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  1. Article: Nonlinear progression across the occult transition establishes cancer lethality.

    Ginzel, Joshua D / Chapman, Henry / Sills, Joelle E / Allen, Edwin J / Barak, Lawrence S / Cardiff, Robert D / Borowsky, Alexander D / Lyerly, H Kim / Rogers, Bruce W / Snyder, Joshua C

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Cancer screening is based upon a linear model of growth and invasion. Yet, early dissemination during the lengthy pre-diagnostic phase suggests that nonlinearity in growth can also occur. Therefore, we quantitatively traced the invisible and visible ... ...

    Abstract Cancer screening is based upon a linear model of growth and invasion. Yet, early dissemination during the lengthy pre-diagnostic phase suggests that nonlinearity in growth can also occur. Therefore, we quantitatively traced the invisible and visible phases of tumorigenesis in the mammary gland for more than two-thousand tumors. Dynamic mathematical models of the invisible phase revealed an occult checkpoint resulting in nonlinear progression of transformed field cells. We found that expansile fields have increased dwell time at the occult checkpoint resulting in a large reservoir of image detectable precursors prior to invasion. In contrast, slowly proliferating lesions disseminate early and then transition rapidly through an occult checkpoint in a process we term nascent lethality. Our data illustrate how nonlinear growth across an occult checkpoint can account for a paradoxical increase in early-stage cancer detection without a dramatic reduction in metastatic burden.
    Highlights: Growth during the invisible phase of tumorigenesis is a nonlinear processField size and field growth rate are uncoupled from metastatic potentialOccult transition rates vary by genotypeNascent lethal lesions are currently undetectable.
    Language English
    Publishing date 2024-04-25
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.04.23.590826
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  2. Article ; Online: Methods of Immunohistochemistry and Immunofluorescence: Converting Invisible to Visible.

    Mori, Hidetoshi / Cardiff, Robert D

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

    2016  Volume 1458, Page(s) 1–12

    Abstract: Observing changes in pathophysiological tissue samples often relies on immunohistochemical or immunofluorescence analysis. These techniques show target microanatomy by visualizing marker molecules on cells and their microenvironment. Here, we describe ... ...

    Abstract Observing changes in pathophysiological tissue samples often relies on immunohistochemical or immunofluorescence analysis. These techniques show target microanatomy by visualizing marker molecules on cells and their microenvironment. Here, we describe the "pros and cons" in each method, along with alternative procedures and the suggested imaging equipment.
    Language English
    Publishing date 2016
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-4939-3801-8_1
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  3. Article: Aging Mouse Models Reveal Complex Tumor-Microenvironment Interactions in Cancer Progression.

    Mori, Hidetoshi / Cardiff, Robert D / Borowsky, Alexander D

    Frontiers in cell and developmental biology

    2018  Volume 6, Page(s) 35

    Abstract: Mouse models and genetically engineered mouse models (GEMM) are essential experimental tools for the understanding molecular mechanisms within complex biological systems. GEMM are especially useful for inferencing phenocopy information to genetic human ... ...

    Abstract Mouse models and genetically engineered mouse models (GEMM) are essential experimental tools for the understanding molecular mechanisms within complex biological systems. GEMM are especially useful for inferencing phenocopy information to genetic human diseases such as breast cancer. Human breast cancer modeling in mice most commonly employs mammary epithelial-specific promoters to investigate gene function(s) and, in particular, putative oncogenes. Models are specifically useful in the mammary epithelial cell in the context of the complete mammary gland environment. Gene targeted knockout mice including conditional targeting to specific mammary cells can reveal developmental defects in mammary organogenesis and demonstrate the importance of putative tumor suppressor genes. Some of these models demonstrate a non-traditional type of tumor suppression which involves interplay between the tumor susceptible cell and its host/environment. These GEMM help to reveal the processes of cancer progression beyond those intrinsic to cancer cells. Furthermore, the, analysis of mouse models requires appropriate consideration of mouse strain, background, and environmental factors. In this review, we compare aging-related factors in mouse models for breast cancer. We introduce databases of GEMM attributes and colony functional variations.
    Language English
    Publishing date 2018-03-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2018.00035
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  4. Article ; Online: Physiological expression of PI3K H1047R mutation reveals its anti-metastatic potential in ErbB2-driven breast cancer.

    Simond, Alexandra M / Bui, Tung / Zuo, Dongmei / Sanguin-Gendreau, Virginie / Rao, Trisha / Phillips, Wayne A / Cardiff, Robert D / Muller, William J

    Oncogene

    2022  Volume 41, Issue 25, Page(s) 3445–3451

    Abstract: p110α is a catalytic subunit of phosphoinositide 3-kinase (PI3K), a major downstream effector of receptor tyrosine kinase ErbB2, that is amplified and overexpressed in 20-30% of breast cancers, 40% of which have an activating mutation in p110α. Despite ... ...

    Abstract p110α is a catalytic subunit of phosphoinositide 3-kinase (PI3K), a major downstream effector of receptor tyrosine kinase ErbB2, that is amplified and overexpressed in 20-30% of breast cancers, 40% of which have an activating mutation in p110α. Despite the high frequency of PIK3CA gain-of-function mutations, their prognostic value is controversial. Here, we employ a knock-in transgenic strategy to restrict the expression of an activated form of ErbB2 and p110α kinase domain mutation (p110α
    MeSH term(s) Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Carcinoma, Intraductal, Noninfiltrating ; Class I Phosphatidylinositol 3-Kinases/genetics ; Female ; Humans ; Mutation ; Phosphatidylinositol 3-Kinase/genetics ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Receptor, ErbB-2/genetics
    Chemical Substances Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2022-05-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-022-02323-9
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  5. Article ; Online: How to phenotype a mouse.

    Cardiff, Robert D

    Disease models & mechanisms

    2009  Volume 2, Issue 7-8, Page(s) 317–321

    MeSH term(s) Animals ; Biology/education ; Disease Models, Animal ; Genetic Techniques ; Genotype ; Mice ; Mice, Transgenic ; Phenotype ; Software
    Language English
    Publishing date 2009-07
    Publishing country England
    Document type Editorial
    ISSN 1754-8411
    ISSN (online) 1754-8411
    DOI 10.1242/dmm.003335
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  6. Article ; Online: At last: classification of human mammary cells elucidates breast cancer origins.

    Cardiff, Robert D / Borowsky, Alexander D

    The Journal of clinical investigation

    2014  Volume 124, Issue 2, Page(s) 478–480

    Abstract: Current breast cancer classification systems are based on molecular evaluation of tumor receptor status and do not account for distinct morphological phenotypes. In other types of cancer, taxonomy based on normal cell phenotypes has been extremely useful ...

    Abstract Current breast cancer classification systems are based on molecular evaluation of tumor receptor status and do not account for distinct morphological phenotypes. In other types of cancer, taxonomy based on normal cell phenotypes has been extremely useful for diagnosis and treatment strategies. In this issue of the JCI, Santagata and colleagues developed a breast cancer classification scheme based on characterization of healthy mammary cells. Reclassification of breast cancer cells and breast cancer tissue microarrays with this system correlated with prognosis better than the standard receptor status designation. This scheme provides a major advance toward our understanding of the origin of the cells in the breast and breast cancers.
    MeSH term(s) Breast/metabolism ; Breast/pathology ; Breast Neoplasms/classification ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Female ; Humans
    Language English
    Publishing date 2014-01-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI73910
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  7. Article: One-health wonders. Interview by R. Scott Nolen.

    Cardiff, Robert D

    Journal of the American Veterinary Medical Association

    2008  Volume 233, Issue 12, Page(s) 1828–1829

    MeSH term(s) Animals ; Animals, Genetically Modified ; Humans ; Interdisciplinary Communication ; Pathology/methods ; Pathology/standards ; Pathology, Veterinary/methods ; Pathology, Veterinary/standards ; Public Health ; Research/organization & administration ; United States ; Veterinary Medicine/standards
    Language English
    Publishing date 2008-12-19
    Publishing country United States
    Document type Interview
    ZDB-ID 390811-2
    ISSN 1943-569X ; 0003-1488
    ISSN (online) 1943-569X
    ISSN 0003-1488
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  8. Article ; Online: Editor's Note: Dual Targeting of the Akt/mTOR Signaling Pathway Inhibits Castration-Resistant Prostate Cancer in a Genetically Engineered Mouse Model.

    Floc'h, Nicola / Kinkade, Carolyn Waugh / Kobayashi, Takashi / Aytes, Alvaro / Lefebvre, Celine / Mitrofanova, Antonina / Cardiff, Robert D / Califano, Andrea / Shen, Michael M / Abate-Shen, Cory

    Cancer research

    2023  Volume 83, Issue 7, Page(s) 1160

    Language English
    Publishing date 2023-04-04
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-23-0516
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  9. Article: Epilog: comparative medicine, one medicine and genomic pathology.

    Cardiff, Robert D

    Breast disease

    2007  Volume 28, Page(s) 107–110

    Abstract: The study of breast cancer has involved comparative pathology since the 1890s. Molecular biology has allowed the detailed examination of human, mouse, and rat genomes. The genes that are associated with breast cancer in humans cause cancer in genetically ...

    Abstract The study of breast cancer has involved comparative pathology since the 1890s. Molecular biology has allowed the detailed examination of human, mouse, and rat genomes. The genes that are associated with breast cancer in humans cause cancer in genetically modified mice and rats. Global genomic analyses demonstrate even broader genomic homologies. The pathology illustrates the principle of One Medicine. This issue examines these contributions and opens the way for the examination of other mammalian species. The development of a new discipline, Genomic Pathology, can now be anticipated.
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/pathology ; Female ; Genomics ; Humans ; Mammary Neoplasms, Animal/genetics ; Mammary Neoplasms, Animal/pathology ; Mice ; Rats
    Language English
    Publishing date 2007-11-14
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 639267-2
    ISSN 0888-6008
    ISSN 0888-6008
    DOI 10.3233/bd-2007-28110
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  10. Article ; Online: Pathologists needed to cope with mutant mice.

    Cardiff, Robert D

    Nature

    2007  Volume 447, Issue 7144, Page(s) 528

    MeSH term(s) Animals ; Humans ; Mice ; Mice, Knockout ; Mice, Mutant Strains ; Models, Animal ; Pathology/education ; Pathology/manpower ; Phenotype
    Language English
    Publishing date 2007-05-31
    Publishing country England
    Document type Comment ; Letter
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/447528c
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