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  1. Article ; Online: The RADx Tech Test Verification Core and the ACME POCT in the Evaluation of COVID-19 Testing Devices

    Eric Nehl / Stacy Heilman / David Ku / David Gottfried / Sarah Farmer / Robert Mannino / Erika Tyburski / Julie Sullivan / Allison Suessmith / Leda Bassit / Janet Figueroa / Anna Wood / Traci Leong / Anuradha Rao / Beverly Rogers / Robert Jerris / Sunita Park / Mark Gonzalez / Jennifer Frediani /
    Claudia Morris / Joshua Levy / Nils Schoof / Maud Mavigner / John Roback / Kristen Herzegh / Natia Saakadze / Jess Ingersoll / Narayana Cheedarla / Andrew Neish / Bradley Hanberry / Christopher Porter / Annette Esper / Russell Kempker / Paulina Rebolledo / Pamela McGuinness / Frederick Balagadde / Rebecca Gore / Ainat Koren / Nira Pollock / Eugene Rogers / Karl Simin / Nathaniel Hafer / Mary Ann Picard / Chiara Ghezzi / David McManus / Bryan Buchholz / Christina Rostad / Viviana Claveria / Thanuja Ramachandra / Yun F. Wang

    IEEE Open Journal of Engineering in Medicine and Biology, Vol 2, Pp 142-

    A Model for Progress and Change

    2021  Volume 151

    Abstract: Faced with the COVID-19 pandemic, the US system for developing and testing technologies was challenged in unparalleled ways. This article describes the multi-institutional, transdisciplinary team of the “RADx SM Tech Test Verification Core” and its role ... ...

    Abstract Faced with the COVID-19 pandemic, the US system for developing and testing technologies was challenged in unparalleled ways. This article describes the multi-institutional, transdisciplinary team of the “RADx SM Tech Test Verification Core” and its role in expediting evaluations of COVID-19 testing devices. Expertise related to aspects of diagnostic testing was coordinated to evaluate testing devices with the goal of significantly expanding the ability to mass screen Americans to preserve lives and facilitate the safe return to work and school. Focal points included: laboratory and clinical device evaluation of the limit of viral detection, sensitivity, and specificity of devices in controlled and community settings; regulatory expertise to provide focused attention to barriers to device approval and distribution; usability testing from the perspective of patients and those using the tests to identify and overcome device limitations, and engineering assessment to evaluate robustness of design including human factors, manufacturability, and scalability.
    Keywords COVID-19 ; Device Testing ; RADx ; Computer applications to medicine. Medical informatics ; R858-859.7 ; Medical technology ; R855-855.5
    Subject code 600
    Language English
    Publishing date 2021-01-01T00:00:00Z
    Publisher IEEE
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: The BRG1 chromatin remodeler protects against ovarian cysts, uterine tumors, and mammary tumors in a lineage-specific manner.

    Daniel W Serber / Allison Rogala / Maisam Makarem / Gary B Rosson / Karl Simin / Virginia Godfrey / Terry Van Dyke / Connie J Eaves / Scott J Bultman

    PLoS ONE, Vol 7, Iss 2, p e

    2012  Volume 31346

    Abstract: The BRG1 catalytic subunit of SWI/SNF-related complexes is required for mammalian development as exemplified by the early embryonic lethality of Brg1 null homozygous mice. BRG1 is also a tumor suppressor and, in mice, 10% of heterozygous (Brg1(null/+)) ... ...

    Abstract The BRG1 catalytic subunit of SWI/SNF-related complexes is required for mammalian development as exemplified by the early embryonic lethality of Brg1 null homozygous mice. BRG1 is also a tumor suppressor and, in mice, 10% of heterozygous (Brg1(null/+)) females develop mammary tumors. We now demonstrate that BRG1 mRNA and protein are expressed in both the luminal and basal cells of the mammary gland, raising the question of which lineage requires BRG1 to promote mammary homeostasis and prevent oncogenic transformation. To investigate this question, we utilized Wap-Cre to mutate both Brg1 floxed alleles in the luminal cells of the mammary epithelium of pregnant mice where WAP is exclusively expressed within the mammary gland. Interestingly, we found that Brg1(Wap-Cre) conditional homozygotes lactated normally and did not develop mammary tumors even when they were maintained on a Brm-deficient background. However, Brg1(Wap-Cre) mutants did develop ovarian cysts and uterine tumors. Analysis of these latter tissues showed that both, like the mammary gland, contain cells that normally express Brg1 and Wap. Thus, tumor formation in Brg1 mutant mice appears to be confined to particular cell types that require BRG1 and also express Wap. Our results now show that such cells exist both in the ovary and the uterus but not in either the luminal or the basal compartments of the mammary gland. Taken together, these findings indicate that SWI/SNF-related complexes are dispensable in the luminal cells of the mammary gland and therefore argue against the notion that SWI/SNF-related complexes are essential for cell survival. These findings also suggest that the tumor-suppressor activity of BRG1 is restricted to the basal cells of the mammary gland and demonstrate that this function extends to other female reproductive organs, consistent with recent observations of recurrent ARID1A/BAF250a mutations in human ovarian and endometrial tumors.
    Keywords Medicine ; R ; Science ; Q
    Subject code 571
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: pRb inactivation in mammary cells reveals common mechanisms for tumor initiation and progression in divergent epithelia.

    Karl Simin / Hua Wu / Lucy Lu / Dan Pinkel / Donna Albertson / Robert D Cardiff / Terry Van Dyke

    PLoS Biology, Vol 2, Iss 2, p E

    2004  Volume 22

    Abstract: Retinoblastoma 1 (pRb) and the related pocket proteins, retinoblastoma-like 1 (p107) and retinoblastoma-like 2 (p130) (pRb(f), collectively), play a pivotal role in regulating eukaryotic cell cycle progression, apoptosis, and terminal differentiation. ... ...

    Abstract Retinoblastoma 1 (pRb) and the related pocket proteins, retinoblastoma-like 1 (p107) and retinoblastoma-like 2 (p130) (pRb(f), collectively), play a pivotal role in regulating eukaryotic cell cycle progression, apoptosis, and terminal differentiation. While aberrations in the pRb-signaling pathway are common in human cancers, the consequence of pRb(f) loss in the mammary gland has not been directly assayed in vivo. We reported previously that inactivating these critical cell cycle regulators in divergent cell types, either brain epithelium or astrocytes, abrogates the cell cycle restriction point, leading to increased cell proliferation and apoptosis, and predisposing to cancer. Here we report that mouse mammary epithelium is similar in its requirements for pRb(f) function; Rb(f) inactivation by T(121), a fragment of SV40 T antigen that binds to and inactivates pRb(f) proteins, increases proliferation and apoptosis. Mammary adenocarcinomas form within 16 mo. Most apoptosis is regulated by p53, which has no impact on proliferation, and heterozygosity for a p53 null allele significantly shortens tumor latency. Most tumors in p53 heterozygous mice undergo loss of the wild-type p53 allele. We show that the mechanism of p53 loss of heterozygosity is not simply the consequence of Chromosome 11 aneuploidy and further that chromosomal instability subsequent to p53 loss is minimal. The mechanisms for pRb and p53 tumor suppression in the epithelia of two distinct tissues, mammary gland and brain, are indistinguishable. Further, this study has produced a highly penetrant breast cancer model based on aberrations commonly observed in the human disease.
    Keywords Biology (General) ; QH301-705.5
    Subject code 572 ; 610
    Language English
    Publishing date 2004-02-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Evidence for phenotypic plasticity in aggressive triple-negative breast cancer

    Nicholas C D'Amato / Julie H Ostrander / Michelle L Bowie / Christopher Sistrunk / Alexander Borowsky / Robert D Cardiff / Katie Bell / Lawrence J T Young / Karl Simin / Robin E Bachelder / Jeff Delrow / Alyssa Dawson / Lisa D Yee / Krzysztof Mrózek / Timothy M Clay / Takuya Osada / Victoria L Seewaldt

    PLoS ONE, Vol 7, Iss 9, p e

    human biology is recapitulated by a novel model system.

    2012  Volume 45684

    Abstract: Breast cancers with a basal-like gene signature are primarily triple-negative, frequently metastatic, and carry a poor prognosis. Basal-like breast cancers are enriched for markers of breast cancer stem cells as well as markers of epithelial-mesenchymal ... ...

    Abstract Breast cancers with a basal-like gene signature are primarily triple-negative, frequently metastatic, and carry a poor prognosis. Basal-like breast cancers are enriched for markers of breast cancer stem cells as well as markers of epithelial-mesenchymal transition (EMT). While EMT is generally thought to be important in the process of metastasis, in vivo evidence of EMT in human disease remains rare. Here we report a novel model of human triple-negative breast cancer, the DKAT cell line, which was isolated from an aggressive, treatment-resistant triple-negative breast cancer that demonstrated morphological and biochemical evidence suggestive of phenotypic plasticity in the patient. The DKAT cell line displays a basal-like phenotype in vitro when cultured in serum-free media, and undergoes phenotypic changes consistent with EMT/MET in response to serum-containing media, a unique property among the breast cancer cell lines we tested. This EMT is marked by increased expression of the transcription factor Zeb1, and Zeb1 is required for the enhanced migratory ability of DKAT cells in the mesenchymal state. DKAT cells also express progenitor-cell markers, and single DKAT cells are able to generate tumorspheres containing both epithelial and mesenchymal cell types. In vivo, as few as ten DKAT cells are capable of forming xenograft tumors which display a range of epithelial and mesenchymal phenotypes. The DKAT model provides a novel model to study the molecular mechanisms regulating phenotypic plasticity and the aggressive biology of triple-negative breast cancers.
    Keywords Medicine ; R ; Science ; Q
    Subject code 610
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Inter-library loan at ZB MED

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  5. Article: Identification of conserved gene expression features between murine mammary carcinoma models and human breast tumors

    Herschkowitz, Jason I / Andrey I Khramtsov / Charles M Perou / Gary A Churchill / Igor Mikaelian / Jeffrey E Green / Jerry Usary / John Quackenbush / Juan P Palazzo / Karen E Rasmussen / Karl Simin / Laundette P Jones / Levy Kopelovich / Michael G Backlund / Olufunmilayo I Olopade / Philip S Bernard / Powel H Brown / Priscilla A Furth / Robert I Glazer /
    Roy Bastein / Shahin Assefnia / Subhashini Chandrasekharan / Terry Van Dyke / Victor J Weigman / Yuzhi Yin / Zhiyuan Hu

    Genome biology. 2007 May, v. 8, no. 5

    2007  

    Abstract: BACKGROUND: Although numerous mouse models of breast carcinomas have been developed, we do not know the extent to which any faithfully represent clinically significant human phenotypes. To address this need, we characterized mammary tumor gene expression ...

    Abstract BACKGROUND: Although numerous mouse models of breast carcinomas have been developed, we do not know the extent to which any faithfully represent clinically significant human phenotypes. To address this need, we characterized mammary tumor gene expression profiles from 13 different murine models using DNA microarrays and compared the resulting data to those from human breast tumors. RESULTS: Unsupervised hierarchical clustering analysis showed that six models (TgWAP-Myc, TgMMTV-Neu, TgMMTV-PyMT, TgWAP-Int3, TgWAP-Tag, and TgC3(1)-Tag) yielded tumors with distinctive and homogeneous expression patterns within each strain. However, in each of four other models (TgWAP-T ₁₂₁ , TgMMTV-Wnt1, Brca1 Cᵒ/Cᵒ ;TgMMTV-Cre;p53⁺/⁻and DMBA-induced), tumors with a variety of histologies and expression profiles developed. In many models, similarities to human breast tumors were recognized, including proliferation and human breast tumor subtype signatures. Significantly, tumors of several models displayed characteristics of human basal-like breast tumors, including two models with induced Brca1 deficiencies. Tumors of other murine models shared features and trended towards significance of gene enrichment with human luminal tumors; however, these murine tumors lacked expression of estrogen receptor (ER) and ER-regulated genes. TgMMTV-Neu tumors did not have a significant gene overlap with the human HER2+/ER- subtype and were more similar to human luminal tumors. CONCLUSION: Many of the defining characteristics of human subtypes were conserved among the mouse models. Although no single mouse model recapitulated all the expression features of a given human subtype, these shared expression features provide a common framework for an improved integration of murine mammary tumor models with human breast tumors.
    Keywords animal models ; breast neoplasms ; carcinoma ; cluster analysis ; DNA microarrays ; estrogen receptors ; gene expression ; genes ; humans ; mammary neoplasms (animal) ; mice ; phenotype ; tumor suppressor proteins
    Language English
    Dates of publication 2007-05
    Size p. 1558.
    Publishing place Springer-Verlag
    Document type Article
    ZDB-ID 2040529-7
    ISSN 1474-760X ; 1465-6914 ; 1465-6906
    ISSN (online) 1474-760X ; 1465-6914
    ISSN 1465-6906
    DOI 10.1186/gb-2007-8-5-r76
    Database NAL-Catalogue (AGRICOLA)

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