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  • 1
    In: Ecology, Wiley, Vol. 103, No. 10 ( 2022-10)
    Abstract: Managing wildlife populations in the face of global change requires regular data on the abundance and distribution of wild animals, but acquiring these over appropriate spatial scales in a sustainable way has proven challenging. Here we present the data from Snapshot USA 2020, a second annual national mammal survey of the USA. This project involved 152 scientists setting camera traps in a standardized protocol at 1485 locations across 103 arrays in 43 states for a total of 52,710 trap‐nights of survey effort. Most (58) of these arrays were also sampled during the same months (September and October) in 2019, providing a direct comparison of animal populations in 2 years that includes data from both during and before the COVID‐19 pandemic. All data were managed by the eMammal system, with all species identifications checked by at least two reviewers. In total, we recorded 117,415 detections of 78 species of wild mammals, 9236 detections of at least 43 species of birds, 15,851 detections of six domestic animals and 23,825 detections of humans or their vehicles. Spatial differences across arrays explained more variation in the relative abundance than temporal variation across years for all 38 species modeled, although there are examples of significant site‐level differences among years for many species. Temporal results show how species allocate their time and can be used to study species interactions, including between humans and wildlife. These data provide a snapshot of the mammal community of the USA for 2020 and will be useful for exploring the drivers of spatial and temporal changes in relative abundance and distribution, and the impacts of species interactions on daily activity patterns. There are no copyright restrictions, and please cite this paper when using these data, or a subset of these data, for publication.
    Type of Medium: Online Resource
    ISSN: 0012-9658 , 1939-9170
    URL: Issue
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    Language: English
    Publisher: Wiley
    Publication Date: 2022
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  • 2
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 11, No. 1 ( 2021-02-05)
    Abstract: Mammosphere assays are widely used in vitro to identify prospective cancer-initiating stem cells that can propagate clonally to form spheres in free-floating conditions. However, the traditional mammosphere assay inevitably introduces cell aggregation that interferes with the measurement of true mammosphere forming efficiency. We developed a method to reduce tumor cell aggregation and increase the probability that the observed mammospheres formed are clonal in origin. Tethering individual tumor cells to lipid anchors prevents cell drift while maintaining free-floating characteristics. This enables real-time monitoring of single tumor cells as they divide to form mammospheres. Monitoring tethered breast cancer cells provided detailed size information that correlates directly to previously published single cell tracking data. We observed that 71% of the Day 7 spheres in lipid-coated wells were between 50 and 150 μm compared to only 37% in traditional low attachment plates. When an equal mixture of MCF7-GFP and MCF7-mCherry cells were seeded, 65% of the mammospheres in lipid-coated wells demonstrated single color expression whereas only 32% were single-colored in low attachment wells. These results indicate that using lipid tethering for mammosphere growth assays can reduce the confounding factor of cell aggregation and increase the formation of clonal mammospheres.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
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  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1123-1123
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1123-1123
    Abstract: Breast cancer is the most frequent malignancy in women, and although many breast cancers are curable via surgery, approximately one quarter maintain a latent and insidious characteristic of slow growth with early metastasis. The loss of the tumor suppressor PTEN has been associated with breast cancer stage, lymph node status, and disease-related death, and the high rate of loss in primary tumors suggests a potential role in initiation and/or progression of the disease. However, specific cellular alterations in human breast epithelium controlled by PTEN inactivation, which lead to an increased metastatic phenotype, remain poorly defined. We have determined that heterozygous and homozygous loss of PTEN in non-tumorigenic mammary epithelial cells (MECs) was insufficient to promote anchorage-independent growth. However, MECs with PTEN loss maintained elevated activation of the PI3K/Akt and MAPK pathways and apoptotic resistance to cell rounding and matrix detatchment. We have also recently determined that PTEN expression loss leads to the production of long, dynamic, tubulin-based membrane protrusions upon detachment, which are increased in frequency, number and length per cell as compared to their isogenic, PTEN-expressing parental counterparts. These novel structures, termed microtentacles (McTNs), are structurally distinct from classical actin-based extensions of adherent cells, persist for days in breast tumor lines that are resistant to anoikis, and aid in the reattachment to matrix or cell monolayers. Therefore, the combination of apoptotic resistance and enhanced McTN formation due to PTEN loss may have important consequences for facilitating tumor cell extravasation and efficient adherence in metastatic sites. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1123.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 4
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 3122-3122
    Abstract: Breast cancer is the most frequent malignancy in women, and although many breast cancers are curable via surgery, approximately one quarter maintain a latent and insidious characteristic of slow growth with early metastasis. The loss of the tumor suppressor PTEN has been associated with breast cancer stage, lymph node status, and disease-related death, and the high rate of loss in primary tumors suggests a potential role in initiation and/or progression of the disease. However, specific cellular alterations in human breast epithelium controlled by PTEN inactivation, which lead to an increased metastatic phenotype, remain poorly defined. We have recently determined that PTEN expression loss leads to the production of long, dynamic, tubulin-based membrane protrusions upon detachment, which increase in frequency, number and length per cell compared to their isogenic, PTEN-expressing parental counterparts. These novel structures, termed microtentacles (McTNs), are structurally distinct from classical actin-based extensions of adherent cells, persist for days in breast tumor lines that are resistant to anoikis, and aid in the reattachment to matrix or cell monolayers and homo- and heterotypic aggregation. McTNs form when the balance of cytoskeletal forces shifts. In order to control morphology, normal cells counteract the expansion of microtubules with tension from the actin cortex. However, altering the balance between microtubules and actin has serious implications for circulating tumor cells (CTCs) dissemination, as metastatically efficient CTCs have been observed to avoid shear-induced fragmentation by undergoing sphere-to-cylinder shape transformations within capillaries. We, therefore, tested the hypothesis that PTEN loss disrupts the actin cortex to allow the increased production of McTNs. We determined that suspended PTEN-null mammary epithelial cells maintained elevated activation of the PI3K/Akt and MAPK pathways and apoptotic resistance to cell rounding and matrix detatchment, but neither activated pathway was responsible for the increased McTNs in these cells. The McTNs produced in the PTEN-null cells aid in cell reattachment, spreading, and homotypic aggregation, and Western blot analysis has proven that the PTEN-null cells show reduced inactivation of cofilin, an actin-binding protein known to sever actin filaments. Thus, the actin cytoskeleton in the PTEN-null cells contains more depolymerized actin, weakening the actin cortex. The combination of apoptotic resistance, the weakening of the actin cortex, and enhanced McTN formation due to PTEN loss may have important consequences for facilitating tumor cell extravasation and efficient adherence in metastatic sites. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3122. doi:10.1158/1538-7445.AM2011-3122
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
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  • 5
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2008
    In:  Cancer Research Vol. 68, No. 14 ( 2008-07-15), p. 5678-5688
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 68, No. 14 ( 2008-07-15), p. 5678-5688
    Abstract: Solid tumor metastasis often involves detachment of epithelial carcinoma cells into the vasculature or lymphatics. However, most studies of cytoskeletal rearrangement in solid tumors focus on attached cells. In this study, we report for the first time that human breast tumor cells produce unique tubulin-based protrusions when detached from extracellular matrix. Tumor cell lines of high metastatic potential show significantly increased extension and frequency of microtubule protrusions, which we have termed tubulin microtentacles. Our previous studies in nontumorigenic mammary epithelial cells showed that such detachment-induced microtentacles are enriched in detyrosinated α-tubulin. However, amounts of detyrosinated tubulin were similar in breast tumor cell lines despite varying microtentacle levels. Because detyrosinated α-tubulin associates strongly with intermediate filament proteins, we examined the contribution of cytokeratin and vimentin filaments to tumor cell microtentacles. Increased microtentacle frequency and extension correlated strongly with loss of cytokeratin expression and up-regulation of vimentin, as is often observed during tumor progression. Moreover, vimentin filaments coaligned with microtentacles, whereas cytokeratin did not. Disruption of vimentin with PP1/PP2A-specific inhibitors significantly reduced microtentacles and inhibited cell reattachment to extracellular matrix. Furthermore, expression of a dominant-negative vimentin mutant disrupted endogenous vimentin filaments and significantly reduced microtentacles, providing specific genetic evidence that vimentin supports microtentacles. Our results define a novel model in which coordination of vimentin and detyrosinated microtubules provides structural support for the extensive microtentacles observed in detached tumor cells and a possible mechanism to promote successful metastatic spread. [Cancer Res 2008;68(14):5678–88]
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
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  • 6
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 20 ( 2010-10-15), p. 7737-7741
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 20 ( 2010-10-15), p. 7737-7741
    Abstract: Detection of circulating tumor cells (CTC) is advancing as an effective predictor of patient outcome and therapeutic response. Unfortunately, our knowledge of CTC biology remains limited, and the impact of drug treatments on CTC metastatic potential is currently unclear. Improved CTC imaging in vivo and analysis of free-floating tumor cells now show that cytoskeletal regulation in CTCs contrasts starkly with tumor cells attached to extracellular matrix. In this review, we examine how persistent microtubule stabilization promotes the formation of microtentacles on the surface of detached breast tumor cells and enhances metastatic potential. Cancer Res; 70(20); 7737–41. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 7
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 20 ( 2010-10-15), p. 8127-8137
    Abstract: Epithelial-to-mesenchymal transition (EMT) is associated with increased breast tumor metastasis; however, the specific mechanisms by which EMT promotes metastasis remain somewhat unclear. Despite the importance of cytoskeletal dynamics during both EMT and metastasis, very few current studies examine the cytoskeleton of detached and circulating tumor cells. Specific posttranslational α-tubulin modifications are critical for adherent cell motility and implicated in numerous pathologies, but also remain understudied in detached cells. We report here that EMT induced through ectopic expression of Twist or Snail promotes α-tubulin detyrosination and the formation of tubulin-based microtentacles in detached HMLEs. Mechanistically, EMT downregulates the tubulin tyrosine ligase enzyme, resulting in an accumulation of detyrosinated α-tubulin (Glu-tubulin), and increases microtentacles that penetrate endothelial layers to facilitate tumor cell reattachment. Confocal microscopy shows that microtentacles are capable of penetrating the junctions between endothelial cells. Suppression of endogenous Twist in metastatic human breast tumor cells is capable of reducing both tubulin detyrosination and microtentacles. Clinical breast tumor samples display high concordance between Glu-tubulin and Twist expression levels, emphasizing the coupling between EMT and tubulin detyrosination in vivo. Coordinated elevation of Twist and Glu-tubulin at invasive tumor fronts, particularly within ductal carcinoma in situ samples, establishes that EMT-induced tubulin detyrosination occurs at the earliest stages of tumor invasion. These data support a novel model where the EMT that occurs during tumor invasion downregulates tubulin tyrosine ligase, increasing α-tubulin detyrosination and promoting microtentacles that could enhance the reattachment of circulating tumor cells to the vascular endothelium during metastasis. Cancer Res; 70(20); 8127–37. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
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  • 8
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1464-1464
    Abstract: Epithelial-to-mesenchymal transition (EMT) is associated with increased breast tumor metastasis, although the specific mechanism by which EMT increases metastasis remains somewhat unclear. We have previously demonstrated that detached human breast tumor cells generate unique microtentacle (McTN) extensions of their plasma membrane that are supported by coordinated vimentin intermediate filaments and detyrosinated microtubules. Microtentacles are specifically induced by EMT and promote the reattachment of tumor cells to each other and endothelial cell layers. We report here that immunohistochemical staining of tumor sections from patients with ductal carcinoma in situ and invasive ductal carcinoma indicates that detyrosination of α-tubulin occurs at invasive fronts where tumor cells are moving through the stromal microenvironment. Costaining with the EMT marker, Twist, demonstrates that tubulin detyrosination occurs specifically within cells that are undergoing EMT. Exogenous expression of either Twist or Snail in immortalized human mammary epithelial cells leads to a downregulation of the tubulin tyrosine ligase (TTL) enzyme that catalyzes the readdition of tyrosine to α-tubulin. This provides a novel molecular mechanism for the increase in detyrosinated microtubules observed in cells undergoing EMT. Addition of the sesquiterpene lactone, Parthenolide, to breast tumor cells reversed this EMT-induced increase in detyrosinated tubulin. Treatment of either breast tumor cells or nontumorigenic MCF10A mammary epithelial cells with 10μM Parthenolide also led to reductions in microtentacles, without affecting cell viability. Given the role of microtentacles in adhesion to endothelial layers, whole-animal bioluminescence imaging was used to track circulating tumor cells following tail vein injection. Pretreating metastatic MDA-MB-231 cells with Parthenolide prior to tail vein injection caused up to a 75% decrease in the lung retention of circulating tumor cells. These data support a model where the tubulin detyrosination that supports microtentacles promotes the ability of circulating tumor cells to reattach in distant capillary beds. Furthermore, the tubulin detyrosination that occurs in cells undergoing EMT at invasive tumor fronts could prime these cells for metastatic success once entering the circulation. These findings provide a possible explanation for why increased levels of detyrosinated tubulin are associated with poor patient survival in breast cancer and a new potential mechanism for how EMT could promote tumor metastasis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1464.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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  • 9
    Online Resource
    Online Resource
    Informa UK Limited ; 2010
    In:  Cancer Biology & Therapy Vol. 9, No. 1 ( 2010-01), p. 66-76
    In: Cancer Biology & Therapy, Informa UK Limited, Vol. 9, No. 1 ( 2010-01), p. 66-76
    Type of Medium: Online Resource
    ISSN: 1538-4047 , 1555-8576
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2010
    detail.hit.zdb_id: 2088895-8
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  • 10
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2010
    In:  Breast Cancer Research and Treatment Vol. 121, No. 1 ( 2010-5), p. 65-78
    In: Breast Cancer Research and Treatment, Springer Science and Business Media LLC, Vol. 121, No. 1 ( 2010-5), p. 65-78
    Type of Medium: Online Resource
    ISSN: 0167-6806 , 1573-7217
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 2004077-5
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