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Article ; Online: Orthogonal immunoassays for IgG antibodies to SARS-CoV-2 antigens reveal that immune response lasts beyond 4 mo post illness onset.

Sasisekharan, Varun / Pentakota, Niharika / Jayaraman, Akila / Tharakaraman, Kannan / Wogan, Gerald N / Narayanasami, Uma

Proceedings of the National Academy of Sciences of the United States of America

2020 Volume 118, Issue 5

Abstract: Immune response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during the current pandemic remains a field of immense interest and active research worldwide. Although the severity of acute infection may depend on the intensity ... ...

Abstract	Immune response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection during the current pandemic remains a field of immense interest and active research worldwide. Although the severity of acute infection may depend on the intensity of innate and adaptive immunity, leading to higher morbidity and mortality, the longevity of IgG antibodies, including neutralizing activity to SARS-CoV-2, is viewed as a key correlate of immune protection. Amid reports and concern that there is a rapid decay of IgG antibody levels within 1 mo to 2 mo after acute infection, we set out to study the pattern and duration of IgG antibody response to various SARS-CoV-2 antigens in asymptomatic and symptomatic patients in a community setting. Herein, we show the correlation of IgG anti-spike protein S1 subunit, receptor binding domain, nucleocapsid, and virus neutralizing antibody titers with each other and with clinical features such as length and severity of COVID-19 illness. More importantly, using orthogonal measurements, we found the IgG titers to persist for more than 4 mo post symptom onset, implying that long-lasting immunity to COVID-19 from infection or vaccination might be observed, as seen with other coronaviruses such as SARS and Middle East respiratory syndrome.
MeSH term(s)	Adult ; Antibodies, Viral/blood ; COVID-19/immunology ; Female ; Humans ; Immunity, Humoral ; Immunoassay ; Immunoglobulin G/blood ; Longitudinal Studies ; Male ; Middle Aged ; SARS-CoV-2/immunology
Chemical Substances	Antibodies, Viral ; Immunoglobulin G
Language	English
Publishing date	2020-12-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2021615118
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Article: Early detection of the aflatoxin B

Fedeles, Bogdan I / Chawanthayatham, Supawadee / Croy, Robert G / Wogan, Gerald N / Essigmann, John M

Molecular & cellular oncology

2017 Volume 4, Issue 4, Page(s) e1329693

Abstract: Using duplex-consensus sequencing technology, we recently identified the characteristic high-resolution mutational spectrum of the liver carcinogen aflatoxin ... ...

Abstract	Using duplex-consensus sequencing technology, we recently identified the characteristic high-resolution mutational spectrum of the liver carcinogen aflatoxin B
Language	English
Publishing date	2017-05-19
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2017.1329693
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Article: Impacts of chemicals on liver cancer risk.

Wogan, G N

Seminars in cancer biology

2000 Volume 10, Issue 3, Page(s) 201–210

Abstract: Primary liver cancer (PLC) is of multifactorial etiology. Chronic infections by hepatitis B (HBV) and hepatitis C (HCV) viruses are major risk factors for most PLC cases worldwide, although mechanisms through which the infections cause PLC are still ... ...

Abstract	Primary liver cancer (PLC) is of multifactorial etiology. Chronic infections by hepatitis B (HBV) and hepatitis C (HCV) viruses are major risk factors for most PLC cases worldwide, although mechanisms through which the infections cause PLC are still unknown. Epidemiologic and experimental evidence indicates that exposure to certain chemicals can also contribute significantly to PLC development, some of which have been designated as human liver carcinogens (Group 1) by the International Agency for Research on Cancer. These include aflatoxins and chronic consumption of alcoholic beverages. Many naturally occurring and synthetic chemicals have been shown to induce liver cancer in experimental animals. Humans are exposed to these carcinogens via accidental contamination of food or water; usually at levels far lower than those that are carcinogenic to experimental animals. Consequently, assessment of possible human PLC risk associated with such exposures is complex and uncertain. Evidence regarding aflatoxin as a human carcinogen has been extensively documented and is reviewed as an example of the usefulness of parallel experimental and epidemiological investigations in cancer risk assessment. Aflatoxins are toxic metabolites of certain spoilage molds that are potent liver carcinogens in experimental animals and frequently contaminate human diets. Collectively, epidemiologic data together with evidence from many types of experimental models defines the role of aflatoxin exposure in PLC causation. Molecular epidemiology involving the use of biomarkers of exposure has been particularly effective in linking aflatoxin exposure to PLC. Biomarkers of aflatoxin exposure have been validated with particular thoroughness. Dose-response relationships between biomarker levels and liver tumor incidence were first established in experimental animals. The biomarkers were then employed in pilot studies of limited scale in humans to define sensitivity, specificity, accuracy, and reliability parameters. Further validation in transitional epidemiological studies assessed intra- and interindividual variability, background levels, external dose-marker relationship, and feasibility for use in larger population-based studies. Finally, prospective epidemiological studies were conducted to evaluate biomarker effectiveness in identifying PLC risk.
MeSH term(s)	Aflatoxin B1/adverse effects ; Aflatoxin B1/metabolism ; Aflatoxin B1/toxicity ; Animals ; Carcinogens/adverse effects ; Carcinogens/metabolism ; Carcinogens/toxicity ; DNA, Neoplasm/chemistry ; Genes, p53/drug effects ; Genes, p53/genetics ; Haplorhini ; Hepatitis B/complications ; Hepatitis C/complications ; Humans ; Liver Neoplasms/chemically induced ; Liver Neoplasms/genetics ; Liver Neoplasms/microbiology ; Liver Neoplasms, Experimental/chemically induced ; Liver Neoplasms, Experimental/genetics ; Liver Neoplasms, Experimental/microbiology ; Mice ; Rats ; Risk Factors
Chemical Substances	Carcinogens ; DNA, Neoplasm ; Aflatoxin B1 (9N2N2Y55MH)
Language	English
Publishing date	2000-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1006/scbi.2000.0320
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Article: Aflatoxin as a human carcinogen.

Wogan, G N

Hepatology (Baltimore, Md.)

1999 Volume 30, Issue 2, Page(s) 573–575

MeSH term(s)	Aflatoxins/toxicity ; Carcinogens/toxicity ; Carcinoma, Hepatocellular/etiology ; Hepatitis B, Chronic/complications ; Humans ; Liver Neoplasms/etiology ; Male
Chemical Substances	Aflatoxins ; Carcinogens
Language	English
Publishing date	1999-08
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.510300231
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Article: Review of the toxicology of tamoxifen.

Wogan, G N

Seminars in oncology

1997 Volume 24, Issue 1 Suppl 1, Page(s) S1–87–S1–97

Abstract: Tamoxifen was carcinogenic to the liver of male and female rats, inducing hepatocellular carcinomas when administered daily by gavage or fed continuously in the diet. It also acted as a promoting agent in a two-stage model of carcinogenesis in rat liver. ...

Abstract	Tamoxifen was carcinogenic to the liver of male and female rats, inducing hepatocellular carcinomas when administered daily by gavage or fed continuously in the diet. It also acted as a promoting agent in a two-stage model of carcinogenesis in rat liver. In contrast, tamoxifen acted as a protective agent in abrogating estrogen-induced hepatotoxicity and hepatocarcinogenesis in hamsters. Tamoxifen did not induce malignancies in mice when administered according to dosing protocols that are effective in inducing hepatocellular carcinomas in rat liver. In the rat, tamoxifen is metabolized to alpha-hydroxytamoxifen, which is further activated to a product that binds principally to the exocyclic amino group of deoxyguanosine in DNA. The same adduct pattern is formed in mouse hepatocytes treated with tamoxifen or its alpha-hydroxylated derivative, and in human hepatocytes exposed to the latter metabolite. However, available data indicate that human cells have a substantially lower capacity than rodent cells for activation of tamoxifen. Tamoxifen also induces aneuploidy in rat hepatocytes in vivo. This evidence has led some investigators to characterize tamoxifen as a carcinogen that acts through both genotoxic and nongenotoxic mechanisms, with the implication that women treated with the drug may be consequently subjected to elevated risk of cancer, particularly of the endometrium. Critical examination of the evidence, however, indicates that extrapolation of these experimental data to humans is subject to very substantial uncertainty. Available data clearly indicate major differences between women and rats with respect to the activation of tamoxifen and formation of DNA adducts, and bring into question the validity of direct extrapolation of data generated in the single susceptible species, the rat, to women in assessing potential risks attendant to tamoxifen administration.
MeSH term(s)	Animals ; Antineoplastic Agents, Hormonal/adverse effects ; Antineoplastic Agents, Hormonal/toxicity ; Carcinogenicity Tests ; DNA Adducts ; Genes, p53/drug effects ; Humans ; Liver Neoplasms/chemically induced ; Mice ; Mutation ; Rats ; Risk Assessment ; Tamoxifen/adverse effects ; Tamoxifen/toxicity
Chemical Substances	Antineoplastic Agents, Hormonal ; DNA Adducts ; Tamoxifen (094ZI81Y45)
Language	English
Publishing date	1997-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	189220-4
ISSN	1532-8708 ; 0093-7754
ISSN (online)	1532-8708
ISSN	0093-7754
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Article ; Online: Infection, inflammation and colon carcinogenesis.

Wogan, Gerald N / Dedon, Peter C / Tannenbaum, Steven R / Fox, James G

Oncotarget

2012 Volume 3, Issue 8, Page(s) 737–738

MeSH term(s)	Animals ; Cell Transformation, Neoplastic ; Colitis/complications ; Colitis/physiopathology ; Colonic Neoplasms/etiology ; Colonic Neoplasms/pathology ; DNA Damage ; Helicobacter Infections/complications ; Helicobacter Infections/immunology ; Helicobacter hepaticus/immunology ; Humans ; Inflammation/physiopathology ; Inflammation Mediators/metabolism ; Mice
Chemical Substances	Inflammation Mediators
Language	English
Publishing date	2012-09-10
Publishing country	United States
Document type	Editorial
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.624
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Article ; Online: Chemistry meets biology in colitis-associated carcinogenesis.

Mangerich, A / Dedon, P C / Fox, J G / Tannenbaum, S R / Wogan, G N

Free radical research

2013 Volume 47, Issue 11, Page(s) 958–986

Abstract: The intestine comprises an exceptional venue for a dynamic and complex interplay of numerous chemical and biological processes. Here, multiple chemical and biological systems, including the intestinal tissue itself, its associated immune system, the gut ... ...

Abstract	The intestine comprises an exceptional venue for a dynamic and complex interplay of numerous chemical and biological processes. Here, multiple chemical and biological systems, including the intestinal tissue itself, its associated immune system, the gut microbiota, xenobiotics, and metabolites meet and interact to form a sophisticated and tightly regulated state of tissue homoeostasis. Disturbance of this homeostasis can cause inflammatory bowel disease (IBD)-a chronic disease of multifactorial etiology that is strongly associated with increased risk for cancer development. This review addresses recent developments in research into chemical and biological mechanisms underlying the etiology of inflammation-induced colon cancer. Beginning with a general overview of reactive chemical species generated during colonic inflammation, the mechanistic interplay between chemical and biological mediators of inflammation, the role of genetic toxicology, and microbial pathogenesis in disease development are discussed. When possible, we systematically compare evidence from studies utilizing human IBD patients with experimental investigations in mice. The comparison reveals that many strong pathological and mechanistic correlates exist between mouse models of colitis-associated cancer, and the clinically relevant situation in humans. We also summarize several emerging issues in the field, such as the carcinogenic potential of novel inflammation-related DNA adducts and genotoxic microbial factors, the systemic dimension of inflammation-induced genotoxicity, and the complex role of genome maintenance mechanisms during these processes. Taken together, current evidence points to the induction of genetic and epigenetic alterations by chemical and biological inflammatory stimuli ultimately leading to cancer formation.
MeSH term(s)	Animals ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Colitis/metabolism ; Colitis/pathology ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; Humans ; Inflammatory Bowel Diseases/metabolism ; Inflammatory Bowel Diseases/pathology ; Mice
Language	English
Publishing date	2013-10-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1194130-3
ISSN	1029-2470 ; 1071-5762
ISSN (online)	1029-2470
ISSN	1071-5762
DOI	10.3109/10715762.2013.832239
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Article: Aflatoxin carcinogenesis: interspecies potency differences and relevance for human risk assessment.

Wogan, G N

Progress in clinical and biological research

1992 Volume 374, Page(s) 123–137

MeSH term(s)	Aflatoxins/toxicity ; Animals ; Carcinoma, Hepatocellular/chemically induced ; Humans ; Liver Neoplasms/chemically induced ; Liver Neoplasms, Experimental/chemically induced ; Risk Factors ; Species Specificity
Chemical Substances	Aflatoxins
Language	English
Publishing date	1992
Publishing country	United States
Document type	Journal Article ; Review
ISSN	0361-7742
ISSN	0361-7742
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Article: Molecular epidemiology in cancer risk assessment and prevention: recent progress and avenues for future research.

Wogan, G N

Environmental health perspectives

1992 Volume 98, Page(s) 167–178

Abstract: ... polycyclic aromatic hydrocarbons, aromatic amines, tobacco-specific nitrosamines); dietary exposures (aflatoxins, N-nitrosamines ... markers (e.g., chromosomal aberrations, sister chromatid exchange, micronuclei), other alterations ... those of the ras family, and inactivation of tumor-suppressor genes (e.g., p53 and Rb) by point mutations and/or ...

Abstract	Molecular epidemiology is increasingly being applied in studies of cancer risks derived from exposure to environmental carcinogens of both endogenous and exogenous origins. Analytical methods have been developed that are capable of detecting and quantifying levels of covalent adducts of several important classes of carcinogens with cellular DNA and blood proteins. Methods of sufficient sensitivity and specificity to detect ambient levels of exposure are in current use. These are being used in studies related to tobacco use (polycyclic aromatic hydrocarbons, aromatic amines, tobacco-specific nitrosamines); dietary exposures (aflatoxins, N-nitrosamines, heterocyclic amines); medicinal exposures (cisplatin, alkylating agents, 8-methoxypsoralen, ultraviolet photoproducts); occupational exposures (aromatic amines, polycyclic aromatic hydrocarbons, oxides of ethylene and styrene, and vinyl chloride); and oxidative damage (8-hydroxyguanine, thymine glycol). Methodologic improvements together with their expanded use in feasibility studies continue to produce results that support the validity of this approach for detecting and quantifying exposure to carcinogens. Genetic markers are also being used to detect early biological responses in efforts to link carcinogen exposure to initiating events in the carcinogenesis process. These include, in addition to traditional cytogenetic markers (e.g., chromosomal aberrations, sister chromatid exchange, micronuclei), other alterations in chromosomal structure such as restriction fragment length polymorphisms, loss of heterozygosity, and translocation markers. Specific genetic changes have recently been identified as critical molecular events in the initiation and development of many cancers. Important among these are activation of oncogenes, especially those of the ras family, and inactivation of tumor-suppressor genes (e.g., p53 and Rb) by point mutations and/or chromosomal deletions and other structural changes. Although some of these changes are known to occur in chemically induced tumors of experimental animals, the possible role of chemical carcinogens in the induction of genetic abnormalities in human cancers has yet to be determined. Continuing investigations employing the methods of molecular epidemiology promise to provide further evidence concerning these relationships. Future investigations employing newly developed molecular biological methods, in particular those based on polymerase chain reaction amplification of DNA, to identify alterations in DNA and chromosomal structure, combined with methods for characterizing exposure to carcinogens and early effects, have great potential for further elucidating the role of genotoxic agents in the etiology of human cancers and also for the development of strategies for their prevention.
MeSH term(s)	Biomarkers, Tumor/genetics ; Carcinogens ; DNA/drug effects ; DNA/metabolism ; DNA Damage ; DNA Mutational Analysis ; Environmental Exposure/adverse effects ; Environmental Exposure/analysis ; Forecasting ; Gene Expression Regulation, Neoplastic/genetics ; Genes, Tumor Suppressor/genetics ; Genes, p53/genetics ; Genes, ras/genetics ; Humans ; Neoplasms/chemically induced ; Neoplasms/epidemiology ; Neoplasms/genetics ; Neoplasms/prevention & control ; Risk Factors
Chemical Substances	Biomarkers, Tumor ; Carcinogens ; DNA (9007-49-2)
Language	English
Publishing date	1992-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	195189-0
ISSN	1552-9924 ; 0091-6765 ; 1078-0475
ISSN (online)	1552-9924
ISSN	0091-6765 ; 1078-0475
DOI	10.1289/ehp.9298167
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Article: Aflatoxins as risk factors for hepatocellular carcinoma in humans.

Wogan, G N

Cancer research

1992 Volume 52, Issue 7 Suppl, Page(s) 2114s–2118s

Abstract: On a global basis, primary liver cancer (PLC) is a very prevalent form of cancer. Wide variation of PLC incidence in different areas of the world suggests the involvement of environmental factors in its etiology. Two major classes of risk factors have ... ...

Abstract	On a global basis, primary liver cancer (PLC) is a very prevalent form of cancer. Wide variation of PLC incidence in different areas of the world suggests the involvement of environmental factors in its etiology. Two major classes of risk factors have been identified. Extensive evidence indicates the importance of infection by the hepatitis B virus as a major risk factor for PLC. Because many organic chemicals induce liver cancer in experimental animals, those to which human exposure is known to occur are also of interest with respect to their possible involvement as risk factors for PLC. Particular emphasis has been placed on aflatoxins because of the frequency with which they occur as food contaminants, together with their potency as liver carcinogens for a large number of experimental animals, including subhuman primates. Other mycotoxins, notably sterigmatocystin and fumonisin, also are relatively potent carcinogens for the liver of animals, but little is known about human exposure to them. Epidemiological surveys carried out over the past 25 years in Asia and Africa have revealed a strong statistical association between aflatoxin ingestion and PLC incidence. The combined experimental and epidemiological evidence has led to designation of aflatoxins as human carcinogens according to International Agency for Cancer Research criteria. Collectively, current evidence strongly suggests that PLC is of multifactorial origin, with probable interactions between viral and chemical agents in populations concurrently exposed to both classes of risk factors. Recently developed methods that permit individual monitoring of aflatoxin exposure, hepatitis B virus infection, and genetic damage caused by these agents are being applied in the design of molecular and biochemical epidemiological studies of the etiology of the disease. Application of this methodology may contribute to elucidation of the relative importance of interacting etiological agents in different populations.
MeSH term(s)	Aflatoxin B1/adverse effects ; Aflatoxin B1/metabolism ; Aflatoxin B1/toxicity ; Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/microbiology ; Codon ; DNA, Neoplasm/chemistry ; Genes, ras/drug effects ; Hepatitis B/complications ; Humans ; Liver Neoplasms/chemically induced ; Liver Neoplasms/genetics ; Liver Neoplasms/microbiology ; Risk Factors ; Serum Albumin/metabolism
Chemical Substances	Codon ; DNA, Neoplasm ; Serum Albumin ; Aflatoxin B1 (9N2N2Y55MH)
Language	English
Publishing date	1992-04-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
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