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  1. Article ; Online: Cancer-Associated Hypercalcemia. Reply.

    Guise, Theresa A / Wysolmerski, John J

    The New England journal of medicine

    2022  Volume 386, Issue 26, Page(s) 2540

    MeSH term(s) Humans ; Hypercalcemia/etiology ; Paraneoplastic Syndromes
    Language English
    Publishing date 2022-06-29
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc2206287
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  2. Article ; Online: Cancer-Associated Hypercalcemia.

    Guise, Theresa A / Wysolmerski, John J

    The New England journal of medicine

    2022  Volume 386, Issue 15, Page(s) 1443–1451

    MeSH term(s) Carcinoma, Squamous Cell/complications ; Humans ; Hypercalcemia/etiology ; Neoplasms/complications ; Paraneoplastic Syndromes/complications
    Language English
    Publishing date 2022-04-13
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcp2113128
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  3. Article ; Online: Systemic effects of abnormal bone resorption on muscle, metabolism, and cognition.

    Trivedi, Trupti / Guise, Theresa A

    Bone

    2021  Volume 154, Page(s) 116245

    Abstract: Skeletal tissue is dynamic, undergoing constant remodeling to maintain musculoskeletal integrity and balance in the human body. Recent evidence shows that apart from maintaining homeostasis in the local microenvironment, the skeleton systemically affects ...

    Abstract Skeletal tissue is dynamic, undergoing constant remodeling to maintain musculoskeletal integrity and balance in the human body. Recent evidence shows that apart from maintaining homeostasis in the local microenvironment, the skeleton systemically affects other tissues. Several cancer-associated and noncancer-associated bone disorders can disrupt the physiological homeostasis locally in the bone microenvironment and indirectly contribute to dysregulation of systemic body function. The systemic effects of bone on the regulation of distant organ function have not been widely explored. Recent evidence suggests that bone can interact with skeletal muscle, pancreas, and brain by releasing factors from mineralized bone matrix. Currently available bone-targeting therapies such as bisphosphonates and denosumab inhibit bone resorption, decrease morbidity associated with bone destruction, and improve survival. Bisphosphonates have been a standard treatment for bone metastases, osteoporosis, and cancer treatment-induced bone diseases. The extraskeletal effects of bisphosphonates on inhibition of tumor growth are known. However, our knowledge of the effects of bisphosphonates on muscle weakness, hyperglycemia, and cognitive defects is currently evolving. To be able to identify the molecular link between bone and distant organs during abnormal bone resorption and then treat these abnormalities and prevent their systemic effects could improve survival benefits. The current review highlights the link between bone resorption and its systemic effects on muscle, pancreas, and brain.
    MeSH term(s) Bone Neoplasms/secondary ; Bone Resorption/drug therapy ; Cognition ; Diphosphonates/pharmacology ; Diphosphonates/therapeutic use ; Humans ; Muscles ; Tumor Microenvironment
    Chemical Substances Diphosphonates
    Language English
    Publishing date 2021-10-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 632515-4
    ISSN 1873-2763 ; 8756-3282
    ISSN (online) 1873-2763
    ISSN 8756-3282
    DOI 10.1016/j.bone.2021.116245
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1571: Show issues Location:
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    Zs.MO 332: Show issues

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  4. Article ; Online: The bone-muscle connection in breast cancer: implications and therapeutic strategies to preserve musculoskeletal health.

    Ballinger, Tarah J / Thompson, William R / Guise, Theresa A

    Breast cancer research : BCR

    2022  Volume 24, Issue 1, Page(s) 84

    Abstract: Breast cancer and its therapies frequently result in significant musculoskeletal morbidity. Skeletal complications include bone metastases, pain, bone loss, osteoporosis, and fracture. In addition, muscle loss or weakness occurring in both the metastatic ...

    Abstract Breast cancer and its therapies frequently result in significant musculoskeletal morbidity. Skeletal complications include bone metastases, pain, bone loss, osteoporosis, and fracture. In addition, muscle loss or weakness occurring in both the metastatic and curative setting is becoming increasingly recognized as systemic complications of disease and treatment, impacting quality of life, responsiveness to therapy, and survival. While the anatomical relationship between bone and muscle is well established, emerging research has led to new insights into the biochemical and molecular crosstalk between the skeletal and muscular systems. Here, we review the importance of both skeletal and muscular health in breast cancer, the significance of crosstalk between bone and muscle, and the influence of mechanical signals on this relationship. Therapeutic exploitation of signaling between bone and muscle has great potential to prevent the full spectrum of musculoskeletal complications across the continuum of breast cancer.
    MeSH term(s) Humans ; Female ; Breast Neoplasms/therapy ; Quality of Life ; Bone Neoplasms/prevention & control ; Muscles ; Osteoporosis
    Language English
    Publishing date 2022-11-23
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2015059-3
    ISSN 1465-542X ; 1465-5411
    ISSN (online) 1465-542X
    ISSN 1465-5411
    DOI 10.1186/s13058-022-01576-2
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    Zs.A 5494: Show issues Location:
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  5. Book: Understanding and optimizing bone health in breast cancer

    Guise, Theresa A. / Brufsky, Adam / Coleman, Robert E.

    (Current medical research and opinion ; 26, Suppl. 3)

    2010  

    Author's details Theresa A. Guise, Adam Brufsky and Robert E. Coleman
    Series title Current medical research and opinion ; 26, Suppl. 3
    Collection
    Language English
    Size 20 S. : Ill.
    Publisher Informa UK
    Publishing place S.l.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT016647402
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Zs A 955 -26,Suppl.3- not available for loan Zeitschriften-Lesesaal

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  6. Article ; Online: Hypercalcemia of Malignancy: A New Twist on an Old Problem.

    Mohammad, Khalid S / Guise, Theresa A

    Journal of oncology practice

    2016  Volume 12, Issue 5, Page(s) 435–436

    Language English
    Publishing date 2016-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2236338-5
    ISSN 1935-469X ; 1554-7477
    ISSN (online) 1935-469X
    ISSN 1554-7477
    DOI 10.1200/JOP.2016.012062
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  7. Article ; Online: The Role of TGF-β in Bone Metastases.

    Trivedi, Trupti / Pagnotti, Gabriel M / Guise, Theresa A / Mohammad, Khalid S

    Biomolecules

    2021  Volume 11, Issue 11

    Abstract: Complications associated with advanced cancer are a major clinical challenge and, if associated with bone metastases, worsen the prognosis and compromise the survival of the patients. Breast and prostate cancer cells exhibit a high propensity to ... ...

    Abstract Complications associated with advanced cancer are a major clinical challenge and, if associated with bone metastases, worsen the prognosis and compromise the survival of the patients. Breast and prostate cancer cells exhibit a high propensity to metastasize to bone. The bone microenvironment is unique, providing fertile soil for cancer cell propagation, while mineralized bone matrices store potent growth factors and cytokines. Biologically active transforming growth factor β (TGF-β), one of the most abundant growth factors, is released following tumor-induced osteoclastic bone resorption. TGF-β promotes tumor cell secretion of factors that accelerate bone loss and fuel tumor cells to colonize. Thus, TGF-β is critical for driving the feed-forward vicious cycle of tumor growth in bone. Further, TGF-β promotes epithelial-mesenchymal transition (EMT), increasing cell invasiveness, angiogenesis, and metastatic progression. Emerging evidence shows TGF-β suppresses immune responses, enabling opportunistic cancer cells to escape immune checkpoints and promote bone metastases. Blocking TGF-β signaling pathways could disrupt the vicious cycle, revert EMT, and enhance immune response. However, TGF-β's dual role as both tumor suppressor and enhancer presents a significant challenge in developing therapeutics that target TGF-β signaling. This review presents TGF-β's role in cancer progression and bone metastases, while highlighting current perspectives on the therapeutic potential of targeting TGF-β pathways.
    MeSH term(s) Bone Neoplasms ; Bone and Bones ; Epithelial-Mesenchymal Transition ; Humans ; Transforming Growth Factor beta
    Chemical Substances Transforming Growth Factor beta
    Language English
    Publishing date 2021-11-06
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom11111643
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  8. Article ; Online: Breast cancer bone metastases: it's all about the neighborhood.

    Guise, Theresa A

    Cell

    2013  Volume 154, Issue 5, Page(s) 957–959

    Abstract: In order to establish themselves in distal sites, metastatic cancer cells need to acquire organ-specific traits. Zhang et al. provide evidence in breast cancer that a tumor cell's acquisition of properties for successful bone metastasis is influenced by ... ...

    Abstract In order to establish themselves in distal sites, metastatic cancer cells need to acquire organ-specific traits. Zhang et al. provide evidence in breast cancer that a tumor cell's acquisition of properties for successful bone metastasis is influenced by signals from the stroma of the primary tumor.
    MeSH term(s) Animals ; Bone Neoplasms/secondary ; Breast Neoplasms/pathology ; Humans ; Neoplasm Metastasis ; Signal Transduction
    Language English
    Publishing date 2013-08-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2013.08.020
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    Zs.A 1167: Show issues Location:
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    Zs.MG 58: Show issues

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  9. Article ; Online: Molecular and clinical effects of aromatase inhibitor therapy on skeletal muscle function in early-stage breast cancer.

    Seibert, Tara A / Shi, Lei / Althouse, Sandra / Hoffman, Richard / Schneider, Bryan P / Russ, Kristen A / Altherr, Cody A / Warden, Stuart J / Guise, Theresa A / Coggan, Andrew R / Ballinger, Tarah J

    Scientific reports

    2024  Volume 14, Issue 1, Page(s) 1029

    Abstract: We evaluated biochemical changes in skeletal muscle of women with breast cancer initiating aromatase inhibitors (AI), including oxidation of ryanodine receptor RyR1 and loss of stabilizing protein calstabin1, and detailed measures of muscle function. ... ...

    Abstract We evaluated biochemical changes in skeletal muscle of women with breast cancer initiating aromatase inhibitors (AI), including oxidation of ryanodine receptor RyR1 and loss of stabilizing protein calstabin1, and detailed measures of muscle function. Fifteen postmenopausal women with stage I-III breast cancer planning to initiate AI enrolled. Quadriceps muscle biopsy, dual-energy x-ray absorptiometry, isokinetic dynamometry, Short Physical Performance Battery, grip strength, 6-min walk, patient-reported outcomes, and serologic measures of bone turnover were assessed before and after 6 months of AI. Post-AI exposure, oxidation of RyR1 significantly increased (0.23 ± 0.37 vs. 0.88 ± 0.80, p < 0.001) and RyR1-bound calstabin1 significantly decreased (1.69 ± 1.53 vs. 0.74 ± 0.85, p < 0.001), consistent with dysfunctional calcium channels in skeletal muscle. Grip strength significantly decreased at 6 months. No significant differences were seen in isokinetic dynamometry measures of muscle contractility, fatigue resistance, or muscle recovery post-AI exposure. However, there was significant correlation between oxidation of RyR1 with muscle power (r = 0.60, p = 0.02) and muscle fatigue (r = 0.57, p = 0.03). Estrogen deprivation therapy for breast cancer resulted in maladaptive changes in skeletal muscle, consistent with the biochemical signature of dysfunctional RyR1 calcium channels. Future studies will evaluate longer trajectories of muscle function change and include other high bone turnover states, such as bone metastases.
    MeSH term(s) Female ; Humans ; Ryanodine Receptor Calcium Release Channel ; Aromatase Inhibitors/pharmacology ; Aromatase Inhibitors/therapeutic use ; Breast Neoplasms/drug therapy ; Muscle, Skeletal ; Walking
    Chemical Substances Ryanodine Receptor Calcium Release Channel ; Aromatase Inhibitors
    Language English
    Publishing date 2024-01-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-024-51751-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Breaking Down Barriers to Chemoresistance: Role of Chemotherapy-Induced Osteoblastic Jagged1.

    Mohammad, Khalid S / Guise, Theresa A

    Cancer cell

    2017  Volume 32, Issue 6, Page(s) 717–718

    Abstract: Bone metastases are incurable. The bone microenvironment has always been a suspect for this clinical enigma, but the exact mechanisms have been unclear. In this issue of Cancer Cell, Zheng and colleagues provide evidence that chemotherapy itself induces ... ...

    Abstract Bone metastases are incurable. The bone microenvironment has always been a suspect for this clinical enigma, but the exact mechanisms have been unclear. In this issue of Cancer Cell, Zheng and colleagues provide evidence that chemotherapy itself induces chemoresistance of bone metastases, mediated by osteoblast Jagged1-induced tumor Notch signaling.
    MeSH term(s) Antineoplastic Agents ; Bone Neoplasms ; Drug Resistance, Neoplasm/drug effects ; Humans ; Jagged-1 Protein ; Osteoblasts ; Receptors, Notch ; Tumor Microenvironment/drug effects
    Chemical Substances Antineoplastic Agents ; Jagged-1 Protein ; Receptors, Notch
    Language English
    Publishing date 2017-12-12
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2017.11.016
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    Zs.MG 104: Show issues

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