Gefitinib, but Not Erlotinib, is a Possible Inducer of Fra-1-mediated Interstitial Lung Disease

Takada, Yasunari; Matsuo, Koichi

doi:10.2302/kjm.2011-0009-oa

Cited by 6 publications

(4 citation statements)

References 24 publications

(35 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…20 Off-target effect of gefitinib causing lung injury by Fra-1-related pathway is not shared by erlotinib, despite being the same class of drug. 21 As a result, erlotinib can be used in patients with gefitinib-induced lung injury, as was done successfully in our case. 22,23 TBLB can establish the pathology in focal and diffuse parenchymal lung diseases as was seen in our cases.…”

Section: Discussionsupporting

confidence: 58%

Chemotherapy-Associated Pulmonary Toxicity—Case Series from a Single Center

Tilak

Handa

Kumar

et al. 2021

South Asian J Cancer

View full text Add to dashboard Cite

Background Pulmonary toxicity due to chemotherapeutic agents can occur with many established and new drugs. Strong clinical suspicion is important as the clinical presentation is usually with nonspecific symptoms like cough, dyspnea, fever, and pulmonary infiltrates. Timely discontinuation of the offending agent alone can improve the condition. Methods A prospective observational study on patients receiving chemotherapy at an 800-bedded tertiary care hospital was performed from 2014 to 2016. Consecutive patients on chemotherapy, presenting with nonresolving respiratory symptoms were evaluated with contrast-enhanced computerized tomography of chest, diffusion lung capacity for carbon monoxide (DLCO), fiberoptic bronchoscopy with lavage, and biopsy, after excluding all causes for pulmonary infections. Descriptive data has been depicted. Results A total of 18 patients were evaluated for persistent symptoms of dry cough, dyspnea, and fever among 624 who received chemotherapy during the study period. Ground-glass opacities on high-resolution CT was the most common imaging finding, others being patchy subpleural consolidation and pleural effusion. Lymphocyte-predominant bronchoalveolar lavage was detected in nine. Eight of the 15 patients who underwent DLCO, had abnormal results. Seven had significant histopathological findings on bronchoscopic lung biopsy, which revealed organizing pneumonia as the most common pattern. Paclitaxel, fluorouracil, gemcitabine, and tyrosine kinase inhibitors were the common culprit drugs. Discontinuation alone of the culprit drug was effective in 15 and 3 needed oral corticosteroids for relief of symptoms. None of the patients died due to the toxicity. Conclusion An incidence of 2.8% for chemotherapy-induced lung injury was seen in our observational study of 3 years, with parenchymal, interstitial, and pleural involvement due to various chemotherapeutic agents. Oral steroids maybe required in a subset of patients not responding to discontinuation of the culprit agent.

show abstract

Section: Discussionsupporting

confidence: 58%

Chemotherapy-Associated Pulmonary Toxicity—Case Series from a Single Center

Tilak

Handa

Kumar

et al. 2021

South Asian J Cancer

View full text Add to dashboard Cite

show abstract

“…The utility of these inhibitors as tools to study the biology of GAK is severely limited. Notably, it has been proposed that GAK inhibition causes clinical toxicity due to pulmonary alveolar dysfunction, but this controversial hypothesis has not been addressed with a selective small molecule GAK inhibitor [16] .…”

Section: Introductionmentioning

confidence: 99%

Identification and Optimization of 4‐Anilinoquinolines as Inhibitors of Cyclin G Associated Kinase

et al. 2017

View full text Add to dashboard Cite

4-Anilinoquinolines were identified as potent and narrow-spectrum inhibitors of the cyclin G associated kinase (GAK), an important regulator of viral and bacterial entry into host cells. Optimization of the 4-anilino group and the 6,7-quinoline substituents produced GAK inhibitors with nanomolar activity, over 50 000-fold selectivity relative to other members of the numb-associated kinase (NAK) subfamily, and a compound (6,7-dimethoxy-N-(3,4,5-trimethoxyphenyl)quinolin-4-amine; 49) with a narrow-spectrum kinome profile. These compounds may be useful tools to explore the therapeutic potential of GAK in prevention of a broad range of infectious and systemic diseases.

show abstract

“…These drugs were designed as inhibitors of EGFR, and their utility as tools to study the biology of GAK is severely limited. Notably, it has been proposed that GAK inhibition causes clinical toxicity due to pulmonary alveolar dysfunction, but this controversial hypothesis has not been addressed with a selective small molecule GAK inhibitor (Tabara, Naito et al 2011, Takada and Matsuo 2012).…”

Section: Introductionmentioning

confidence: 99%

Identification and Optimization of 4-Anilinoquinolines as Inhibitors of Cyclin G Associated Kinase

Asquith¹,

Laitinen

Bennett

et al. 2017

Preprint

View full text Add to dashboard Cite

ABSTRACT4-Anilinoquinolines were identified as potent and narrow spectrum inhibitors of the cyclin G associated kinase (GAK), an important regulator of viral and bacterial entry into host cells. Optimization of the 4-anilino group and the 6,7-quinoline substituents produced GAK inhibitors with nanomolar activity and over 50,000-fold selectivity relative to other members of the numb-associated kinase (NAK) sub-family. These compounds may be useful tools to explore the therapeutic potential of GAK in prevention of a broad range of infectious diseases.

show abstract

Gefitinib, but Not Erlotinib, is a Possible Inducer of Fra-1-mediated Interstitial Lung Disease

Cited by 6 publications

References 24 publications

Chemotherapy-Associated Pulmonary Toxicity—Case Series from a Single Center

Chemotherapy-Associated Pulmonary Toxicity—Case Series from a Single Center

Identification and Optimization of 4‐Anilinoquinolines as Inhibitors of Cyclin G Associated Kinase

Identification and Optimization of 4-Anilinoquinolines as Inhibitors of Cyclin G Associated Kinase

Contact Info

Product

Resources

About