Effects of tyrosine kinase inhibition on bone metabolism: untargeted consequences of targeted therapies

Alemán, José O.; Farooki, Azeez; Girotra, Monica

doi:10.1530/erc-12-0400

Cited by 64 publications

(40 citation statements)

References 62 publications

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“…In particular, Sorafenib, Sunitinib, Vandetanib and Cabozantinib have been reported to prevent OB differentiation in vitro, as well as the production of RANKL, an essential factor for OC activation. Dasatinib, another BCR-ABL inhibitor, also inhibits Rous sarcoma (Src) kinase that is involved in OC differentiation and bone resorption [75].…”

Section: Targeted Therapymentioning

confidence: 99%

Cancer treatment-induced bone loss (CTIBL): Pathogenesis and clinical implications

D’Oronzo

Stucci

Tucci

et al. 2015

Cancer Treatment Reviews

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Section: Targeted Therapymentioning

confidence: 99%

Cancer treatment-induced bone loss (CTIBL): Pathogenesis and clinical implications

D’Oronzo

Stucci

Tucci

et al. 2015

Cancer Treatment Reviews

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“…Tyrosine kinase inhibitors, the newest cancer-targeting agents, have off-target class effects on cells of the osteoclast and/or osteoblast lineage, which results in a bone-sparing effect 95 . Mast/stem cell growth factor receptor Kit (commonly known as proto-oncogene c-KIT), platelet-derived growth factor receptor α (PDGFR-α) and PDGFR-β, macrophage colony-stimulating factor 1 receptor (commonly known as M-CSF-R), proto-oncogene tyrosine-protein kinase Src (commonly known as SRC) and rearranged during transfection (RET) induce osteoclastogenesis when stimulated by their respective ligands 95 .…”

Section: Managing Skeletal Complications Of Cancermentioning

confidence: 99%

The best of both worlds — managing the cancer, saving the bone

et al. 2015

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In the context of breast cancer, the importance of the skeleton in the regulation of primary tumour development and as a site for subsequent metastasis is well characterized. Our understanding of the contributions made by the host bone and bone marrow cells increasingly demonstrates the extent of the interaction between tumour cells and normal host cells. As a result, the need to develop and utilize therapies that can impede the growth and/or function of tumour cells while sparing normal host bone and bone marrow cells is immense and expanding. The need for these new treatments is, however, superimposed on the orthopaedic management of patients’ quality of life, where pain control and continued locomotion are paramount. Indeed, the majority of the anticancer therapies used to date often result in direct or indirect damage to bone. Thus, although the bone microenvironment regulates tumour cell growth in bone, cells within the bone marrow niche also mediate many of the orthopaedic consequences of tumour progression as well as resistance to the antitumour effects of existing therapies. In this Review, we highlight the effects of existing cancer treatments on bone and the bone marrow microenvironment as well as the mechanisms mediating these effects and the current utility of modern orthopaedic interventions.

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“…Hypophosphatemia is often accompanied by increased phosphaturia, low to normal levels of calcium, secondary hyperparathyroidism, and biphasic modifications of markers of bone formation and resorption [59,60]. In imatinib-treated adult patients, bone mineral density remains stable or slightly increases over time [60,61]. Growth retardation has been described in prepubertal patients receiving imatinib or dasatinib, but this effect occurs through TKI-induced disturbances in the growth hormone/insulin-like growth factor-1 axis [62].…”

Section: Metabolic and Endocrine Side Effectsmentioning

confidence: 99%

Management of adverse events associated with tyrosine kinase inhibitors in chronic myeloid leukemia

Réa

2015

Ann Hematol

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Tyrosine kinase inhibitors (TKIs) targeting the breakpoint cluster region-Abelson 1 (BCR-ABL1) oncoprotein represent an outstanding progress in chronic myeloid leukemia (CML), and long-term survival has become a reality. However, the majority of patients need to be treated during their entire life span; thus, outcome does not solely depend on treatment efficacy but also on how well therapy is tolerated. TKIs have an overall favorable safety profile in clinical practice. Although many patients may encounter adverse events, these usually occur early after treatment initiation, are mild to moderate in intensity and resolve spontaneously, or are easily controlled with adequate supportive care. Whenever treatment interruption is necessary, re-exposition to the same TKI or switch to an alternative TKI is successful in the majority of the cases. However, long-term safety issues have not been fully elucidated at present, especially for new-generation TKIs. Recent evidence has emerged that these new agents may sometimes impinge on vital organs such as the heart and lung in an irreversible fashion especially when comorbidities are present; thus, decision regarding of which TKI should be used must take into account disease-related, TKI-related, and patient-related variables. The purpose of this article is to provide an up-to-date review of common adverse events associated with TKIs and how these events may be optimally managed.

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Effects of tyrosine kinase inhibition on bone metabolism: untargeted consequences of targeted therapies

Cited by 64 publications

References 62 publications

Cancer treatment-induced bone loss (CTIBL): Pathogenesis and clinical implications

Cancer treatment-induced bone loss (CTIBL): Pathogenesis and clinical implications

The best of both worlds — managing the cancer, saving the bone

Management of adverse events associated with tyrosine kinase inhibitors in chronic myeloid leukemia

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