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  1. Article ; Online: Understanding sexual violence perpetration.

    Goodson, William H

    JAMA pediatrics

    2014  Volume 168, Issue 6, Page(s) 580–581

    MeSH term(s) Adolescent Behavior ; Caregivers/statistics & numerical data ; Female ; Humans ; Male ; Sex Offenses/statistics & numerical data ; Sexual Behavior/statistics & numerical data
    Language English
    Publishing date 2014-06
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 2701223-2
    ISSN 2168-6211 ; 2168-6203
    ISSN (online) 2168-6211
    ISSN 2168-6203
    DOI 10.1001/jamapediatrics.2013.5405
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  2. Article ; Online: Reduction of daily-use parabens and phthalates reverses accumulation of cancer-associated phenotypes within disease-free breast tissue of study subjects

    Dairkee, Shanaz H. / Moore, Dan H. / Luciani, M. Gloria / Anderle, Nicole / Gerona, Roy / Ky, Karina / Torres, Samantha M. / Marshall, Polly V. / Goodson, William H.

    Chemosphere. 2023 Feb. 04, p.138014-

    2023  , Page(s) 138014–

    Abstract: Estrogenic overstimulation is carcinogenic to the human breast. Personal care products (PCPs) commonly contain xenoestrogens (XE), such as parabens and phthalates. Here, we identified the adverse effects of persistent exposure to such PCPs directly ... ...

    Abstract Estrogenic overstimulation is carcinogenic to the human breast. Personal care products (PCPs) commonly contain xenoestrogens (XE), such as parabens and phthalates. Here, we identified the adverse effects of persistent exposure to such PCPs directly within human estrogen responsive breast tissue of subjects enrolled in a regimen of reduced XE use (REDUXE). Pre- and post-intervention fine needle aspirates (FNAs) of the breast were collected from healthy volunteers who discontinued the use of paraben and phthalate containing PCPs over a 28 d period. Based on high-dimensional gene expression data of matched FNA pairs of study subjects, we demonstrate a striking reversal of cancer-associated phenotypes, including the PI3K-AKT/mTOR pathway, autophagy, and apoptotic signaling networks within breast cells of REDUXE compliant subjects. These, and other altered phenotypes were detected together with a significant reduction in urinary parabens and phthalate metabolites. Moreover, in vitro treatment of paired FNAs with 17β-estradiol (E2), displayed a ‘normalizing’ impact of REDUXE on gene expression within known E2-modulated pathways, and on functional endpoints, including estrogen receptor alpha: beta ratio, and S-phase fraction of the cell cycle. In a paradigm shifting approach facilitated by community-based participatory research, REDUXE reveals unfavorable consequences from exposure to XEs from daily-use PCPs. Our findings illustrate the potential for REDUXE to suppress pro-carcinogenic phenotypes at the cellular level towards the goal of breast cancer prevention.
    Keywords apoptosis ; autophagy ; breast neoplasms ; breasts ; carcinogenicity ; cell cycle ; cooperative research ; estrogen receptors ; estrogens ; gene expression ; humans ; metabolites ; phthalates ; xenoestrogens ; Endocrine disruption ; Biomarkers ; Nonmalignant breast tissue ; Paired human samples ; Pan-cancer pathways ; PCP ; XE ; REDUXE ; FNA ; E2 ; Pg ; SHBG ; REDUXExE2 ; DEG
    Language English
    Dates of publication 2023-0204
    Publishing place Elsevier Ltd
    Document type Article ; Online
    Note Pre-press version
    ZDB-ID 120089-6
    ISSN 1879-1298 ; 0045-6535 ; 0366-7111
    ISSN (online) 1879-1298
    ISSN 0045-6535 ; 0366-7111
    DOI 10.1016/j.chemosphere.2023.138014
    Database NAL-Catalogue (AGRICOLA)

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  3. Article ; Online: Testing the low dose mixtures hypothesis from the Halifax project.

    Goodson, William H / Lowe, Leroy / Gilbertson, Michael / Carpenter, David O

    Reviews on environmental health

    2020  Volume 35, Issue 4, Page(s) 333–357

    Abstract: In 2013, 60 scientists, representing a larger group of 174 scientists from 26 nations, met in Halifax, Nova Scotia to consider whether - using published research - it was logical to anticipate that a mixture of chemicals, each thought to be non- ... ...

    Abstract In 2013, 60 scientists, representing a larger group of 174 scientists from 26 nations, met in Halifax, Nova Scotia to consider whether - using published research - it was logical to anticipate that a mixture of chemicals, each thought to be non-carcinogenic, might act together in that mixture as a
    MeSH term(s) Animals ; Carcinogenesis/chemically induced ; Carcinogens/toxicity ; Humans ; Nova Scotia
    Chemical Substances Carcinogens
    Language English
    Publishing date 2020-08-24
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 184450-7
    ISSN 2191-0308 ; 0048-7562 ; 0048-7554
    ISSN (online) 2191-0308
    ISSN 0048-7562 ; 0048-7554
    DOI 10.1515/reveh-2020-0033
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  4. Article: Closure of partial mastectomy.

    Goodson, William H

    American journal of surgery

    2006  Volume 191, Issue 1, Page(s) 117–120

    Abstract: A longstanding controversy surrounds whether to close breast parenchyma at the completion of a partial mastectomy for breast cancer. Modification of a technique described 80 years ago finds the middle ground between various opinions and simultaneously ... ...

    Abstract A longstanding controversy surrounds whether to close breast parenchyma at the completion of a partial mastectomy for breast cancer. Modification of a technique described 80 years ago finds the middle ground between various opinions and simultaneously addresses 2 issues: (1) approximation of the deep and superficial surfaces of the parenchyma, without sutures within the parenchyma, minimizes "dents;" and (2) a radial suture line preserves the distance from the nipple to the periphery of the breast which minimizes traction on the nipple.
    MeSH term(s) Breast Neoplasms/surgery ; Cicatrix/prevention & control ; Female ; Humans ; Mastectomy, Segmental/methods ; Suture Techniques ; Wound Healing
    Language English
    Publishing date 2006-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2953-1
    ISSN 1879-1883 ; 0002-9610
    ISSN (online) 1879-1883
    ISSN 0002-9610
    DOI 10.1016/j.amjsurg.2005.10.012
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  5. Article ; Online: Molecular prediction of recurrence of breast cancer.

    Goodson, William H

    The New England journal of medicine

    2005  Volume 352, Issue 15, Page(s) 1605–7; author reply 1605–7

    MeSH term(s) Biomarkers, Tumor/analysis ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Gene Expression ; Humans ; Observer Variation ; Pathology/standards ; Recurrence ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2005-04-14
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
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  6. Article: Breast cancer reporting practice and guidelines.

    Goodson, William H

    Journal of the American College of Surgeons

    2004  Volume 199, Issue 1, Page(s) 170; author reply 171

    MeSH term(s) Breast Neoplasms/pathology ; Female ; Humans ; Practice Guidelines as Topic/standards ; Specimen Handling/methods ; Specimen Handling/standards
    Language English
    Publishing date 2004-07
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 1181115-8
    ISSN 1879-1190 ; 1072-7515
    ISSN (online) 1879-1190
    ISSN 1072-7515
    DOI 10.1016/j.jamcollsurg.2004.03.006
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  7. Article ; Online: Optimal recall rates following mammography.

    Goodson, William H

    JAMA

    2004  Volume 291, Issue 7, Page(s) 821–2; author reply 822

    MeSH term(s) Biopsy ; Breast Neoplasms/diagnosis ; Breast Neoplasms/epidemiology ; Humans ; Mammography/statistics & numerical data ; Mass Screening/statistics & numerical data ; United Kingdom/epidemiology ; United States/epidemiology
    Language English
    Publishing date 2004-02-18
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 2958-0
    ISSN 1538-3598 ; 0254-9077 ; 0002-9955 ; 0098-7484
    ISSN (online) 1538-3598
    ISSN 0254-9077 ; 0002-9955 ; 0098-7484
    DOI 10.1001/jama.291.7.821-b
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  8. Article ; Online: A Ternary Mixture of Common Chemicals Perturbs Benign Human Breast Epithelial Cells More Than the Same Chemicals Do Individually.

    Dairkee, Shanaz H / Luciani-Torres, Gloria / Moore, Dan H / Jaffee, Ian M / Goodson, William H

    Toxicological sciences : an official journal of the Society of Toxicology

    2018  Volume 165, Issue 1, Page(s) 131–144

    Abstract: As a continuous source of hormonal stimulation, environmentally ubiquitous estrogenic chemicals, ie, xenoestrogens (XEs), are a potential risk factor for breast carcinogenesis. Given their wide distribution in the environment and the fact that bisphenol- ... ...

    Abstract As a continuous source of hormonal stimulation, environmentally ubiquitous estrogenic chemicals, ie, xenoestrogens (XEs), are a potential risk factor for breast carcinogenesis. Given their wide distribution in the environment and the fact that bisphenol-A (BPA), methylparaben (MP), and perfluorooctanoic acid (PFOA) are uniformly detected in unselected body fluid samples, it must be assumed that humans are simultaneously exposed to these chemicals almost daily. We studied the effects of a ternary mixture of BPA, MP, and PFOA on benign breast epithelial cells at the range of concentrations observed for single chemicals in human samples. Measurements of exposure impact relevant to the breast were based on endpoints associated with "hallmarks" of cancer and "key characteristics" of carcinogens. These included modulation of total estrogen receptor (ER)α, phosphorylated ERα (pERα), total ERβ, S-phase induction, and apoptotic evasion. Data from live cell measurements were fit to a log-linear dose-response model. Concentration-dependent reduction of ERβ and apoptosis evasion was observed concurrently with the induction of ERα, pERα, and S-phase fraction, and an increased rate of cell proliferation. Beyond additive effects predicted by the sum of individual test XEs, mixture treatment demonstrated synergism for the ERβ and apoptosis suppression phenotypes (p > .001). Nonmalignant breast cells were more sensitive than commonly used breast cancer lines to XE treatment in 3 of 5 endpoints. All observations were validated with cells isolated from the normal breast tissue of 14 individuals. At relatively low concentrations, a chemical mixture has striking effects on normal cell function that are missed by evaluation of single components.
    MeSH term(s) Apoptosis/drug effects ; Benzhydryl Compounds/administration & dosage ; Benzhydryl Compounds/toxicity ; Breast/drug effects ; Breast/metabolism ; Breast/pathology ; Caprylates/administration & dosage ; Caprylates/toxicity ; Cell Line ; Dose-Response Relationship, Drug ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Estrogen Receptor alpha/metabolism ; Estrogen Receptor beta/metabolism ; Fluorocarbons/administration & dosage ; Fluorocarbons/toxicity ; Humans ; Parabens/administration & dosage ; Parabens/toxicity ; Phenols/administration & dosage ; Phenols/toxicity ; Xenobiotics/administration & dosage ; Xenobiotics/toxicity
    Chemical Substances Benzhydryl Compounds ; Caprylates ; ESR1 protein, human ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Fluorocarbons ; Parabens ; Phenols ; Xenobiotics ; perfluorooctanoic acid (947VD76D3L) ; methylparaben (A2I8C7HI9T) ; bisphenol A (MLT3645I99)
    Language English
    Publishing date 2018-05-30
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfy126
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  9. Article: Risks of postmenopausal hormone replacement.

    Goodson, William H

    JAMA

    2002  Volume 288, Issue 22, Page(s) 2820–1; author reply 2823–4

    MeSH term(s) Breast Neoplasms/epidemiology ; Colonic Neoplasms/epidemiology ; Estrogen Replacement Therapy ; Female ; Hip Fractures/epidemiology ; Humans ; Postmenopause ; Risk
    Language English
    Publishing date 2002-08-23
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 2958-0
    ISSN 1538-3598 ; 0098-7484 ; 0254-9077 ; 0002-9955
    ISSN (online) 1538-3598
    ISSN 0098-7484 ; 0254-9077 ; 0002-9955
    DOI 10.1001/jama.288.22.2820-jlt1211-1-5
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  10. Article ; Online: Low-Dose Mixture Hypothesis of Carcinogenesis Workshop: Scientific Underpinnings and Research Recommendations.

    Miller, Mark F / Goodson, William H / Manjili, Masoud H / Kleinstreuer, Nicole / Bisson, William H / Lowe, Leroy

    Environmental health perspectives

    2017  Volume 125, Issue 2, Page(s) 163–169

    Abstract: Background: The current single-chemical-as-carcinogen risk assessment paradigm might underestimate or miss the cumulative effects of exposure to chemical mixtures, as highlighted in recent work from the Halifax Project. This is particularly important ... ...

    Abstract Background: The current single-chemical-as-carcinogen risk assessment paradigm might underestimate or miss the cumulative effects of exposure to chemical mixtures, as highlighted in recent work from the Halifax Project. This is particularly important for chemical exposures in the low-dose range that may be affecting crucial cancer hallmark mechanisms that serve to enable carcinogenesis.
    Objective: Could ongoing low-dose exposures to a mixture of commonly encountered environmental chemicals produce effects in concert that lead to carcinogenesis? A workshop held at the NIEHS in August 2015 evaluated the scientific support for the low-dose mixture hypothesis of carcinogenesis and developed a research agenda. Here we describe the science that supports this novel theory, identify knowledge gaps, recommend future methodologies, and explore preventative risk assessment and policy decision-making that incorporates cancer biology, environmental health science, translational toxicology, and clinical epidemiology.
    Discussion and conclusions: The theoretical merits of the low-dose carcinogenesis hypothesis are well founded with clear biological relevance, and therefore, the premise warrants further investigation. Expert recommendations include the need for better insights into the ways in which noncarcinogenic constituents might combine to uniquely affect the process of cellular transformation (in vitro) and environmental carcinogenesis (in vivo), including investigations of the role of key defense mechanisms in maintaining transformed cells in a dormant state. The scientific community will need to acknowledge limitations of animal-based models in predicting human responses; evaluate biological events leading to carcinogenesis both spatially and temporally; examine the overlap between measurable cancer hallmarks and characteristics of carcinogens; incorporate epigenetic biomarkers, in silico modelling, high-performance computing and high-resolution imaging, microbiome, metabolomics, and transcriptomics into future research efforts; and build molecular annotations of network perturbations. The restructuring of many existing regulatory frameworks will require adequate testing of relevant environmental mixtures to build a critical mass of evidence on which to base policy decisions. Citation: Miller MF, Goodson WH III, Manjili MH, Kleinstreuer N, Bisson WH, Lowe L. 2017. Low-Dose Mixture Hypothesis of Carcinogenesis Workshop: scientific underpinnings and research recommendations. Environ Health Perspect 125:163-169; http://dx.doi.org/10.1289/EHP411.
    MeSH term(s) Carcinogenesis ; Carcinogens/toxicity ; Complex Mixtures ; Consensus ; Dose-Response Relationship, Drug ; Education ; Environmental Exposure/statistics & numerical data ; Environmental Pollution/statistics & numerical data ; Models, Animal ; Neoplasms ; Risk Assessment
    Chemical Substances Carcinogens ; Complex Mixtures
    Language English
    Publishing date 2017-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 195189-0
    ISSN 1552-9924 ; 0091-6765 ; 1078-0475
    ISSN (online) 1552-9924
    ISSN 0091-6765 ; 1078-0475
    DOI 10.1289/EHP411
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