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Article: Reactivation of telomerase reverse transcriptase expression in cancer: the role of TERT promoter mutations.

Tornesello, Maria Lina / Cerasuolo, Andrea / Starita, Noemy / Amiranda, Sara / Bonelli, Patrizia / Tuccillo, Franca Maria / Buonaguro, Franco M / Buonaguro, Luigi / Tornesello, Anna Lucia

Frontiers in cell and developmental biology

2023 Volume 11, Page(s) 1286683

Abstract: Telomerase activity and telomere elongation are essential conditions for the unlimited proliferation of neoplastic cells. Point mutations in the core promoter region of the telomerase reverse transcriptase (TERT) gene have been found to occur at high ... ...

Abstract	Telomerase activity and telomere elongation are essential conditions for the unlimited proliferation of neoplastic cells. Point mutations in the core promoter region of the telomerase reverse transcriptase (TERT) gene have been found to occur at high frequencies in several tumour types and considered a primary cause of telomerase reactivation in cancer cells. These mutations promote TERT gene expression by multiple mechanisms, including the generation of novel binding sites for nuclear transcription factors, displacement of negative regulators from DNA G-quadruplexes, recruitment of epigenetic activators and disruption of long-range interactions between TERT locus and telomeres. Furthermore, TERT promoter mutations cooperate with TPP1 promoter nucleotide changes to lengthen telomeres and with mutated BRAF and FGFR3 oncoproteins to enhance oncogenic signalling in cancer cells. TERT promoter mutations have been recognized as an early marker of tumour development or a major indicator of poor outcome and reduced patients survival in several cancer types. In this review, we summarize recent findings on the role of TERT promoter mutations, telomerase expression and telomeres elongation in cancer development, their clinical significance and therapeutic opportunities.
Language	English
Publishing date	2023-11-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2023.1286683
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Article: The Role of circRNAs in Human Papillomavirus (HPV)-Associated Cancers.

Bonelli, Patrizia / Borrelli, Antonella / Tuccillo, Franca Maria / Buonaguro, Franco Maria / Tornesello, Maria Lina

Cancers

2021 Volume 13, Issue 5

Abstract: Circular RNAs (circRNAs) are a new class of "non-coding RNAs" that originate from non-sequential back-splicing of exons and/or introns of precursor messenger RNAs (pre-mRNAs). These molecules are generally produced at low levels in a cell-type-specific ... ...

Abstract	Circular RNAs (circRNAs) are a new class of "non-coding RNAs" that originate from non-sequential back-splicing of exons and/or introns of precursor messenger RNAs (pre-mRNAs). These molecules are generally produced at low levels in a cell-type-specific manner in mammalian tissues, but due to their circular conformation they are unaffected by the cell mRNA decay machinery. circRNAs can sponge multiple microRNAs or RNA-binding proteins and play a crucial role in the regulation of gene expression and protein translation. Many circRNAs have been shown to be aberrantly expressed in several cancer types, and to sustain specific oncogenic processes. Particularly, in virus-associated malignancies such as human papillomavirus (HPV)-associated anogenital carcinoma and oropharyngeal and oral cancers, circRNAs have been shown to be involved in tumorigenesis and cancer progression, as well as in drug resistance, and some are useful diagnostic and prognostic markers. HPV-derived circRNAs, encompassing the HPV E7 oncogene, have been shown to be expressed and to serve as transcript for synthesis of the E7 oncoprotein, thus reinforcing the virus oncogenic activity in HPV-associated cancers. In this review, we summarize research advances in the biogenesis of cell and viral circRNAs, their features and functions in the pathophysiology of HPV-associated tumors, and their importance as diagnostic, prognostic, and therapeutic targets in anogenital and oropharyngeal and oral cancers.
Language	English
Publishing date	2021-03-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13051173
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Article: The Molecular Interplay between Human Oncoviruses and Telomerase in Cancer Development.

Tornesello, Maria Lina / Cerasuolo, Andrea / Starita, Noemy / Tornesello, Anna Lucia / Bonelli, Patrizia / Tuccillo, Franca Maria / Buonaguro, Luigi / Isaguliants, Maria G / Buonaguro, Franco M

Cancers

2022 Volume 14, Issue 21

Abstract: Human oncoviruses are able to subvert telomerase function in cancer cells through multiple strategies. The activity of the catalytic subunit of telomerase (TERT) is universally enhanced in virus-related cancers. Viral oncoproteins, such as high-risk ... ...

Abstract	Human oncoviruses are able to subvert telomerase function in cancer cells through multiple strategies. The activity of the catalytic subunit of telomerase (TERT) is universally enhanced in virus-related cancers. Viral oncoproteins, such as high-risk human papillomavirus (HPV) E6, Epstein-Barr virus (EBV) LMP1, Kaposi's sarcoma-associated herpesvirus (HHV-8) LANA, hepatitis B virus (HBV) HBVx, hepatitis C virus (HCV) core protein and human T-cell leukemia virus-1 (HTLV-1) Tax protein, interact with regulatory elements in the infected cells and contribute to the transcriptional activation of TERT gene. Specifically, viral oncoproteins have been shown to bind TERT promoter, to induce post-transcriptional alterations of TERT mRNA and to cause epigenetic modifications, which have important effects on the regulation of telomeric and extra-telomeric functions of the telomerase. Other viruses, such as herpesviruses, operate by integrating their genomes within the telomeres or by inducing alternative lengthening of telomeres (ALT) in non-ALT cells. In this review, we recapitulate on recent findings on virus-telomerase/telomeres interplay and the importance of TERT-related oncogenic pathways activated by cancer-causing viruses.
Language	English
Publishing date	2022-10-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14215257
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Article: Precision medicine in gastric cancer.

Bonelli, Patrizia / Borrelli, Antonella / Tuccillo, Franca Maria / Silvestro, Lucrezia / Palaia, Raffaele / Buonaguro, Franco Maria

World journal of gastrointestinal oncology

2018 Volume 11, Issue 10, Page(s) 804–829

Abstract: Gastric cancer (GC) is a complex disease linked to a series of environmental factors and unhealthy lifestyle habits, and especially to genetic alterations. GC represents the second leading cause of cancer-related deaths worldwide. Its onset is subtle, ... ...

Abstract	Gastric cancer (GC) is a complex disease linked to a series of environmental factors and unhealthy lifestyle habits, and especially to genetic alterations. GC represents the second leading cause of cancer-related deaths worldwide. Its onset is subtle, and the majority of patients are diagnosed once the cancer is already advanced. In recent years, there have been innovations in the management of advanced GC including the introduction of new classifications based on its molecular characteristics. Thanks to new technologies such as next-generation sequencing and microarray, the Cancer Genome Atlas and Asian Cancer Research Group classifications have also paved the way for precision medicine in GC, making it possible to integrate diagnostic and therapeutic methods. Among the objectives of the subdivision of GC into subtypes is to select patients in whom molecular targeted drugs can achieve the best results; many lines of research have been initiated to this end. After phase III clinical trials, trastuzumab, anti-Erb-B2 receptor tyrosine kinase 2 (commonly known as ERBB2) and ramucirumab, anti-vascular endothelial growth factor receptor 2 (commonly known as VEGFR2) monoclonal antibodies, were approved and introduced into first- and second-line therapies for patients with advanced/metastatic GC. However, the heterogeneity of this neoplasia makes the practical application of such approaches difficult. Unfortunately, scientific progress has not been matched by progress in clinical practice in terms of significant improvements in prognosis. Survival continues to be low in contrast to the reduction in deaths from many common cancers such as colorectal, lung, breast, and prostate cancers. Although several target molecules have been identified on which targeted drugs can act and novel products have been introduced into experimental therapeutic protocols, the overall approach to treating advanced stage GC has not substantially changed. Currently, surgical resection with adjuvant or neoadjuvant radiotherapy and chemotherapy are the most effective treatments for this disease. Future research should not underestimate the heterogeneity of GC when developing diagnostic and therapeutic strategies aimed toward improving patient survival.
Language	English
Publishing date	2018-11-16
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2573696-6
ISSN	1948-5204
ISSN	1948-5204
DOI	10.4251/wjgo.v11.i10.804
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Article ; Online: UMG1/CD3ε-bispecific T-cell engager redirects T-cell cytotoxicity against diffuse large B-cell lymphoma.

British journal of haematology

2023 Volume 204, Issue 2, Page(s) 555–560

Abstract: UMG1 is a unique epitope of CD43, not expressed by normal cells and tissues of haematopoietic and non-haematopoietic origin, except thymocytes and a minority (<5%) of peripheral blood T lymphocytes. By immunohistochemistry analysis of tissue microarray ... ...

Abstract	UMG1 is a unique epitope of CD43, not expressed by normal cells and tissues of haematopoietic and non-haematopoietic origin, except thymocytes and a minority (<5%) of peripheral blood T lymphocytes. By immunohistochemistry analysis of tissue microarray and pathology slides, we found high UMG1 expression in 20%-24% of diffuse large B-cell lymphomas (DLBCLs), including highly aggressive BCL2
MeSH term(s)	Humans ; T-Lymphocytes/metabolism ; Lymphoma, Large B-Cell, Diffuse/pathology ; Immunohistochemistry
Language	English
Publishing date	2023-11-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.19183
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Article ; Online: Role of gut microbiota and oxidative stress in the progression of non-alcoholic fatty liver disease to hepatocarcinoma: Current and innovative therapeutic approaches.

Borrelli, Antonella / Bonelli, Patrizia / Tuccillo, Franca Maria / Goldfine, Ira D / Evans, Joseph L / Buonaguro, Franco Maria / Mancini, Aldo

Redox biology

2018 Volume 15, Page(s) 467–479

Abstract: Non-alcoholic fatty liver disease (NAFLD) represents the most common chronic liver disease in industrialized countries. NAFLD progresses through the inflammatory phase of non-alcoholic steatohepatitis (NASH) to fibrosis and cirrhosis, with some cases ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) represents the most common chronic liver disease in industrialized countries. NAFLD progresses through the inflammatory phase of non-alcoholic steatohepatitis (NASH) to fibrosis and cirrhosis, with some cases developing liver failure or hepatocellular carcinoma (HCC). Liver biopsy remains the gold standard approach to a definitive diagnosis of NAFLD and the distinction between simple steatosis and NASH. The pathogenesis of NASH is still not clear. Several theories have been proposed ranging from the "Two Hit Theory" to the "Multiple Hit Theory". However, the general consensus is that the gut microbiota, oxidative stress, and mitochondrial damage play key roles in the pathogenesis of NASH. The interaction between the gut epithelia and some commensal bacteria induces the rapid generation of reactive oxygen species (ROS). The main goal of any therapy addressing NASH is to reverse or prevent progression to liver fibrosis/cirrhosis. This problem represents the first "Achilles' heel" of the new molecules being evaluated in most ongoing clinical trials. The second is the inability of these molecules to reach the mitochondria, the primary sites of energy production and ROS generation. Recently, a variety of non-pharmacological and pharmacological treatment approaches for NASH have been evaluated including vitamin E, the thiazolidinediones, and novel molecules related to NASH pathogenesis (including obeticholic acid and elafibranor). Recently, a new isoform of human manganese superoxide dismutase (MnSOD) was isolated and obtained in a synthetic recombinant form designated rMnSOD. This protein has been shown to be a powerful antioxidant capable of mediating ROS dismutation, penetrating biological barriers via its uncleaved leader peptide, and reducing portal hypertension and fibrosis in rats affected by liver cirrhosis. Based on these distinctive characteristics, it can be hypothesized that this novel recombinant protein (rMnSOD) potentially represents a new and highly efficient adjuvant therapy to counteract the progression from NASH to HCC.
MeSH term(s)	Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/microbiology ; Carcinoma, Hepatocellular/pathology ; Gastrointestinal Microbiome ; Humans ; Liver/metabolism ; Liver/microbiology ; Liver/pathology ; Liver Neoplasms/metabolism ; Liver Neoplasms/microbiology ; Liver Neoplasms/pathology ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/microbiology ; Non-alcoholic Fatty Liver Disease/pathology ; Oxidative Stress/genetics ; Reactive Oxygen Species/toxicity
Chemical Substances	Reactive Oxygen Species
Language	English
Publishing date	2018-02-03
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2018.01.009
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Article: A Novel Bispecific T-Cell Engager (CD1a x CD3ε) BTCE Is Effective against Cortical-Derived T Cell Acute Lymphoblastic Leukemia (T-ALL) Cells.

Riillo, Caterina / Caracciolo, Daniele / Grillone, Katia / Polerà, Nicoletta / Tuccillo, Franca Maria / Bonelli, Patrizia / Juli, Giada / Ascrizzi, Serena / Scionti, Francesca / Arbitrio, Mariamena / Lopreiato, Mariangela / Siciliano, Maria Anna / Sestito, Simona / Talarico, Gabriella / Galea, Eulalia / Galati, Maria Concetta / Pensabene, Licia / Loprete, Giovanni / Rossi, Marco /

Ballerini, Andrea / Gentile, Massimo / Britti, Domenico / Di Martino, Maria Teresa / Tagliaferri, Pierosandro / Tassone, Pierfrancesco

Cancers

2022 Volume 14, Issue 12

Abstract: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy burdened by poor prognosis. While huge progress of immunotherapy has recently improved the outcome of B-cell malignancies, the lack of tumor-restricted T-cell antigens still hampers ... ...

Abstract	T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy burdened by poor prognosis. While huge progress of immunotherapy has recently improved the outcome of B-cell malignancies, the lack of tumor-restricted T-cell antigens still hampers its progress in T-ALL. Therefore, innovative immunotherapeutic agents are eagerly awaited. To this end, we generated a novel asymmetric (2 + 1) bispecific T-cell engager (BTCE) targeting CD1a and CD3ε (CD1a x CD3ε) starting from the development of a novel mAb named UMG2. UMG2 mAb reacts against CD1a, a glycoprotein highly expressed by cortical T-ALL cells. Importantly, no UMG2 binding was found on normal T-cells. CD1a x CD3ε induced high T-cell mediated cytotoxicity against CD1a+ T-ALL cells in vitro, as demonstrated by the concentration-dependent increase of T-cell proliferation, degranulation, induction of cell surface activation markers, and secretion of pro-inflammatory cytokines. Most importantly, in a PBMC-reconstituted NGS mouse model bearing human T-ALL, CD1a x CD3ε significantly inhibited the growth of human T-ALL xenografts, translating into a significant survival advantage of treated animals. In conclusion, CD1a x CD3ε is a novel BTCE highly active against CD1a-expressing cortical-derived T-ALL cells suitable for clinical development as an effective therapeutic option for this rare and aggressive disease.
Language	English
Publishing date	2022-06-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14122886
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Article ; Online: The functional role of MnSOD as a biomarker of human diseases and therapeutic potential of a new isoform of a human recombinant MnSOD.

Borrelli, Antonella / Schiattarella, Antonietta / Bonelli, Patrizia / Tuccillo, Franca Maria / Buonaguro, Franco Maria / Mancini, Aldo

BioMed research international

2014 Volume 2014, Page(s) 476789

Abstract: Reactive oxygen species (ROS) are generated as a consequence of metabolic reactions in the mitochondria of eukaryotic cells. This work describes the role of the manganese superoxide dismutase (MnSOD) as a biomarker of different human diseases and ... ...

Abstract	Reactive oxygen species (ROS) are generated as a consequence of metabolic reactions in the mitochondria of eukaryotic cells. This work describes the role of the manganese superoxide dismutase (MnSOD) as a biomarker of different human diseases and proposes a new therapeutic application for the prevention of cancer and its treatment. The paper also describes how a new form of human MnSOD was discovered, its initial application, and its clinical potentials. The MnSOD isolated from a human liposarcoma cell line (LSA) was able to kill cancer cells expressing estrogen receptors, but it did not have cytotoxic effects on normal cells. Together with its oncotoxic activity, the recombinant MnSOD (rMnSOD) exerts a radioprotective effect on normal cells irradiated with X-rays. The rMnSOD is characterized by the presence of a leader peptide, which allows the protein to enter cells: this unique property can be used in the radiodiagnosis of cancer or chemotherapy, conjugating radioactive substances or chemotherapic drugs to the leader peptide of the MnSOD. Compared to traditional chemotherapic agents, the drugs conjugated with the leader peptide of MnSOD can selectively reach and enter cancer cells, thus reducing the side effects of traditional treatments.
MeSH term(s)	Antioxidants/metabolism ; Biomarkers ; Cell Line, Tumor ; Humans ; Liposarcoma/genetics ; Liposarcoma/pathology ; Liposarcoma/therapy ; Mitochondria/metabolism ; Mitochondria/pathology ; Molecular Targeted Therapy ; Protein Isoforms/genetics ; Protein Isoforms/therapeutic use ; Reactive Oxygen Species/metabolism ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Superoxide Dismutase/therapeutic use
Chemical Substances	Antioxidants ; Biomarkers ; Protein Isoforms ; Reactive Oxygen Species ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2014-01-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2014/476789
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Article ; Online: CDK/CCN and CDKI alterations for cancer prognosis and therapeutic predictivity.

Bonelli, Patrizia / Tuccillo, Franca Maria / Borrelli, Antonella / Schiattarella, Antonietta / Buonaguro, Franco Maria

BioMed research international

2014 Volume 2014, Page(s) 361020

Abstract: The regulation of cell growth and division occurs in an accurate sequential manner. It is dictated by the accumulation of cyclins (CCNs) and cyclin-dependent kinases (CDKs) complexes and degradation of CCNs. In human tumors, instead, the cell cycle is ... ...

Abstract	The regulation of cell growth and division occurs in an accurate sequential manner. It is dictated by the accumulation of cyclins (CCNs) and cyclin-dependent kinases (CDKs) complexes and degradation of CCNs. In human tumors, instead, the cell cycle is deregulated, causing absence of differentiation and aberrant cell growth. Oncogenic alterations of CCNs, CDKs, and CDKIs have been reported in more than 90% of human cancers, and the most frequent are those related to the G1 phase. Several molecular mechanisms, including gene overexpression, chromosomal translocations, point mutations, insertions and deletions, missense and frame shift mutation, splicing, or methylation, may be responsible for these alterations. The cell cycle regulators are involved in tumor progression given their association with cancers characterized by higher incidence of relapses and chemotherapy resistance. In the last decade anticancer drug researches focused on new compounds, able to target molecules related to changes in genes associated with tumor status. Recently, the studies have focused on the restoration of cell cycle control modulating molecular targets involved in cancer-cell alterations. This paper aims to correlate alterations of cell cycle regulators with human cancers and therapeutic responsivity.
MeSH term(s)	Animals ; Cell Cycle ; Cyclin-Dependent Kinase Inhibitor Proteins/metabolism ; Cyclin-Dependent Kinases/metabolism ; Cyclins/metabolism ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Prognosis
Chemical Substances	Cyclin-Dependent Kinase Inhibitor Proteins ; Cyclins ; Cyclin-Dependent Kinases (EC 2.7.11.22)
Language	English
Publishing date	2014-01-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2014/361020
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Article ; Online: A new hexapeptide from the leader peptide of rMnSOD enters cells through the oestrogen receptor to deliver therapeutic molecules.

Borrelli, Antonella / Schiattarella, Antonietta / Mancini, Roberto / Pica, Alessandra / Pollio, Maria Laura / Ruggiero, Maria Grazia / Bonelli, Patrizia / De Luca, Viviana / Tuccillo, Franca Maria / Capasso, Clemente / Gori, Enrico / Sanseverino, Marina / Carpentieri, Andrea / Birolo, Leila / Pucci, Piero / Rommelaere, Jean / Mancini, Aldo

Scientific reports

2016 Volume 6, Page(s) 18691

Abstract: A 24-amino acid leader peptide of a new human recombinant manganese superoxide dismutase can enter cells and carry molecules. Here, we demonstrated that six of the 24 amino acids penetrate cells through a particular gate represented by a specific amino ... ...

Abstract	A 24-amino acid leader peptide of a new human recombinant manganese superoxide dismutase can enter cells and carry molecules. Here, we demonstrated that six of the 24 amino acids penetrate cells through a particular gate represented by a specific amino acid sequence of the oestrogen receptor (ER). We analysed the internalization of the synthetic hexapeptide and the cytotoxic activity of the hexapeptide conjugated to cisplatin on a cell line panel. In most cell lines, the hexapeptide delivered an amount of cisplatin that was 2 to 8 times greater than that released by cisplatin when the drug was used alone. This increased delivery increases the therapeutic index of cisplatin and reduces side effects caused by a high dosage or long-term treatment times. We may consider this hexapeptide a new molecular carrier to deliver molecules with therapeutic activity into ER(+) cells for diagnostic purposes and clinical or immune therapy.
MeSH term(s)	Amino Acid Sequence ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/metabolism ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cisplatin/chemistry ; Cisplatin/metabolism ; Cisplatin/pharmacology ; Drug Carriers/chemistry ; Drug Carriers/metabolism ; Drug Carriers/pharmacology ; Drug Screening Assays, Antitumor ; Endoplasmic Reticulum/metabolism ; Fluorescein/chemistry ; Fluorescein/metabolism ; Fluorescent Dyes/chemistry ; Fluorescent Dyes/metabolism ; Humans ; Inhibitory Concentration 50 ; Peptide Fragments/chemistry ; Peptide Fragments/metabolism ; Peptide Fragments/pharmacology ; Protein Sorting Signals ; Receptors, Estrogen/metabolism ; Recombinant Proteins/chemistry ; Superoxide Dismutase/chemistry
Chemical Substances	Antineoplastic Agents ; Drug Carriers ; Fluorescent Dyes ; Peptide Fragments ; Protein Sorting Signals ; Receptors, Estrogen ; Recombinant Proteins ; Superoxide Dismutase (EC 1.15.1.1) ; Cisplatin (Q20Q21Q62J) ; Fluorescein (TPY09G7XIR)
Language	English
Publishing date	2016-01-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep18691
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