several ... ...

Abstract	New vessel formation (angiogenesis) is an essential physiological process for embryologic development, normal growth, and tissue repair. Angiogenesis is tightly regulated at the molecular level; however, this process is dysregulated in several pathological conditions such as cancer. The imbalance between pro- and antiangiogenic signaling molecules within tumors creates an abnormal vascular network that is characterized by dilated, tortuous, and leaky vessels. The pathophysiological consequences of these vascular abnormalities include temporal and spatial heterogeneity in tumor blood flow, oxygenation, and increased tumor interstitial fluid pressure. The resultant microenvironment deeply impacts on tumor progression, and also leads to a reduction in therapy efficacy. The discovery of vascular endothelial growth factor (VEGF) as a major driver of tumor angiogenesis has led to efforts to develop novel therapeutics aimed at inhibiting its activity. Anti-VEGF therapy has become an important option for the management of several human malignancies; however, a significant number of patients do not respond to anti-VEGF therapy when used either as single agent or in combination with chemotherapy. In addition, the benefit of antiangiogenic therapy is relatively short lived and the majority of patients relapse and progress. An increasing amount of reports suggest several potential mechanisms of resistance to antiangiogenic therapy including, but not limited to, tumor hypoxia. This chapter discusses the role of the VEGF axis in tumor biology and highlights the clinical application of anti-VEGF therapies elaborating on pitfalls and strategies to improve clinical outcome.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Animals ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/metabolism ; Humans ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Receptors, Vascular Endothelial Growth Factor/metabolism ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Angiogenesis Inhibitors ; Vascular Endothelial Growth Factor A ; Receptors, Vascular Endothelial Growth Factor (EC 2.7.10.1)
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	127-2
ISSN	2162-5557 ; 0065-230X
ISSN (online)	2162-5557
ISSN	0065-230X
DOI	10.1016/B978-0-12-386503-8.00006-5
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Article ; Online: Overcoming disappointing results with antiangiogenic therapy by targeting hypoxia.

Rapisarda, Annamaria / Melillo, Giovanni

Nature reviews. Clinical oncology

2012 Volume 9, Issue 7, Page(s) 378–390

Abstract: Cancer cells rely on angiogenesis to fulfil their need for oxygen and nutrients; hence, agents targeting angiogenic pathways and mediators have been investigated as potential cancer drugs. Although this strategy has demonstrated delayed tumour ... ...

Abstract	Cancer cells rely on angiogenesis to fulfil their need for oxygen and nutrients; hence, agents targeting angiogenic pathways and mediators have been investigated as potential cancer drugs. Although this strategy has demonstrated delayed tumour progression--leading to progression-free survival and overall survival benefits compared with standard therapy--in some patients, the results are more modest than predicted. A significant number of patients either do not respond to antiangiogenic agents or fairly rapidly develop resistance to them, which raises questions about how resistance develops and how it can be overcome. Furthermore, whether cancers, once they develop resistance, become more invasive or lead to metastatic disease remains unclear. Several mechanisms of resistance have been recently proposed and emerging evidence indicates that, under certain experimental conditions, antiangiogenic agents increase intratumour hypoxia by promoting vessel pruning and inhibiting neoangiogenesis. Indeed, several studies have highlighted the possibility that inhibitors of VEGF (and its receptors) can promote an invasive metastatic switch, in part by creating an increasingly hypoxic tumour microenvironment. As a potential remedy, a number of therapeutic approaches have been investigated that target the hypoxic tumour compartment to improve the clinical outcome of antiangiogenic therapy.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Animals ; Drug Resistance, Neoplasm/drug effects ; Humans ; Hypoxia/drug therapy ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neovascularization, Pathologic/drug therapy
Chemical Substances	Angiogenesis Inhibitors
Language	English
Publishing date	2012-04-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/nrclinonc.2012.64
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Article ; Online: Role of the hypoxic tumor microenvironment in the resistance to anti-angiogenic therapies.

Rapisarda, Annamaria / Melillo, Giovanni

Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

2009 Volume 12, Issue 3, Page(s) 74–80

Abstract: Angiogenesis, a key process for the growth of human cancers, has recently been exploited for the development of a novel class of cancer therapeutics that was thought to have wide applications and not to induce resistance in the clinical setting. Indeed, ... ...

Abstract	Angiogenesis, a key process for the growth of human cancers, has recently been exploited for the development of a novel class of cancer therapeutics that was thought to have wide applications and not to induce resistance in the clinical setting. Indeed, anti-angiogenic therapy has become an important option for the management of several human malignancies. However, a significant number of patients either do not respond to anti-angiogenic agents or fairly rapidly develop resistance. In addition, the benefit of anti-angiogenic therapy is relatively short-lived and the majority of patients eventually relapses and progresses. Several mechanisms of resistance to anti-angiogenic therapy have been recently proposed. The current review focuses on the role of intra-tumor hypoxia as a mechanism of resistance to anti-angiogenic agents and speculates on therapeutic approaches that might circumvent resistance and thereby improve clinical outcome.
MeSH term(s)	Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/therapeutic use ; Cell Hypoxia/drug effects ; Cell Hypoxia/physiology ; Combined Modality Therapy ; Drug Resistance, Neoplasm/physiology ; Humans ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neoplasms/physiopathology ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/physiopathology
Chemical Substances	Angiogenesis Inhibitors
Language	English
Publishing date	2009-04-25
Publishing country	Scotland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1474513-6
ISSN	1532-2084 ; 1368-7646
ISSN (online)	1532-2084
ISSN	1368-7646
DOI	10.1016/j.drup.2009.03.002
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Article ; Online: Epigenome-wide DNA methylation analysis of small cell lung cancer cell lines suggests potential chemotherapy targets.

Krushkal, Julia / Silvers, Thomas / Reinhold, William C / Sonkin, Dmitriy / Vural, Suleyman / Connelly, John / Varma, Sudhir / Meltzer, Paul S / Kunkel, Mark / Rapisarda, Annamaria / Evans, David / Pommier, Yves / Teicher, Beverly A

Clinical epigenetics

2020 Volume 12, Issue 1, Page(s) 93

Abstract: Background: Small cell lung cancer (SCLC) is an aggressive neuroendocrine lung cancer. SCLC progression and treatment resistance involve epigenetic processes. However, links between SCLC DNA methylation and drug response remain unclear. We performed an ... ...

Abstract	Background: Small cell lung cancer (SCLC) is an aggressive neuroendocrine lung cancer. SCLC progression and treatment resistance involve epigenetic processes. However, links between SCLC DNA methylation and drug response remain unclear. We performed an epigenome-wide study of 66 human SCLC cell lines using the Illumina Infinium MethylationEPIC BeadChip array. Correlations of SCLC DNA methylation and gene expression with in vitro response to 526 antitumor agents were examined. Results: We found multiple significant correlations between DNA methylation and chemosensitivity. A potentially important association was observed for TREX1, which encodes the 3' exonuclease I that serves as a STING antagonist in the regulation of a cytosolic DNA-sensing pathway. Increased methylation and low expression of TREX1 were associated with the sensitivity to Aurora kinase inhibitors AZD-1152, SCH-1473759, SNS-314, and TAK-901; the CDK inhibitor R-547; the Vertex ATR inhibitor Cpd 45; and the mitotic spindle disruptor vinorelbine. Compared with cell lines of other cancer types, TREX1 had low mRNA expression and increased upstream region methylation in SCLC, suggesting a possible relationship with SCLC sensitivity to Aurora kinase inhibitors. We also identified multiple additional correlations indicative of potential mechanisms of chemosensitivity. Methylation of the 3'UTR of CEP350 and MLPH, involved in centrosome machinery and microtubule tracking, respectively, was associated with response to Aurora kinase inhibitors and other agents. EPAS1 methylation was associated with response to Aurora kinase inhibitors, a PLK-1 inhibitor and a Bcl-2 inhibitor. KDM1A methylation was associated with PLK-1 inhibitors and a KSP inhibitor. Increased promoter methylation of SLFN11 was correlated with resistance to DNA damaging agents, as a result of low or no SLFN11 expression. The 5' UTR of the epigenetic modifier EZH2 was associated with response to Aurora kinase inhibitors and a FGFR inhibitor. Methylation and expression of YAP1 were correlated with response to an mTOR inhibitor. Among non-neuroendocrine markers, EPHA2 was associated with response to Aurora kinase inhibitors and a PLK-1 inhibitor and CD151 with Bcl-2 inhibitors. Conclusions: Multiple associations indicate potential epigenetic mechanisms affecting SCLC response to chemotherapy and suggest targets for combination therapies. While many correlations were not specific to SCLC lineages, several lineage markers were associated with specific agents.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents, Phytogenic/pharmacology ; Aurora Kinases/antagonists & inhibitors ; Cell Cycle Proteins/antagonists & inhibitors ; Cell Line, Tumor/drug effects ; Cyclin-Dependent Kinase Inhibitor Proteins/pharmacology ; DNA Methylation/drug effects ; DNA Methylation/genetics ; Drug Therapy, Combination/statistics & numerical data ; Epigenome/genetics ; Exodeoxyribonucleases/genetics ; Exodeoxyribonucleases/metabolism ; Gene Expression/drug effects ; Gene Expression/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; High-Throughput Nucleotide Sequencing/methods ; Histone Demethylases/drug effects ; Histone Demethylases/genetics ; Humans ; Lung Neoplasms/pathology ; Membrane Proteins/antagonists & inhibitors ; Nuclear Proteins/drug effects ; Nuclear Proteins/genetics ; Phosphoproteins/genetics ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Proto-Oncogene Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins c-bcl-2/antagonists & inhibitors ; Small Cell Lung Carcinoma/diagnosis ; Small Cell Lung Carcinoma/genetics ; Polo-Like Kinase 1
Chemical Substances	Antineoplastic Agents ; Antineoplastic Agents, Phytogenic ; Cell Cycle Proteins ; Cyclin-Dependent Kinase Inhibitor Proteins ; Membrane Proteins ; Nuclear Proteins ; Phosphoproteins ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2 ; SLFN11 protein, human ; STING1 protein, human ; Histone Demethylases (EC 1.14.11.-) ; KDM1A protein, human (EC 1.5.-) ; Aurora Kinases (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Exodeoxyribonucleases (EC 3.1.-) ; exodeoxyribonuclease I (EC 3.1.11.1) ; three prime repair exonuclease 1 (EC 3.1.16.-)
Language	English
Publishing date	2020-06-25
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2553921-8
ISSN	1868-7083 ; 1868-7075
ISSN (online)	1868-7083
ISSN	1868-7075
DOI	10.1186/s13148-020-00876-8
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Article ; Online: Development of HIF-1 inhibitors for cancer therapy.

Onnis, Barbara / Rapisarda, Annamaria / Melillo, Giovanni

Journal of cellular and molecular medicine

2009 Volume 13, Issue 9A, Page(s) 2780–2786

Abstract: Intratumour hypoxia has long been considered a driving force of tumour progression and a negative prognostic factor in human cancers. The discovery of hypoxia inducible factors (HIFs), which mediate transcriptional responses to changes in oxygen levels, ... ...

Abstract	Intratumour hypoxia has long been considered a driving force of tumour progression and a negative prognostic factor in human cancers. The discovery of hypoxia inducible factors (HIFs), which mediate transcriptional responses to changes in oxygen levels, has renewed enthusiasm for the discovery and development of targeted therapies exploiting the hypoxic tumour microenvironment. In spite of an ever increasing number of putative small molecule inhibitors of HIF, only few progress through pre-clinical and early clinical development. In this review, we will focus primarily on: (1) HIF inhibitors that have been more recently described and (2) small molecules targeting HIF that are being tested in early clinical trials or that are already approved for use in patients. A rigorous 'validation' of HIF targeted therapies in relevant pre-clinical models and eventually in pharmacodynamic-based early clinical trials is essential for 'credentialing' HIF-1 as a legitimate target that can be pharmacologically modulated in cancer patients.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Drug Discovery ; Humans ; Hypoxia-Inducible Factor 1/antagonists & inhibitors ; Neoplasms/drug therapy
Chemical Substances	Antineoplastic Agents ; Hypoxia-Inducible Factor 1
Language	English
Publishing date	2009-08-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/j.1582-4934.2009.00876.x
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Article ; Online: Antiangiogenic agents and HIF-1 inhibitors meet at the crossroads.

Rapisarda, Annamaria / Shoemaker, Robert H / Melillo, Giovanni

Cell cycle (Georgetown, Tex.)

2009 Volume 8, Issue 24, Page(s) 4040–4043

Abstract: Novel molecularly targeted therapies aim at exploiting oncogenic and non-oncogenic alterations that epitomize potential vulnerable aspects of tumorigenesis, with the hope to ultimately target cancer cells and spare normal tissues. Hypoxia, a decrease in ... ...

Abstract	Novel molecularly targeted therapies aim at exploiting oncogenic and non-oncogenic alterations that epitomize potential vulnerable aspects of tumorigenesis, with the hope to ultimately target cancer cells and spare normal tissues. Hypoxia, a decrease in tissue oxygen levels, is a feature of the tumor microenvironment that has attracted considerable interest for its potential contribution to increasing the tumorigenicity of cancer cells, by selecting more aggressive and metastatic clones and by activating pathways that contribute to cancer cells survival, all of which may have important therapeutic implications. In this article, we discuss how two therapeutic strategies, which have been developed over the last few years to target aspects dependent on or associated with intratumor hypoxia, may provide the rationale for a novel combination strategy aimed at blocking compensatory circuits that maintain cancer cells survival and propagate the cancer phenotype. We hypothesized that concurrent inhibition of HIF-1 and VEGF, which are mechanistically linked to intratumor hypoxia, represents a logical therapeutic combination that may find applications in a number of solid tumors, irrespective of their underlying genetic alterations. Indeed, intrinsic limitations of HIF-1 inhibitors and mechanisms of acquired resistance to anti-VEGF therapies may counter-balance each other in combination approaches that block vicious compensatory pathways exploited by cancer cells to overcome environmental stresses.
MeSH term(s)	Angiogenesis Inhibitors/therapeutic use ; Antineoplastic Agents/therapeutic use ; Drug Resistance, Neoplasm ; Drug Therapy, Combination ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors ; Neoplasms/blood supply ; Neoplasms/drug therapy ; Neovascularization, Pathologic/drug therapy
Chemical Substances	Angiogenesis Inhibitors ; Antineoplastic Agents ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit
Language	English
Publishing date	2009-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.8.24.10145
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Article ; Online: Autocrine production of IL-11 mediates tumorigenicity in hypoxic cancer cells.

Onnis, Barbara / Fer, Nicole / Rapisarda, Annamaria / Perez, Victor S / Melillo, Giovanni

The Journal of clinical investigation

2013 Volume 123, Issue 4, Page(s) 1615–1629

Abstract: IL-11 and its receptor, IL-11Ra, are expressed in human cancers; however, the functional role of IL-11 in tumor progression is not known. We found that IL11 is a hypoxia-inducible, VHL-regulated gene in human cancer cells and that expression of IL11 mRNA ...

Abstract	IL-11 and its receptor, IL-11Ra, are expressed in human cancers; however, the functional role of IL-11 in tumor progression is not known. We found that IL11 is a hypoxia-inducible, VHL-regulated gene in human cancer cells and that expression of IL11 mRNA was dependent, at least in part, on HIF-1. A cooperative interaction between HIF-1 and AP-1 mediated transcriptional activation of the IL11 promoter. Additionally, we found that human cancer cells expressed a functional IL-11Ra subunit, which triggered signal transduction either by exogenous recombinant human IL-11 or by autocrine production of IL-11 in cells cultured under hypoxic conditions. Silencing of IL11 dramatically abrogated the ability of hypoxia to increase anchorage-independent growth and significantly reduced tumor growth in xenograft models. Notably, these results were phenocopied by partial knockdown of STAT1 in a human prostate cancer cell line (PC3), suggesting that this pathway may play an important role in mediating the effects of IL-11 under hypoxic conditions. In conclusion, these results identify IL11 as an oxygen- and VHL-regulated gene and provide evidence of a pathway "hijacked" by hypoxic cancer cells that may contribute to tumor progression.
MeSH term(s)	Animals ; Antigens, Neoplasm/genetics ; Antigens, Neoplasm/metabolism ; Autocrine Communication ; Basic Helix-Loop-Helix Transcription Factors/physiology ; Binding Sites ; Carbonic Anhydrase IX ; Carbonic Anhydrases/genetics ; Carbonic Anhydrases/metabolism ; Cell Hypoxia ; Cell Proliferation ; Cell Transformation, Neoplastic/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; HCT116 Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/physiology ; Interleukin-11/genetics ; Interleukin-11/metabolism ; Interleukin-11/physiology ; Interleukin-11 Receptor alpha Subunit/genetics ; Interleukin-11 Receptor alpha Subunit/metabolism ; Interleukin-11 Receptor alpha Subunit/physiology ; MAP Kinase Signaling System ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Phosphorylation ; Protein Processing, Post-Translational ; RNA Interference ; Response Elements ; STAT1 Transcription Factor/metabolism ; Transcription Factor AP-1/physiology ; Transcriptional Activation ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Von Hippel-Lindau Tumor Suppressor Protein/physiology
Chemical Substances	Antigens, Neoplasm ; Basic Helix-Loop-Helix Transcription Factors ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; IL11 protein, human ; IL11RA protein, human ; Interleukin-11 ; Interleukin-11 Receptor alpha Subunit ; STAT1 Transcription Factor ; STAT1 protein, human ; Transcription Factor AP-1 ; VEGFA protein, human ; Vascular Endothelial Growth Factor A ; endothelial PAS domain-containing protein 1 (1B37H0967P) ; Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27) ; CA9 protein, human (EC 4.2.1.1) ; Carbonic Anhydrase IX (EC 4.2.1.1) ; Carbonic Anhydrases (EC 4.2.1.1) ; VHL protein, human (EC 6.3.2.-)
Language	English
Publishing date	2013-03-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI59623
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Article: Targeting topoisomerase I to inhibit hypoxia inducible factor 1.

Rapisarda, Annamaria / Shoemaker, Robert H / Melillo, Giovanni

Cell cycle (Georgetown, Tex.)

2004 Volume 3, Issue 2, Page(s) 172–175

Abstract: HIF-1 is a key factor in cancer progression. Efforts are underway to identify and develop small molecules that inhibit HIF-1 transcriptional activity. What are the best targets and the best ways to develop HIF-1 inhibitors are open questions. However, ... ...

Abstract	HIF-1 is a key factor in cancer progression. Efforts are underway to identify and develop small molecules that inhibit HIF-1 transcriptional activity. What are the best targets and the best ways to develop HIF-1 inhibitors are open questions. However, several "nonselective" HIF-1 inhibitors have been identified, which are either in the clinic or under development. In this article, we discuss how topoisomerase I poisons, which inhibit HIF-1a protein accumulation and transcriptional activity, can be "rationally" used to target HIF-1 for cancer therapy.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Cell Hypoxia/physiology ; Cyclooxygenase 2 ; DNA Topoisomerases, Type I/metabolism ; DNA-Binding Proteins/antagonists & inhibitors ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/physiology ; Helix-Loop-Helix Motifs/physiology ; Humans ; Hypoxia-Inducible Factor 1 ; Hypoxia-Inducible Factor 1, alpha Subunit ; Isoenzymes/metabolism ; Membrane Proteins ; Nuclear Proteins/antagonists & inhibitors ; Nuclear Proteins/metabolism ; Prostaglandin-Endoperoxide Synthases/metabolism ; Signal Transduction/physiology ; Topoisomerase I Inhibitors ; Topotecan/pharmacology ; Transcription Factors ; Tumor Cells, Cultured ; Vascular Endothelial Growth Factor A/metabolism
Chemical Substances	Antineoplastic Agents ; DNA-Binding Proteins ; HIF1A protein, human ; Hypoxia-Inducible Factor 1 ; Hypoxia-Inducible Factor 1, alpha Subunit ; Isoenzymes ; Membrane Proteins ; Nuclear Proteins ; Topoisomerase I Inhibitors ; Transcription Factors ; Vascular Endothelial Growth Factor A ; Topotecan (7M7YKX2N15) ; Cyclooxygenase 2 (EC 1.14.99.1) ; PTGS2 protein, human (EC 1.14.99.1) ; Prostaglandin-Endoperoxide Synthases (EC 1.14.99.1) ; DNA Topoisomerases, Type I (EC 5.99.1.2)
Language	English
Publishing date	2004-01-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
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