Tumor lysis syndrome after starting treatment with Gleevec in a patient with chronic myelogenous leukemia

Al‐Kali, Aref; Farooq, Saba; Tfayli, Arafat

doi:10.1111/j.1365-2710.2009.01035.x

Cited by 28 publications

(19 citation statements)

References 6 publications

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“…Although tumor lysis in highly treatment‐responsive malignancies can be associated with acute kidney injury, we found no correlation between the percentage of tumor shrinkage as per RECIST and the amount of change in the eGFR at the closest time point to the radiographic assessment (r, −0.052; P = .798) (Fig. 4) . Within a subgroup of patients in whom we could capture eGFR changes both on crizotinib and after a period of time after therapy with crizotinib but before the introduction of any other systemic anticancer therapy, we were able to isolate the effect of crizotinib separate from exposure to other potential nephrotoxic agents including NSAIDs, diuretics, and iv contrast from imaging studies (Table 4).…”

Section: Discussionmentioning

confidence: 86%

Drug‐induced reduction in estimated glomerular filtration rate in patients with ALK‐positive non‐small cell lung cancer treated with the ALK inhibitor crizotinib

Brosnan

Weickhardt

et al. 2013

Cancer

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Background Renal side effects of crizotinib have not been investigated previously. Methods Estimated Glomerular Filtration Rate (eGFR) was calculated using the CKD-EPI creatinine-based prediction equation during the first 12 weeks of crizotinib and post-crizotinib prior to the introduction of any further systemic therapy. Results 38 stage IV ALK+ NSCLC patients treated with crizotinib were identified. Mean eGFR fell 23.9% compared to baseline (p<0.0001, 95%CI: 21.3% - 26.6%), with most of the fall occurring within the first 2 weeks of therapy. Clinical history and BUN/creatinine ratios did not suggest prerenal causes. The objective response rate among evaluable patients (n=27) was 41%. Tumor shrinkage was not correlated with changes in eGFR (r = -0.052 (p=0.798)). Among 16 patients with post-crizotinib data, recovery to within 84% of baseline eGFR occurred in all patients. After adjusting for the number of scans with IV contrast and use of known nephrotoxic drugs, whether a patient was on or off crizotinib was significantly associated with changes in eGFR (p<0.0001). Conclusions Assessed by the CKI-EPI prediction equation, eGFR is reduced by crizotinib but most patients will recover their eGFR after cessation of therapy. The early onset, size of change, minimal cumulative effect and rapid reversibility raise the possibility that this may be a pharmacological and/or tubular creatinine secretion effect rather than a direct nephrotoxic effect. Increased vigilance with regard to the concomitant use of renally cleared medications or nephrotoxic agents should be considered for patients receiving crizotinib and, when eGFR is reduced, additional renal investigations undertaken.

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Section: Discussionmentioning

confidence: 86%

Drug‐induced reduction in estimated glomerular filtration rate in patients with ALK‐positive non‐small cell lung cancer treated with the ALK inhibitor crizotinib

Brosnan

Weickhardt

et al. 2013

Cancer

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“…Intriguingly, the 421C>A SNP of ABCG2/BCRP may have another effect on tumor lysis syndrome with hyperuricemia during TKI-based molecular-targeted therapy. Several studies have reported renal failure and tumor lysis syndrome during TKI-based molecular-targeted therapies, including with sorafenib for hepatocellular carcinoma, with imatinib for chronic myelogenous leukemia, and with flavopiridol for chronic lymphocytic leukemia 138–141. Because the Q141K variant of ABCG2/BCRP corresponding to SNP 421C>A reduces uric acid transport68 and those TKIs are substrates/inhibitors of ABCG2/BCRP, TKI therapy in patients with the SNP 421C>A (Q141K) may be at higher risk of tumor lysis syndrome 5…”

Section: Pharmacological Interaction Of Abcg2/bcrp With Molecular-tarmentioning

confidence: 99%

Human ABC transporter ABCG2/BCRP expression in chemoresistance: basic and clinical perspectives for molecular cancer therapeutics

Noguchi¹,

Katayama²,

Sugimoto³

2014

PGPM

130

111

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Adenine triphosphate (ATP)-binding cassette (ABC) transporter proteins, such as ABCB1/P-glycoprotein (P-gp) and ABCG2/breast cancer resistance protein (BCRP), transport various structurally unrelated compounds out of cells. ABCG2/BCRP is referred to as a “half-type” ABC transporter, functioning as a homodimer, and transports anticancer agents such as irinotecan, 7-ethyl-10-hydroxycamptothecin (SN-38), gefitinib, imatinib, methotrexate, and mitoxantrone from cells. The expression of ABCG2/BCRP can confer a multidrug-resistant phenotype on cancer cells and affect drug absorption, distribution, metabolism, and excretion in normal tissues, thus modulating the in vivo efficacy of chemotherapeutic agents. Clarification of the substrate preferences and structural relationships of ABCG2/BCRP is essential for our understanding of the molecular mechanisms underlying its effects in vivo during chemotherapy. Its single-nucleotide polymorphisms are also involved in determining the efficacy of chemotherapeutics, and those that reduce the functional activity of ABCG2/BCRP might be associated with unexpected adverse effects from normal doses of anticancer drugs that are ABCG2/BCRP substrates. Importantly, many recently developed molecular-targeted cancer drugs, such as the tyrosine kinase inhisbitors, imatinib mesylate, gefitinib, and others, can also interact with ABCG2/BCRP. Both functional single-nucleotide polymorphisms and inhibitory agents of ABCG2/BCRP modulate the in vivo pharmacokinetics and pharmacodynamics of these molecular cancer treatments, so the pharmacogenetics of ABCG2/BCRP is an important consideration in the application of molecular-targeted chemotherapies.

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“…Indeed, it is striking to note the number of case reports in the literature of tumor lysis syndrome in the context of diseases or drugs not conventionally thought associated with this complication – sorafenib in hepatocellular carcinoma, imatinib in chronic myelogenous leukemia, flavopiridol in chronic lymphocytic leukemia 98–101 . Given that these compounds are all substrates of ABCG2, and inhibitors at higher concentrations, it is tempting to speculate that these isolated cases occur in patients with the Q141K SNP.…”

Section: Clinically Important Normal Tissue Expressionmentioning

confidence: 99%

The Challenge of Exploiting ABCG2 in the Clinic

Robey

Ieranò

Zhan

et al. 2011

CPB

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ABCG2, or breast cancer resistance protein (BCRP), is an ATP-binding cassette half transporter that has been shown to transport a wide range of substrates including chemotherapeutics, antivirals, antibiotics and flavonoids. Given its wide range of substrates, much work has been dedicated to developing ABCG2 as a clinical target. But where can we intervene clinically and how can we avoid the mistakes made in past clinical trials targeting P-glycoprotein? This review will summarize the normal tissue distribution, cancer tissue expression, substrates and inhibitors of ABCG2, and highlight the challenges presented in exploiting ABCG2 in the clinic. We discuss the possibility of inhibiting ABCG2, so as to increase oral bioavailability or increase drug penetration into sanctuary sites, especially the central nervous system; and at the other end of the spectrum, the possibility of improving ABCG2 function, in the case of gout caused by a single nucleotide polymphism. Together, these aspects of ABCG2/BCRP make the protein a target of continuing interest for oncologists, biologists, and pharmacologists.

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Tumor lysis syndrome after starting treatment with Gleevec in a patient with chronic myelogenous leukemia

Cited by 28 publications

References 6 publications

Drug‐induced reduction in estimated glomerular filtration rate in patients with ALK‐positive non‐small cell lung cancer treated with the ALK inhibitor crizotinib

Drug‐induced reduction in estimated glomerular filtration rate in patients with ALK‐positive non‐small cell lung cancer treated with the ALK inhibitor crizotinib

Human ABC transporter ABCG2/BCRP expression in chemoresistance: basic and clinical perspectives for molecular cancer therapeutics

The Challenge of Exploiting ABCG2 in the Clinic

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