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Article ; Online: Intraductal papillary mucinous neoplasm: clinical surveillance and management decisions.

Chin, Joanna Y / Pitman, Martha B / Hong, Theodore S

2014 Volume 24, Issue 2, Page(s) 77–84

Abstract: Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is a relatively rare cystic neoplasm. Although most IPMNs appear to be benign and may be managed by surveillance, all IPMNs are considered premalignant lesions with malignant potential. As ... ...

Abstract	Intraductal papillary mucinous neoplasm (IPMN) of the pancreas is a relatively rare cystic neoplasm. Although most IPMNs appear to be benign and may be managed by surveillance, all IPMNs are considered premalignant lesions with malignant potential. As such, current efforts are focused on identifying those neoplasms that are at high risk for malignancy to optimize treatment strategy and outcome. IPMNs with invasive carcinoma have clinical outcomes that approach those of conventional pancreatic ductal adenocarcinoma. Management guidelines recommend surgical resection for IPMNs with high-risk imaging or cytologic features. The role of adjuvant therapy is unclear, and we review the evidence for chemoradiation here. Some studies suggest adjuvant chemoradiation may have the greatest impact in malignant IPMNs with adverse histologic features, that is, lymph node metastasis at the time of diagnosis or positive surgical margins. As more IPMNs are recognized and treated, more evidence will accumulate to guide clinicians regarding appropriate use of radiotherapy in the management of IPMN.
MeSH term(s)	Adenocarcinoma, Mucinous/diagnosis ; Adenocarcinoma, Mucinous/radiotherapy ; Adenocarcinoma, Mucinous/surgery ; Carcinoma, Pancreatic Ductal/diagnosis ; Carcinoma, Pancreatic Ductal/radiotherapy ; Carcinoma, Pancreatic Ductal/surgery ; Carcinoma, Papillary/diagnosis ; Carcinoma, Papillary/radiotherapy ; Carcinoma, Papillary/surgery ; Humans ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/radiotherapy ; Pancreatic Neoplasms/surgery ; Prognosis ; Radiotherapy, Adjuvant
Language	English
Publishing date	2014-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1146999-7
ISSN	1532-9461 ; 1053-4296
ISSN (online)	1532-9461
ISSN	1053-4296
DOI	10.1016/j.semradonc.2013.11.005
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Article ; Online: Tumor Biomechanics Alters Metastatic Dissemination of Triple Negative Breast Cancer via Rewiring Fatty Acid Metabolism.

Filipe, Elysse C / Velayuthar, Sipiththa / Philp, Ashleigh / Nobis, Max / Latham, Sharissa L / Parker, Amelia L / Murphy, Kendelle J / Wyllie, Kaitlin / Major, Gretel S / Contreras, Osvaldo / Mok, Ellie T Y / Enriquez, Ronaldo F / McGowan, Suzanne / Feher, Kristen / Quek, Lake-Ee / Hancock, Sarah E / Yam, Michelle / Tran, Emmi / Setargew, Yordanos F I /

Skhinas, Joanna N / Chitty, Jessica L / Phimmachanh, Monica / Han, Jeremy Z R / Cadell, Antonia L / Papanicolaou, Michael / Mahmodi, Hadi / Kiedik, Beata / Junankar, Simon / Ross, Samuel E / Lam, Natasha / Coulson, Rhiannon / Yang, Jessica / Zaratzian, Anaiis / Da Silva, Andrew M / Tayao, Michael / Chin, Ian L / Cazet, Aurélie / Kansara, Maya / Segara, Davendra / Parker, Andrew / Hoy, Andrew J / Harvey, Richard P / Bogdanovic, Ozren / Timpson, Paul / Croucher, David R / Lim, Elgene / Swarbrick, Alexander / Holst, Jeff / Turner, Nigel / Choi, Yu Suk / Kabakova, Irina V / Philp, Andrew / Cox, Thomas R

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

2024 , Page(s) e2307963

Abstract: In recent decades, the role of tumor biomechanics on cancer cell behavior at the primary site has been increasingly appreciated. However, the effect of primary tumor biomechanics on the latter stages of the metastatic cascade, such as metastatic seeding ... ...

Abstract	In recent decades, the role of tumor biomechanics on cancer cell behavior at the primary site has been increasingly appreciated. However, the effect of primary tumor biomechanics on the latter stages of the metastatic cascade, such as metastatic seeding of secondary sites and outgrowth remains underappreciated. This work sought to address this in the context of triple negative breast cancer (TNBC), a cancer type known to aggressively disseminate at all stages of disease progression. Using mechanically tuneable model systems, mimicking the range of stiffness's typically found within breast tumors, it is found that, contrary to expectations, cancer cells exposed to softer microenvironments are more able to colonize secondary tissues. It is shown that heightened cell survival is driven by enhanced metabolism of fatty acids within TNBC cells exposed to softer microenvironments. It is demonstrated that uncoupling cellular mechanosensing through integrin β1 blocking antibody effectively causes stiff primed TNBC cells to behave like their soft counterparts, both in vitro and in vivo. This work is the first to show that softer tumor microenvironments may be contributing to changes in disease outcome by imprinting on TNBC cells a greater metabolic flexibility and conferring discrete cell survival advantages.
Language	English
Publishing date	2024-04-11
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2808093-2
ISSN	2198-3844 ; 2198-3844
ISSN (online)	2198-3844
ISSN	2198-3844
DOI	10.1002/advs.202307963
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Article ; Online: Triplex-forming peptide nucleic acids induce heritable elevations in gamma-globin expression in hematopoietic progenitor cells.

Chin, Joanna Y / Reza, Faisal / Glazer, Peter M

Molecular therapy : the journal of the American Society of Gene Therapy

2013 Volume 21, Issue 3, Page(s) 580–587

Abstract: Potentiating homologous recombination using triplex-forming peptide nucleic acids (PNAs) can be used to mediate targeted sequence editing by donor DNAs and thereby induce functional gene expression to supplant non-functional counterparts. Mutations that ... ...

Abstract	Potentiating homologous recombination using triplex-forming peptide nucleic acids (PNAs) can be used to mediate targeted sequence editing by donor DNAs and thereby induce functional gene expression to supplant non-functional counterparts. Mutations that disrupt the normal function of the β-globin subunit cause hemoglobinopathies such as sickle cell disease and β-thalassemias. However, expression of the functional γ-globin subunit in adults, a benign condition called hereditary persistence of fetal hemoglobin (HPFH), can ameliorate the severity of these disorders, but this expression is normally silenced. Here, we harness triplex-forming PNA-induced donor DNA recombination to create HPFH mutations that increase the expression of γ-globin in adult mammalian cells, including β-yeast artificial chromosome (YAC) bone marrow and hematopoietic progenitor cells (HPCs). Transfection of human cells led to site-specific modification frequencies of 1.63% using triplex-forming PNA γ-194-3K in conjunction with donor DNAs, compared with 0.29% using donor DNAs alone. We also concurrently modified the γ-globin promoter to insert both HPFH-associated point mutations and a hypoxia-responsive element (HRE), conferring increased expression that was also regulated by oxygen tension. This work demonstrates application of oligonucleotide-based gene therapy to induce a quiescent gene promoter in mammalian cells and regulate its expression via an introduced HRE transcription factor binding site for potential therapeutic purposes.
MeSH term(s)	Adult ; Animals ; Antigens, CD34/metabolism ; Cell Line ; Chromosomes, Artificial, Yeast/metabolism ; DNA/chemistry ; DNA/genetics ; Fetal Hemoglobin/genetics ; Fetal Hemoglobin/metabolism ; Gene Expression Regulation ; Genetic Therapy ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Hemoglobinopathies/therapy ; Humans ; K562 Cells ; Mice ; Mice, Transgenic ; Mutation ; Peptide Nucleic Acids/chemistry ; Peptide Nucleic Acids/genetics ; Promoter Regions, Genetic ; Transfection ; gamma-Globins/genetics ; gamma-Globins/metabolism
Chemical Substances	Antigens, CD34 ; Peptide Nucleic Acids ; gamma-Globins ; triplex DNA ; DNA (9007-49-2) ; Fetal Hemoglobin (9034-63-3)
Language	English
Publishing date	2013-01-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1038/mt.2012.262
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Zs.A 5640: Show issues

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Article ; Online: Mitomycin in anal cancer: still the standard of care.

Chin, Joanna Y / Hong, Theodore S / Ryan, David P

Journal of clinical oncology : official journal of the American Society of Clinical Oncology

2012 Volume 30, Issue 35, Page(s) 4297–4301

Abstract: A 52-year-old woman presents with a 2-month history of bright red blood per rectum. Her bleeding is associated with bowel movements and a sense of incomplete evacuation. She denies fecal incontinence or change in stool caliber. On digital rectal ... ...

Abstract	A 52-year-old woman presents with a 2-month history of bright red blood per rectum. Her bleeding is associated with bowel movements and a sense of incomplete evacuation. She denies fecal incontinence or change in stool caliber. On digital rectal examination, the tumor is palpated approximately 3 cm from the anal verge, posterior and slightly to the right, positioned at the top of the anal canal and extending into the rectum, measuring approximately 2.5 cm. Additionally, a firm 1.5-cm left-sided inguinal node is palpated. The patient is then referred for colonoscopy, which reveals a mass in the anal canal; biopsy of the mass shows squamous cell carcinoma. Positron emission tomography-computed tomography (PET-CT) demonstrates thickening in the low rectum with [(18)F]fluorodeoxyglucose (FDG) avidity (Figs 1A, 1B). The left inguinal node is visualized, as is a perirectal lymph node with associated FDG avidity (Figs 1C, 1D). The patient is staged as having T2N3 squamous cell carcinoma of the anal canal (Table 1). Her medical history is otherwise unremarkable, including for HIV, prior abnormal Papanicolaou smears, and other risk factors for human papillomavirus (HPV) exposure.
MeSH term(s)	Antibiotics, Antineoplastic/therapeutic use ; Anus Neoplasms/diagnostic imaging ; Anus Neoplasms/drug therapy ; Anus Neoplasms/pathology ; Carcinoma, Squamous Cell/diagnostic imaging ; Carcinoma, Squamous Cell/drug therapy ; Carcinoma, Squamous Cell/pathology ; Female ; Humans ; Middle Aged ; Mitomycin/therapeutic use ; Positron-Emission Tomography
Chemical Substances	Antibiotics, Antineoplastic ; Mitomycin (50SG953SK6)
Language	English
Publishing date	2012-12-10
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	604914-x
ISSN	1527-7755 ; 0732-183X
ISSN (online)	1527-7755
ISSN	0732-183X
DOI	10.1200/JCO.2012.44.8878
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Zs.A 1847: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 650: Show issues

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Article ; Online: Repair of DNA lesions associated with triplex-forming oligonucleotides.

Chin, Joanna Y / Glazer, Peter M

Molecular carcinogenesis

2006 Volume 48, Issue 4, Page(s) 389–399

Abstract: Triplex-forming oligonucleotides (TFOs) are gene targeting tools that can bind in the major groove of duplex DNA in a sequence-specific manner. When bound to DNA, TFOs can inhibit gene expression, can position DNA-reactive agents to specific locations in ...

Abstract	Triplex-forming oligonucleotides (TFOs) are gene targeting tools that can bind in the major groove of duplex DNA in a sequence-specific manner. When bound to DNA, TFOs can inhibit gene expression, can position DNA-reactive agents to specific locations in the genome, or can induce targeted mutagenesis and recombination. There is evidence that third strand binding, alone or with an associated cross-link, is recognized and metabolized by DNA repair factors, particularly the nucleotide excision repair pathway. This review examines the evidence for DNA repair of triplex-associated lesions.
MeSH term(s)	Animals ; DNA/chemistry ; DNA/genetics ; DNA/metabolism ; DNA Damage ; DNA Repair ; Humans ; Nucleic Acid Conformation ; Oligonucleotides/chemistry ; Oligonucleotides/genetics ; Oligonucleotides/metabolism
Chemical Substances	Oligonucleotides ; triplex DNA ; DNA (9007-49-2)
Language	English
Publishing date	2006-12-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.20501
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Zs.A 2664: Show issues

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Article: Triplex-mediated gene modification.

Schleifman, Erica B / Chin, Joanna Y / Glazer, Peter M

Methods in molecular biology (Clifton, N.J.)

2008 Volume 435, Page(s) 175–190

Abstract: Gene targeting with DNA-binding molecules such as triplex-forming oligonucleotides or peptide nucleic acids can be utilized to direct mutagenesis or induce recombination site-specifically. In this chapter, several detailed protocols are described for the ...

Abstract	Gene targeting with DNA-binding molecules such as triplex-forming oligonucleotides or peptide nucleic acids can be utilized to direct mutagenesis or induce recombination site-specifically. In this chapter, several detailed protocols are described for the design and use of triplex-forming molecules to bind and mediate gene modification at specific chromosomal targets. Target site identification, binding molecule design, as well as various methods to test binding and assess gene modification are described.
MeSH term(s)	Animals ; Base Sequence ; Binding Sites/genetics ; CHO Cells ; Cricetinae ; Cricetulus ; DNA/genetics ; DNA/metabolism ; Gene Targeting/methods ; Genes, Reporter ; Genetic Techniques ; Luciferases/genetics ; Molecular Sequence Data ; Mutagenesis, Site-Directed/methods ; Nucleic Acid Conformation ; Oligonucleotides/chemistry ; Oligonucleotides/genetics ; Oligonucleotides/metabolism ; Peptide Nucleic Acids/chemistry ; Peptide Nucleic Acids/genetics ; Peptide Nucleic Acids/metabolism ; Recombination, Genetic
Chemical Substances	Oligonucleotides ; Peptide Nucleic Acids ; DNA (9007-49-2) ; Luciferases (EC 1.13.12.-)
Language	English
Publishing date	2008
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1064-3745
ISSN	1064-3745
DOI	10.1007/978-1-59745-232-8_13
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Article: Repair and recombination induced by triple helix DNA.

Chin, Joanna Y / Schleifman, Erica B / Glazer, Peter M

Frontiers in bioscience : a journal and virtual library

2007 Volume 12, Page(s) 4288–4297

Abstract: Triple-helix DNA structures can form endogenously at mirror repeat polypurine/polypyrimidine sequences or by introduction of triplex-forming oligonucleotides (TFOs). Recent evidence suggests that triple helices are sources of genetic instability, and are ...

Abstract	Triple-helix DNA structures can form endogenously at mirror repeat polypurine/polypyrimidine sequences or by introduction of triplex-forming oligonucleotides (TFOs). Recent evidence suggests that triple helices are sources of genetic instability, and are subject to increased rates of mutagenesis and recruitment of repair factors. Indeed, observations using TFOs suggest that triple helices provoke a variety of biological processes which can be harnessed to modulate gene expression and induce heritable changes in targeted genes. This review surveys the biological applications of TFOs, with particular attention to their recombinogenic and mutagenic potential, and summarizes available evidence for the mechanism of triplex and triplex-associated repair.
MeSH term(s)	DNA/chemistry ; DNA/physiology ; DNA Repair ; Nucleic Acid Conformation ; Recombination, Genetic
Chemical Substances	triplex DNA ; DNA (9007-49-2)
Language	English
Publishing date	2007-05-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2141320-4
ISSN	1093-9946
ISSN	1093-9946
DOI	10.2741/2388
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Zs.A 5867: Show issues

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Article ; Online: Nanoparticles deliver triplex-forming PNAs for site-specific genomic recombination in CD34+ human hematopoietic progenitors.

McNeer, Nicole A / Chin, Joanna Y / Schleifman, Erica B / Fields, Rachel J / Glazer, Peter M / Saltzman, W Mark

Molecular therapy : the journal of the American Society of Gene Therapy

2010 Volume 19, Issue 1, Page(s) 172–180

Abstract: Triplex-forming peptide nucleic acids (PNAs) are powerful gene therapy agents that can enhance recombination of short donor DNAs with genomic DNA, leading to targeted and specific correction of disease-causing genetic mutations. Therapeutic use of PNAs ... ...

Abstract	Triplex-forming peptide nucleic acids (PNAs) are powerful gene therapy agents that can enhance recombination of short donor DNAs with genomic DNA, leading to targeted and specific correction of disease-causing genetic mutations. Therapeutic use of PNAs is severely limited, however, by challenges in intracellular delivery, particularly in clinically relevant targets such as hematopoietic stem and progenitor cells. Here, we demonstrate efficient and nontoxic PNA-mediated recombination in human CD34(+) cells using poly(lactic-co-glycolic acid) (PLGA) nanoparticles for intracellular oligonucleotide delivery. Treatment of progenitor cells with nanoparticles loaded with PNAs and DNAs targeting the β-globin locus led to levels of site-specific modification in the range of 0.5-1% in a single treatment, without detectable loss in cell viability, resulting in a 60-fold increase in modified and viable cells as compared to nucleofection. As well, the differentiation capacity of the progenitor cells treated with nanoparticles did not change relative to untreated progenitor cells, indicating that nanoparticles are safe and minimally disruptive delivery vectors for PNAs and DNAs to mediate gene modification in human primary cells. This is the first demonstration of the use of biodegradable nanoparticles to deliver genome-editing agents to human primary cells, and provides a strong rationale for systemic delivery of complex nucleic acid mixtures designed for gene correction.
MeSH term(s)	Antigens, CD34/biosynthesis ; Cell Survival/drug effects ; Cells, Cultured ; DNA/genetics ; Gene Targeting/methods ; Gene Transfer Techniques ; Genome ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/physiology ; Humans ; Lactic Acid/pharmacology ; Nanoparticles/administration & dosage ; Nanoparticles/chemistry ; Oligonucleotides/pharmacology ; Particle Size ; Peptide Nucleic Acids/administration & dosage ; Peptide Nucleic Acids/genetics ; Polyglycolic Acid/pharmacology ; Polylactic Acid-Polyglycolic Acid Copolymer ; Receptors, CCR5/genetics ; Recombination, Genetic ; Targeted Gene Repair ; beta-Globins/genetics
Chemical Substances	Antigens, CD34 ; Oligonucleotides ; Peptide Nucleic Acids ; Receptors, CCR5 ; beta-Globins ; triplex DNA ; Polylactic Acid-Polyglycolic Acid Copolymer (1SIA8062RS) ; Polyglycolic Acid (26009-03-0) ; Lactic Acid (33X04XA5AT) ; DNA (9007-49-2)
Language	English
Publishing date	2010-09-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1038/mt.2010.200
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Zs.A 5640: Show issues

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Article ; Online: DNA hypomethylation silences anti-tumor immune genes in early prostate cancer and CTCs.

Cell

2023 Volume 186, Issue 13, Page(s) 2765–2782.e28

Abstract: Cancer is characterized by hypomethylation-associated silencing of large chromatin domains, whose contribution to tumorigenesis is uncertain. Through high-resolution genome-wide single-cell DNA methylation sequencing, we identify 40 core domains that are ...

Abstract	Cancer is characterized by hypomethylation-associated silencing of large chromatin domains, whose contribution to tumorigenesis is uncertain. Through high-resolution genome-wide single-cell DNA methylation sequencing, we identify 40 core domains that are uniformly hypomethylated from the earliest detectable stages of prostate malignancy through metastatic circulating tumor cells (CTCs). Nested among these repressive domains are smaller loci with preserved methylation that escape silencing and are enriched for cell proliferation genes. Transcriptionally silenced genes within the core hypomethylated domains are enriched for immune-related genes; prominent among these is a single gene cluster harboring all five CD1 genes that present lipid antigens to NKT cells and four IFI16-related interferon-inducible genes implicated in innate immunity. The re-expression of CD1 or IFI16 murine orthologs in immuno-competent mice abrogates tumorigenesis, accompanied by the activation of anti-tumor immunity. Thus, early epigenetic changes may shape tumorigenesis, targeting co-located genes within defined chromosomal loci. Hypomethylation domains are detectable in blood specimens enriched for CTCs.
MeSH term(s)	Animals ; Humans ; Male ; Mice ; Carcinogenesis/genetics ; DNA ; DNA Methylation ; Epigenesis, Genetic ; Prostatic Neoplasms/genetics ; Neoplastic Cells, Circulating
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2023-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2023.05.028
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Zs.A 1167: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 58: Show issues

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Article: Correction of a splice-site mutation in the beta-globin gene stimulated by triplex-forming peptide nucleic acids

Chin, Joanna Y / Kuan, Jean Y / Lonkar, Pallavi S / Krause, Diane S / Seidman, Michael M / Peterson, Kenneth R / Nielsen, Peter E / Kole, Ryszard / Glazer, Peter M

Proceedings of the National Academy of Sciences of the United States of America. 2008 Sept. 9, v. 105, no. 36

2008

Abstract: Splice-site mutations in the beta-globin gene can lead to aberrant transcripts and decreased functional beta-globin, causing beta-thalassemia. Triplex-forming DNA oligonucleotides (TFOs) and peptide nucleic acids (PNAs) have been shown to stimulate ... ...

Abstract	Splice-site mutations in the beta-globin gene can lead to aberrant transcripts and decreased functional beta-globin, causing beta-thalassemia. Triplex-forming DNA oligonucleotides (TFOs) and peptide nucleic acids (PNAs) have been shown to stimulate recombination in reporter gene loci in mammalian cells via site-specific binding and creation of altered helical structures that provoke DNA repair. We have designed a series of triplex-forming PNAs that can specifically bind to sequences in the human beta-globin gene. We demonstrate here that these PNAs, when cotransfected with recombinatory donor DNA fragments, can promote single base-pair modification at the start of the second intron of the beta-globin gene, the site of a common thalassemia-associated mutation. This single base pair change was detected by the restoration of proper splicing of transcripts produced from a green fluorescent protein-beta-globin fusion gene. The ability of these PNAs to induce recombination was dependent on dose, sequence, cell-cycle stage, and the presence of a homologous donor DNA molecule. Enhanced recombination, with frequencies up to 0.4%, was observed with use of the lysomotropic agent chloroquine. Finally, we demonstrate that these PNAs were effective in stimulating the modification of the endogenous beta-globin locus in human cells, including primary hematopoietic progenitor cells. This work suggests that PNAs can be effective tools to induce heritable, site-specific modification of disease-related genes in human cells.
Language	English
Dates of publication	2008-0909
Size	p. 13514-13519.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
Database	NAL-Catalogue (AGRICOLA)

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