Inhibition of collagen-induced discoidin domain receptor 1 and 2 activation by imatinib, nilotinib and dasatinib

Day, Elizabeth; Waters, Beatrice; Spiegel, Katrin; Alnadaf, Tanja; Manley, Paul W.; Buchdunger, Elisabeth; Walker, Christoph; Járai, Gábor

doi:10.1016/j.ejphar.2008.10.014

Cited by 242 publications

(230 citation statements)

References 31 publications

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“…However, other kinase targets may preferentially be recognized by nilotinib [19,20]. One of the more interesting kinase-targets in terms of vascular cells and events is the discoidin domain receptor 1 (DDR1) [20,29]. This receptor has recently been implicated in plaque formation in artherosclerosis [30][31][32].…”

Section: Other Severe Non-hematologic Events Observed During Nilotinibmentioning

confidence: 99%

Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML

et al. 2011

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The second generation BCR/ABL kinase inhibitor nilotinib is increasingly used for the treatment of imatinib‐resistant chronic myeloid leukemia (CML). So far, nilotinib is considered a well‐tolerated drug with little if any side effects, although an increase in the fasting glucose level has been reported. We examined a series of 24 consecutive CML patients treated with nilotinib in our center for the development of non‐hematologic adverse events. Three of these 24 CML patients developed a rapidly progressive peripheral arterial occlusive disease (PAOD) during treatment with nilotinib. In all three cases, PAOD required repeated angioplasty and/or multiple surgeries within a few months. No PAOD was known before nilotinib‐therapy in these patients, although all three had received imatinib. In two patients, pre‐existing risk factors predisposing for PAOD were known, and one of them had developed diabetes mellitus during nilotinib. In the other 21 patients treated with nilotinib in our center, one less severe PAOD, one myocardial infarction, one spinal infarction, one subdural hematoma, and one sudden death of unknown etiology were recorded. In summary, treatment with nilotinib may be associated with an increased risk of vascular adverse events, including PAOD development. In a subgroup of patients, these events are severe or even life‐threatening. Although the exact mechanisms remain unknown, we recommend screening for pre‐existing PAOD and for vascular risk factors such as diabetes mellitus in all patients before starting nilotinib and in the follow up during nilotinib‐therapy. Am. J. Hematol. 2011. © 2011 Wiley‐Liss, Inc.

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Section: Other Severe Non-hematologic Events Observed During Nilotinibmentioning

confidence: 99%

Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML

et al. 2011

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“…8 In the kidney, DDRs are widely expressed in cells such as epithelia, fibroblasts, vascular smooth muscle cells, and mesangial cells. 50 DDRs are potent mediators of inflammation and fibrosis, and DDR1 null mice have reduced collagen accumulation and infiltrating inflammatory cells in both angiotensin II-induced renal injury and the UUO model of fibrosis.…”

Section: Ddrmentioning

confidence: 99%

“…51 Imatinib inhibits DDRs in vitro, and this effect probably plays a role in imatinib's attenuation of fibrosis and inflammation observed in murine models of kidney disease. 8 …”

Section: Ddrmentioning

confidence: 99%

Imatinib

Wallace

Gewin

2013

Journal of the American Society of Nephrology

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The treatments for many autoimmune diseases are limited in efficacy, and long-term use is associated with severe adverse events. The tyrosine kinase inhibitors have proven to be well tolerated for long treatment periods, with minimal adverse events, in the oncology population. These agents have recently been used to treat autoimmune diseases. We review the potential mechanisms whereby tyrosine kinase inhibitors may modulate the immune response and inhibit fibrogenesis and discuss the current evidence for their use in the treatment of autoimmune diseases of the kidney.

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“…While DDR2 has not been regarded as a main target of drug research, a recent report suggests that ABL kinase suppressors suppress DDR2, including imatinib, nilotinib, and dasatinib [31]. In addition, dasatinib can inhibit proliferation of lung tumor cells with DDR2 mutations.…”

Section: Ddr2 Mutationsmentioning

confidence: 99%

The development of potential targets in the treatment of non-small cell lung cancer

Zhang

Lin

2016

Open Life Sciences

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The oncogenic driver mutations have been found that not only have potential sensitivity to epidermal growth factor receptor but also can inhibit anaplastic lymphoma kinase tyrosine kinase; more and more interest has been evoked in discovering additional targets to non-small cell lung cancer (NSCLC). Recently, many novel underlying oncogenic gene alterations have been identified, such as HER2 insertions, BRAF mutations, PIK3 mutations, FGFR1 amplifications, DDR2 mutations, KRAS mutations, MET amplification, ROS1 rearrangements, ALK rearrangements, and RET rearrangements. In this review, we will discuss the discovery of these potential targets and the application of each in NSCLC and of small molecular inhibitors on these potential targets.

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Inhibition of collagen-induced discoidin domain receptor 1 and 2 activation by imatinib, nilotinib and dasatinib

Cited by 242 publications

References 31 publications

Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML

Progressive peripheral arterial occlusive disease and other vascular events during nilotinib therapy in CML

Imatinib

The development of potential targets in the treatment of non-small cell lung cancer

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