Outcome in advanced non-small cell lung cancer patients with successful rechallenge after recovery from epidermal growth factor receptor tyrosine kinase inhibitor-induced interstitial lung disease

Kashiwabara, Kosuke; Semba, Hiroshi; Fujii, Shigehiko; Tsumura, Shinsuke

doi:10.1007/s00280-017-3261-5

Cited by 27 publications

(34 citation statements)

References 23 publications

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“…Kashiwabara et al. reported five patients who refused to continue treatment using first EGFR‐TKI, but were subsequently rechallenged using a second EGFR‐TKI . Neither report examined the safety of the second EGFR‐TKI treatment and whether it provided a beneficial effect or not.…”

Section: Discussionmentioning

confidence: 99%

“…6,7 Although there are some case reports describing successful EGFR-TKI rechallenge after recovery from EGFR-TKI-induced AEs, few studies have examined first EGFR-TKI, but were subsequently rechallenged using a second EGFR-TKI. 9 Neither report examined the safety of the second EGFR-TKI treatment and whether it provided a beneficial effect or not. Thus, the present study builds on the experience of those researchers.…”

Section: Discussionmentioning

confidence: 99%

“…In clinical practice, one approach to this development is switching from one EGFR‐TKI to another. However, to the best of our knowledge, only a few case series have evaluated treatment response after switching EGFR‐TKIs because of AEs, rather than disease progression (PD) . Therefore, this retrospective study evaluated the efficacy and outcomes of switching EGFR‐TKIs because of AEs.…”

Section: Introductionmentioning

confidence: 99%

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The effects of switching EGFR‐TKI treatments for non‐small cell lung cancer because of adverse events

Sakata

Kawamura

Shingu

et al. 2018

Asia-Pac J Clncl Oncology

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Background Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR‐TKIs) are used to treat patients with non‐small cell lung cancer (NSCLC) and EGFR driver mutations. Although some patients discontinued these treatments because of adverse events, it is unclear whether switching EGFR‐TKI because of adverse events provides a benefit. Methods This retrospective study evaluated data from 22 patients with EGFR mutation‐positive NSCLC who received at least two EGFR‐TKIs that were switched because of adverse events (March 2011 to September 2017). Progression‐free survival 2 (PFS2) was defined as the time from starting of the first EGFR‐TKI treatment to disease progression during the second EGFR‐TKI treatment. Results Seventeen patients received gefitinib as the first EGFR‐TKI treatment, while four patients received afatinib and one patient received erlotinib. The median time to failure of the first EGFR‐TKI treatment was 1.6 months. The EGFR‐TKIs were switched because of hepatotoxicity (n = 16), interstitial lung disease (n = 3), and other reasons (n = 3). The median washout period was 1.1 months. Seventeen patients received erlotinib as the second EGFR‐TKI treatment, while three patients received gefitinib and two patients received afatinib. The median PFS for the second EGFR‐TKI treatment was 15.2 months. The median PFS2 was 17.7 months and the median overall survival was 32.8 months. Conclusions Switching EGFR‐TKIs because of adverse events provided a clinical benefit for patients with EGFR mutation‐positive NSCLC. Appropriate judgment regarding switching from one EGFR‐TKI to another may improve the performance status and prognosis of patients with EGFR mutation‐positive NSCLC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The effects of switching EGFR‐TKI treatments for non‐small cell lung cancer because of adverse events

Sakata

Kawamura

Shingu

et al. 2018

Asia-Pac J Clncl Oncology

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“…Ultérieurement, pourra se poser l'épineuse question de la réintroduction en l'absence d'alternative qui peut être vitale en cas de cancer ; dans certains cas, elle est possible sous une couverture éventuelle par corticoïdes [19].…”

Section: Quel Traitement ?unclassified

“…• l'arrêt d'un traitement présumé pneumotoxique par erreur peut être dramatique en cancérologie, en l'absence de traitement alternatif [19].…”

Section: Introductionunclassified

Toxicité pulmonaire des médicaments : ce que le réanimateur doit connaître ?

Parrot

Gibelin

Issoufaly

et al. 2018

Méd. Intensive Réa.

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Résumé Le diagnostic d'insuffisance respiratoire aiguë d'origine médicamenteuse est un véritable défi. Les traitements à l'origine d'une toxicité pulmonaire sont très nombreux. Les nouveaux traitements, notamment en oncohématologie (thé-rapie ciblée, immunothérapie), ne sont pas en reste. L'expression clinique très hétérogène est sous-tendue par des mécanis-mes lésionnels très différents. Après avoir écarté une infection ou un oedème pulmonaire, il faut savoir évoquer une pneumopathie médicamenteuse. La réalisation d'un scanner thoracique et d'une fibroscopie bronchique avec lavage bronchoalvéolaire peut être utile pour exclure une pathologie infectieuse et suggérer une pathologie médicamenteuse. Le traitement est l'arrêt du médicament et repose fréquemment dans ces formes graves sur une corticothérapie. Mots clés Détresse respiratoire · Pneumopathie médicamenteuse · Toxicité pulmonaireAbstract Acute respiratory failure related to drug toxicity is challenging. Several drugs, also including targeted therapy and immunotherapy, have been reported to induce lung toxicity. Clinical and pathological presentations are heterogeneous suggesting different toxicity pulmonary mechanisms. Infection or pulmonary edema should be ruled out, and then drug-induced pneumonitis diagnosis should be considered. CT scan and bronchoscopy with bronchoalveolar lavage are helpful for the disease diagnosis. Due to the severity, the identified drug should be stopped and more frequently steroids should be started.

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Inhibition of NF‐κB improves sensitivity to irradiation and EGFR‐TKIs and decreases irradiation‐induced lung toxicity

Wang

Peng

Zhang

et al. 2018

Intl Journal of Cancer

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Resistance to radiotherapy and to EGFR tyrosine kinase inhibitors (EGFR‐TKIs), as well as therapy‐related lung toxicity, are serious problems in the treatment of lung cancer. NF‐κB has been reported to be associated with radioresistance. Therefore, we evaluated its effects on sensitivity to irradiation and to EGFR‐TKIs; irradiation‐induced lung toxicity; and the effects of irradiation on sensitivity to EGFR‐TKIs. We used IKKβ inhibitor IMD 0354 or p65 depletion to explore their effects on sensitivity to irradiation and to EGFR‐TKIs in vitro and in vivo. We evaluated the efficacy of IMD 0354 in a radiation‐induced pulmonary‐fibrosis mouse model. Irradiation enhanced activation and expression of MET and therefore suppressed the sensitivity of lung cancer cells to irradiation or EGFR‐TKIs. Inhibition of NF‐κB by IMD 0354 or by p65 depletion reversed irradiation‐induced MET activation and increased the sensitivity of lung cancer cells to irradiation, to EGFR‐TKIs and to the combination thereof in vitro and in vivo. In addition, IMD 0354 significantly reduced lung toxicity in a murine model of irradiation‐induced pneumonia and lung fibrosis. These findings indicated that NF‐κB inhibition can improve sensitivity to irradiation and to EGFR‐TKIs and can decrease irradiation‐induced lung toxicity in lung cancer.

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Outcome in advanced non-small cell lung cancer patients with successful rechallenge after recovery from epidermal growth factor receptor tyrosine kinase inhibitor-induced interstitial lung disease

Abstract: EGFR-TKI rechallenge with concurrent prednisolone therapy might be salvage therapy in advanced NSCLC patients with active EGFR mutations after recovery from EGFR-TKI-induced ILD.

Cited by 27 publications

References 23 publications

The effects of switching EGFR‐TKI treatments for non‐small cell lung cancer because of adverse events

The effects of switching EGFR‐TKI treatments for non‐small cell lung cancer because of adverse events

Toxicité pulmonaire des médicaments : ce que le réanimateur doit connaître ?

Inhibition of NF‐κB improves sensitivity to irradiation and EGFR‐TKIs and decreases irradiation‐induced lung toxicity

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