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  1. Article ; Online: Thinking outside the box: using metastasis suppressors as molecular tools.

    Thiolloy, Sophie / Rinker-Schaeffer, Carrie W

    Seminars in cancer biology

    2011  Volume 21, Issue 2, Page(s) 89–98

    Abstract: Metastasis, the process in which tumor cells move from a primary tumor through the circulation, lodge, and grow in distant locations, is a significant contributor to cancer patient morbidity and mortality, yet remains poorly understood. The molecular ... ...

    Abstract Metastasis, the process in which tumor cells move from a primary tumor through the circulation, lodge, and grow in distant locations, is a significant contributor to cancer patient morbidity and mortality, yet remains poorly understood. The molecular processes regulating tumorigenicity and metastasis are distinguishable, suggesting that it is possible to design therapeutic interventions to specifically control metastasis formation. Metastasis suppressors, which specifically regulate metastasis, are being used in "reverse genetics" approaches to discover the phenotypic alterations caused by modulating their levels and/or activity. This strategy is allowing the identification of tumor-host interactions that are crucial for efficient colonization and their disruption can be targeted to suppress metastases formation. In this review we discuss studies addressing invasion and migration, key functions for both early and late in the metastatic process. Metastasis suppressor functions, which modulate lodging and subsequent colonization of the secondary site, are also described. In sum this review focuses on metastasis suppressors that have yielded insight into mechanisms controlling metastasis formation. These serve as platform for out of the box thinking which will enable the discovery of new paradigms in metastasis research.
    MeSH term(s) Animals ; Cell Adhesion/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Molecular Biology ; Neoplasm Metastasis/genetics ; Signal Transduction ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism
    Chemical Substances Tumor Suppressor Proteins
    Language English
    Publishing date 2011-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1033980-2
    ISSN 1096-3650 ; 1044-579X
    ISSN (online) 1096-3650
    ISSN 1044-579X
    DOI 10.1016/j.semcancer.2010.12.008
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    Zs.A 2922: Show issues Location:
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  2. Article ; Online: Disrupting ovarian cancer metastatic colonization: insights from metastasis suppressor studies.

    Khan, Shaheena / Taylor, Jennifer L / Rinker-Schaeffer, Carrie W

    Journal of oncology

    2010  Volume 2010, Page(s) 286925

    Abstract: Ovarian cancer affects approximately 25,000 women in the United States each year and remains one of the most lethal female malignancies. A standard approach to therapy is surgical cytoreduction, after which the remaining microscopic residual disease is ... ...

    Abstract Ovarian cancer affects approximately 25,000 women in the United States each year and remains one of the most lethal female malignancies. A standard approach to therapy is surgical cytoreduction, after which the remaining microscopic residual disease is treated with chemotherapy. The vast majority of patients have disease recurrence, underscoring the crucial need for approaches to control the regrowth, or colonization, of tissues after local treatment. Improved therapies require mechanistic information about the process of metastatic colonization, the final step in metastasis, in which cancer cells undergo progressive growth at secondary sites. Studies of metastasis suppressors are providing insights into events controlling metastatic colonization. This paper reviews our laboratory's approach to the identification, characterization, and functional testing of the JNKK1/MKK4 metastasis suppressor in ovarian cancer metastatic colonization. Specifically, we demonstrate that interaction of ovarian caner cells with the omental microenvironment activates JNKK1/MKK4 resulting in decreased proliferation without affecting apoptosis. The potential role of the omental microenvironment, specifically milky spot structures, is also described. It is our goal to provide this work as a usable paradigm that will enable others to study metastasis suppressors in clinical and experimental ovarian cancer metastases.
    Language English
    Publishing date 2010-03-14
    Publishing country Egypt
    Document type Journal Article
    ZDB-ID 2461349-6
    ISSN 1687-8469 ; 1687-8450
    ISSN (online) 1687-8469
    ISSN 1687-8450
    DOI 10.1155/2010/286925
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  3. Article ; Online: Metastasis-suppressor genes in clinical practice: lost in translation?

    Shoushtari, Alexander N / Szmulewitz, Russell Z / Rinker-Schaeffer, Carrie W

    Nature reviews. Clinical oncology

    2011  Volume 8, Issue 6, Page(s) 333–342

    Abstract: Over the past 25 years, an expanding set of metastasis-suppressor genes (MSGs) has been identified that specifically regulate metastasis formation without affecting primary growth. MSGs are involved in diverse molecular processes in multiple tumor types. ...

    Abstract Over the past 25 years, an expanding set of metastasis-suppressor genes (MSGs) has been identified that specifically regulate metastasis formation without affecting primary growth. MSGs are involved in diverse molecular processes in multiple tumor types. Given the wealth of metastasis biology that underlies their functions, treatment strategies based on MSGs have an unparalleled potential to improve patient care. Using NM23 as a prime example, we discuss how specific MSGs have been used as prognostic markers, tools for predicting response to treatment, and targets for the development of novel therapies. Barriers specific to the translation of MSG biology into clinical practice are reviewed and future research directions necessary for clinical advances are delineated. Although to date the impact of MSGs on patient care is limited, it is an expanding field with vast potential to help develop new treatments and identify patients who will most benefit from them.
    MeSH term(s) Genes, Tumor Suppressor ; Humans ; Neoplasm Metastasis ; Neoplasms/genetics ; Neoplasms/prevention & control ; Signal Transduction
    Language English
    Publishing date 2011-04-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2491410-1
    ISSN 1759-4782 ; 1759-4774
    ISSN (online) 1759-4782
    ISSN 1759-4774
    DOI 10.1038/nrclinonc.2011.65
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    Zs.A 6029: Show issues Location:
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  4. Article ; Online: Flexible peritoneal windows for quantitative fluorescence and bioluminescence preclinical imaging.

    Souris, Jeffrey S / Hickson, Jonathan A / Msezane, Lambda / Rinker-Schaeffer, Carrie W / Chen, Chin-Tu

    Molecular imaging

    2013  Volume 12, Issue 1, Page(s) 28–38

    Abstract: At present, there is considerable interest in the use of in vivo fluorescence and bioluminescence imaging to track the onset and progression of pathologic processes in preclinical models of human disease. Optical quantitation of such phenomena, however, ... ...

    Abstract At present, there is considerable interest in the use of in vivo fluorescence and bioluminescence imaging to track the onset and progression of pathologic processes in preclinical models of human disease. Optical quantitation of such phenomena, however, is often problematic, frequently complicated by the overlying tissue's scattering and absorption of light, as well as the presence of endogenous cutaneous and subcutaneous fluorophores. To partially circumvent this information loss, we report here the development of flexible, surgically implanted, transparent windows that enhance quantitative in vivo fluorescence and bioluminescence imaging of optical reporters. These windows are metal and glass free and thus compatible with computed tomography, magnetic resonance imaging, positron emission tomography, and single-photon emission computed tomography; they also permit visualization of much larger areas with fewer impediments to animal locomotion and grooming than those previously described. To evaluate their utility in preclinical imaging, we surgically implanted these windows in the abdominal walls of female athymic nude mice and subsequently inoculated each animal with 1 × 10(4) to 1 × 10(6) bioluminescent human ovarian cancer cells (SKOV3ip.1-luc). Longitudinal imaging studies of fenestrated animals revealed up to 48-fold gains in imaging sensitivity relative to nonfenestrated animals, with relatively few complications, allowing wide-field in vivo visualization of nascent metastatic ovarian cancer colonization.
    MeSH term(s) Abdomen/surgery ; Animals ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Humans ; Implants, Experimental ; Kaplan-Meier Estimate ; Luminescent Measurements/methods ; Materials Testing ; Mice ; Mice, Nude ; Molecular Imaging/methods ; Optical Imaging/methods ; Peritoneum/surgery ; Polyvinyl Chloride/chemistry
    Chemical Substances Polyvinyl Chloride (9002-86-2)
    Language English
    Publishing date 2013-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2137435-1
    ISSN 1536-0121 ; 1535-3508
    ISSN (online) 1536-0121
    ISSN 1535-3508
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  5. Article: Stopping cancer before it colonizes.

    Rinker-Schaeffer, Carrie W / Hickson, Jonathan A

    Nature medicine

    2006  Volume 12, Issue 8, Page(s) 887–888

    MeSH term(s) Amino Acid Sequence ; Animals ; Biomarkers/metabolism ; Cell Proliferation ; Cellular Senescence/physiology ; Duffy Blood-Group System/chemistry ; Duffy Blood-Group System/metabolism ; Endothelium, Vascular/metabolism ; Humans ; Immunohistochemistry ; Kangai-1 Protein/chemistry ; Kangai-1 Protein/metabolism ; Lung Neoplasms/pathology ; Membrane Glycoproteins/chemistry ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Knockout ; Models, Biological ; Neoplasm Metastasis/prevention & control ; Neoplasm Transplantation ; Receptors, Cell Surface/chemistry ; Receptors, Cell Surface/metabolism ; Transplantation, Heterologous ; beta-Galactosidase/metabolism
    Chemical Substances ACKR1 protein, human ; Biomarkers ; Duffy Blood-Group System ; Kangai-1 Protein ; Membrane Glycoproteins ; Receptors, Cell Surface ; beta-Galactosidase (EC 3.2.1.23)
    Language English
    Publishing date 2006-08-03
    Publishing country United States
    Document type Comparative Study ; News ; Comment
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm0806-887
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    Zs.A 4212: Show issues Location:
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  6. Article: From prostate to bone: key players in prostate cancer bone metastasis.

    Thobe, Megan N / Clark, Robert J / Bainer, Russell O / Prasad, Sandip M / Rinker-Schaeffer, Carrie W

    Cancers

    2011  Volume 3, Issue 1, Page(s) 478–493

    Abstract: Bone is the most common site for metastasis in human prostate cancer patients. Skeletal metastases are a significant cause of morbidity and mortality and overall greatly affect the quality of life of prostate cancer patients. Despite advances in our ... ...

    Abstract Bone is the most common site for metastasis in human prostate cancer patients. Skeletal metastases are a significant cause of morbidity and mortality and overall greatly affect the quality of life of prostate cancer patients. Despite advances in our understanding of the biology of primary prostate tumors, our knowledge of how and why secondary tumors derived from prostate cancer cells preferentially localize bone remains limited. The physiochemical properties of bone, and signaling molecules including specific chemokines and their receptors, are distinct in nature and function, yet play intricate and significant roles in prostate cancer bone metastasis. Examining the impact of these facets of bone metastasis in vivo remains a significant challenge, as animal models that mimic the natural history and malignant progression clinical prostate cancer are rare. The goals of this article are to discuss (1) characteristics of bone that most likely render it a favorable environment for prostate tumor cell growth, (2) chemokine signaling that is critical in the recruitment and migration of prostate cancer cells to the bone, and (3) current animal models utilized in studying prostate cancer bone metastasis. Further research is necessary to elucidate the mechanisms underlying the extravasation of disseminated prostate cancer cells into the bone and to provide a better understanding of the basis of cancer cell survival within the bone microenvironment. The development of animal models that recapitulate more closely the human clinical scenario of prostate cancer will greatly benefit the generation of better therapies.
    Language English
    Publishing date 2011-04-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers3010478
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  7. Article ; Online: Disrupting Ovarian Cancer Metastatic Colonization

    Jennifer L. Taylor / Carrie W. Rinker-Schaeffer / Shaheena Khan

    Journal of Oncology, Vol

    Insights from Metastasis Suppressor Studies

    2010  Volume 2010

    Keywords Neoplasms. Tumors. Oncology. Including cancer and carcinogens ; RC254-282 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Oncology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2010-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: A new look at an old problem: the survival and organ-specific growth of metastases.

    Vander Griend, Donald J / Rinker-Schaeffer, Carrie W

    Science's STKE : signal transduction knowledge environment

    2004  Volume 2004, Issue 216, Page(s) pe3

    Abstract: Despite improvements in cancer detection and therapy, metastatic disease is largely incurable. Recent research indicates that tumor cells disseminate widely early in the process of pathogenesis, and that the survival and proliferation of these cells--and ...

    Abstract Despite improvements in cancer detection and therapy, metastatic disease is largely incurable. Recent research indicates that tumor cells disseminate widely early in the process of pathogenesis, and that the survival and proliferation of these cells--and thus the development of metastases--depend on interactions between the disseminated cells and their particular microenvironment. Proliferative signals and the inhibition of proapoptotic responses are both critically involved in the development of clinically significant metastases. Identification of the underlying signaling cascades may provide additional targets for antimetastatic therapy.
    MeSH term(s) Animals ; Cell Division ; Cell Survival ; Humans ; Neoplasm Metastasis/pathology ; Organ Specificity
    Language English
    Publishing date 2004-01-13
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1525-8882
    ISSN (online) 1525-8882
    DOI 10.1126/stke.2162004pe3
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  9. Article ; Online: Time-dependent transcriptional profiling links gene expression to mitogen-activated protein kinase kinase 4 (MKK4)-mediated suppression of omental metastatic colonization.

    Bainer, Russell O / Veneris, Jennifer Taylor / Yamada, S Diane / Montag, Anthony / Lingen, Mark W / Gilad, Yoav / Rinker-Schaeffer, Carrie W

    Clinical & experimental metastasis

    2012  Volume 29, Issue 5, Page(s) 397–408

    Abstract: Although metastasis is the most lethal attribute of cancer, critical gaps in our knowledge of how cancer cells effectively colonize distant sites remain. For example, little is known about the cellular and molecular events that occur during the ... ...

    Abstract Although metastasis is the most lethal attribute of cancer, critical gaps in our knowledge of how cancer cells effectively colonize distant sites remain. For example, little is known about the cellular and molecular events that occur during the timecourse of metastatic colonization. To address this we are using the mitogen-activated protein kinase kinase 4 (MKK4) metastasis suppressor as a tool to identify these events. Specifically, we report a microarray expression-based strategy to identify genes whose transcription is altered in SKOV3ip.1 human ovarian cancer cells that express ectopic MKK4 throughout the course of in vivo metastatic colonization. The majority of genes identified fell into the categories of cytokinesis, cytoskeleton remodeling, and cell adhesion, and their expression was repressed in MKK4-expressing cells relative to vector controls. The greatest transcriptional divergence was concomitant with impaired proliferation at 14 days post injection (dpi). Specifically, 763 genes were differentially expressed (FDR < 0.05) between lesions that expressed ectopic MKK4 and paired controls. In contrast, only seven genes were differentially expressed at the experimental endpoint, when MKK4-expressing and control cells had formed macroscopic metastases. Application of our cohort of differentially expressed genes to three independent clinical datasets demonstrated a strong correlation between our findings and metastatic phenotypes in patient samples. Our results highlight the dynamic nature of metastatic colonization and reinforce the importance of examining both molecular and cellular phenotypes over time when studying metastasis formation.
    MeSH term(s) Animals ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Blotting, Western ; Female ; Gene Expression Profiling ; Humans ; Immunoenzyme Techniques ; MAP Kinase Kinase 4/genetics ; MAP Kinase Kinase 4/metabolism ; Mice ; Oligonucleotide Array Sequence Analysis ; Omentum/metabolism ; Omentum/pathology ; Ovarian Neoplasms/enzymology ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/secondary ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Tumor Cells, Cultured ; Tumor Stem Cell Assay
    Chemical Substances Biomarkers, Tumor ; RNA, Messenger ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; MAP2K4 protein, human (EC 2.7.12.2)
    Language English
    Publishing date 2012-02-21
    Publishing country Netherlands
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 604952-7
    ISSN 1573-7276 ; 0262-0898
    ISSN (online) 1573-7276
    ISSN 0262-0898
    DOI 10.1007/s10585-011-9448-y
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    Zs.A 1855: Show issues Location:
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  10. Article: Mitogen-activated protein kinase kinase 4/c-Jun NH2-terminal kinase kinase 1 protein expression is subject to translational regulation in prostate cancer cell lines.

    Robinson, Victoria L / Shalhav, Ore / Otto, Kristen / Kawai, Tomoko / Gorospe, Myriam / Rinker-Schaeffer, Carrie W

    Molecular cancer research : MCR

    2008  Volume 6, Issue 3, Page(s) 501–508

    Abstract: Mitogen-activated protein kinase kinase 4/c-Jun NH(2)-terminal kinase kinase 1 (MKK4/JNKK1; hereafter referred to as MKK4) is a dual-specificity kinase with a critical role in regulating the activity of c-Jun NH(2)-terminal kinase and p38 kinases. We ... ...

    Abstract Mitogen-activated protein kinase kinase 4/c-Jun NH(2)-terminal kinase kinase 1 (MKK4/JNKK1; hereafter referred to as MKK4) is a dual-specificity kinase with a critical role in regulating the activity of c-Jun NH(2)-terminal kinase and p38 kinases. We identified a novel biological function for MKK4 in the regulation of growth of ovarian and prostate cancer metastases. Clinical correlative studies showed that MKK4 protein levels were reduced in high-grade prostate cancer and prostate and ovarian cancer metastases compared with normal tissue, which prompted investigation into the mechanism(s) responsible for down-regulation of MKK4 in a panel of cancer cell lines. Initial studies found that low levels of MKK4 protein did not correlate with either exon deletion or decreased levels of MKK4 mRNA, suggesting that MKK4 protein levels were regulated posttranscriptionally by either reduced translation or reduced protein stability. Endogenous MKK4 was highly stable and not subject to altered proteolysis. Instead, MKK4 biosynthesis seemed to be regulated by altered translation. In support of this assertion, we found that cytosolic MKK4 mRNA was shifted toward active polysomes in cells with higher levels of MKK4 protein, suggesting that MKK4 mRNA was translated more efficiently in these cells. This study supports a novel mechanism for the regulation of MKK4 protein levels. Further, these findings have potential therapeutic implications for modulating the expression of a signaling kinase involved in the regulation of metastatic growth.
    MeSH term(s) Acetylcysteine/analogs & derivatives ; Acetylcysteine/pharmacology ; Blotting, Northern ; Cell Line, Tumor ; Cycloheximide/pharmacology ; Dactinomycin/pharmacology ; Ethanol/pharmacology ; Female ; Gene Expression Regulation, Enzymologic/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; MAP Kinase Kinase 4/genetics ; Male ; Neoplasm Metastasis ; Ovarian Neoplasms/enzymology ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Polymerase Chain Reaction ; Prostatic Neoplasms/enzymology ; Prostatic Neoplasms/genetics ; Protein Biosynthesis
    Chemical Substances lactacystin (133343-34-7) ; Dactinomycin (1CC1JFE158) ; Ethanol (3K9958V90M) ; Cycloheximide (98600C0908) ; MAP Kinase Kinase 4 (EC 2.7.12.2) ; MAP2K4 protein, human (EC 2.7.12.2) ; Acetylcysteine (WYQ7N0BPYC)
    Language English
    Publishing date 2008-03-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-07-2075
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