scholarly journals Pneumothorax during Pazopanib Treatment in Patients with Soft-Tissue Sarcoma: Two Case Reports and a Review of the Literature

2017 ◽  
Vol 10 (1) ◽  
pp. 333-338 ◽  
Author(s):  
Yoshiro Nakahara ◽  
Tomoya Fukui ◽  
Ken Katono ◽  
Yuuki Nishizawa ◽  
Yusuke Okuma ◽  
...  
Keyword(s):  
Soft Tissue ◽  
Soft Tissue Sarcoma ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Lung Metastases ◽  
Case Reports ◽  
Single Agent ◽  
Review Of The Literature ◽  
Advanced Soft Tissue Sarcoma

Pazopanib, a multitargeting tyrosine kinase inhibitor, has single-agent activity in patients with advanced soft-tissue sarcoma. Herein, we describe 2 cases of pneumothorax that occurred during pazopanib treatment in patients with soft-tissue sarcoma. These 2 patients had multiple lung metastases. According to previous reports and our past experience, the risk of pneumothorax may be higher in patients with multiple lung metastases. Although a causal relationship is uncertain, the risk of pneumothorax when prescribing pazopanib for these patients should be considered.

Clinical outcomes and toxicities of pazopanib administered orally in crushed form: Case reports and review of the literature

2019 ◽  
Vol 26 (1) ◽  
pp. 232-235 ◽  
Author(s):  
Jill Stein ◽  
Mohammed Milhem ◽  
Daniel Vaena
Keyword(s):  
Renal Cell Carcinoma ◽  
Soft Tissue ◽  
Soft Tissue Sarcoma ◽  
Kinase Inhibitor ◽  
Case Reports ◽  
Clinical Activity ◽  
Review Of The Literature ◽  
Advanced Soft Tissue Sarcoma ◽  
Feeding Tubes ◽  
Tumor Types

Cancer treatment has changed dramatically with the development of oral targeted therapies. Pazopanib, an oral VEGF tyrosine kinase inhibitor, is currently approved for advanced renal cell carcinoma, advanced soft tissue sarcoma, and is being studied for various tumor types. Due to the potential of increased exposure to pazopanib when crushed, pazopanib should be given as an intact whole tablet. Thus, in patients with difficulty swallowing medications or feeding tubes, pazopanib is usually not considered to be an option. Here, we describe two cases which show the administration of crushed pazopanib was feasible and had apparent clinical activity.

Efficacy of STI571, an Abl tyrosine kinase inhibitor, in conjunction with other antileukemic agents against Bcr-Abl–positive cells

Blood ◽  
2000 ◽  
Vol 96 (9) ◽  
pp. 3195-3199 ◽  
Author(s):  
J. Tyler Thiesing ◽  
Sayuri Ohno-Jones ◽  
Kathryn S. Kolibaba ◽  
Brian J. Druker
Keyword(s):  
Clinical Trials ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Kinase Inhibitor ◽  
Single Agent ◽  
Myelogenous Leukemia ◽  
Hematopoietic Stem ◽  
Abl Tyrosine Kinase ◽  
Abl Tyrosine Kinase Inhibitor

Abstract Chronic myelogenous leukemia (CML), a malignancy of a hematopoietic stem cell, is caused by the Bcr-Abl tyrosine kinase. STI571(formerly CGP 57148B), an Abl tyrosine kinase inhibitor, has specific in vitro antileukemic activity against Bcr-Abl–positive cells and is currently in Phase II clinical trials. As it is likely that resistance to a single agent would be observed, combinations of STI571 with other antileukemic agents have been evaluated for activity against Bcr-Abl–positive cell lines and in colony-forming assays in vitro. The specific antileukemic agents tested included several agents currently used for the treatment of CML: interferon-alpha (IFN), hydroxyurea (HU), daunorubicin (DNR), and cytosine arabinoside (Ara-C). In proliferation assays that use Bcr-Abl–expressing cells lines, the combination of STI571 with IFN, DNR, and Ara-C showed additive or synergistic effects, whereas the combination of STI571 and HU demonstrated antagonistic effects. However, in colony-forming assays that use CML patient samples, all combinations showed increased antiproliferative effects as compared with STI571 alone. These data indicate that combinations of STI571 with IFN, DNR, or Ara-C may be more useful than STI571 alone in the treatment of CML and suggest consideration of clinical trials of these combinations.

scholarly journals Atypical Posterior Reversible Encephalopathy Syndrome due to Oral Tyrosine Kinase Inhibitor Cabozantinib: First Case Report

2020 ◽  
Vol 13 (2) ◽  
pp. 1013-1019 ◽  
Author(s):  
Anannya Patwari ◽  
Vineel Bhatlapenumarthi ◽  
Sheila K. Pascual
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
Kinase Inhibitor ◽  
Case Reports ◽  
Cell Cancer ◽  
Mri Findings ◽  
Posterior Reversible Encephalopathy ◽  
First Case ◽  
Reversible Encephalopathy

We report here a rare case of atypical posterior reversible encephalopathy syndrome (PRES) due to oral tyrosine kinase inhibitor cabozantinib. No case reports of such have been found in our literature search. The patient, a 70-year-old female with metastatic renal cell cancer on oral tyrosine kinase inhibitor cabozantinib, was brought into the emergency room because of confusion and seizures, found to have elevated blood pressure and atypical MRI findings consistent with PRES due to cabozantinib.

A phase I trial of doxorubicin and flavopiridol in soft tissue sarcoma

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 9523-9523 ◽  
Author(s):  
D. R. D’Adamo ◽  
K. Scheu ◽  
S. Singer ◽  
G. K. Schwartz ◽  
R. G. Maki
Keyword(s):  
Soft Tissue ◽  
Soft Tissue Sarcoma ◽  
Phase I ◽  
Stable Disease ◽  
Kinase Inhibitor ◽  
Single Agent ◽  
Xenograft Model ◽  
Fixed Dose ◽  
Preclinical Model ◽  
Combination Methods

9523 Background: Flavopiridol, a potent cyclin dependent kinase inhibitor, has been shown in vitro to enhance doxorubicin induced apoptosis. Using the BWH dediffentiated liposarcoma xenograft model we have shown that sequential therapy with doxorubicin (D) followed 1 hour later by flavopiridol (F) is superior to doxorubicin alone (p=0.006). Single agent flavopiridol was also active in this xenograft model, but less so than the combination. Methods: We have commenced an ongoing phase I study of the combination of D and F on the basis of this preclinical data in soft tissue sarcoma with fixed dose D (60 mg/m2), followed 1 hour later by escalating doses of F (40–70 mg/m2) administered over one hour, every 3 weeks. Standard phase I eligibility criteria apply. No prior anthracycline therapy is allowed. At 300 mg/m2 D, dexrazoxane is added to D F. Patients with responsive or stable disease after cumulative D dose of 600mg/m2 can receive single agent flavopiridol. Results: Median characteristics of 7 evaluable patients: age 52 (31–65), KPS 80% (70–90), 3 males / 4 females, 0 prior regimens (range 0–2). The combination has been well-tolerated, with no dose limiting toxicity (DLT) yet. There has been 1 grade 3 bleed in the setting of progressive disease and 1 grade 4 neutropenia without fever. Grade 1 and 2 diarrhea, related to flavopiridol have been observed. Pharmacokinetic (PK) studies are ongoing. We have observed no partial responses (PR). Prolonged stable disease (SD) has been seen in 3 patients for 6, 6 and 11 months. Two patients with SD have liposarcoma. One patient with liposarcoma continues on single agent flavopiridol with stable disease after having reached the prescribed limit of D of 600 mg/m2. Conclusions: The combination of doxorubicin and flavopiridol is safe, with no unexpected toxicities. Disease stabilization in STS has been observed. This appears to be an encouraging combination in liposarcoma and is consistent with our preclinical model. Flavopiridol dose escalation is continuing. No significant financial relationships to disclose.

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