Virtual Library

Start Your Search

Angela Tiganas



Author of

  • +

    EP1.14 - Targeted Therapy (ID 204)

    • Event: WCLC 2019
    • Type: E-Poster Viewing in the Exhibit Hall
    • Track: Targeted Therapy
    • Presentations: 1
    • Now Available
    • Moderators:
    • Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
    • +

      EP1.14-27 - Retroperitoneal Pseudotumor Induced by Crizotinib Treatment for CMET ex14 Skip Mutation NCSLC (Now Available) (ID 292)

      08:00 - 18:00  |  Author(s): Angela Tiganas

      • Abstract
      • Slides

      Background

      MET-exon-14-skipping(METex14) mutations have been described in 0.6-7% of non-small-cell-lung-carcinomas(NSCLC). METex14 enhance MET receptor pathway signalling through increasing MET protein stability. Patients with NSCLC harboring METex14 mutations may respond to MET tyrosine-kinase-inhibitors(TKI) such as crizotinib. A.E. Drilon et al presented in the Profile-1001 study that crizotinib also demonstrated clinical activity in NSCLC with MET amplification and further data were associated with METex14 skip mutation.

      Method

      A 63-year-old, non-smoking, female presented with right-upper-lobe (RUL) mass, Lymphangitis spread and bilateral mediastinal nodal involvement (figure 1). Lung adenocarcinoma (TTF1(+), PDL>20%) was diagnosed. The patient refused radiation nor chemo-therapy and therefore treated by pembrolizumab (KeyNote-042). Upon the presence of CMET ex 14 skip mutation detected on ctDNA (Gaurdnat360TM), crizotinib was started with a significant response that allowed a RUL lobectomy with free surgical margins (R0), 4 months later (pT1aN0M0). Following the surgery, she has continued crizotinib therapy and a retroperitoneal pseudotumor was seen on the 9th months post-surgery (figure 2). Needle biopsy indicated a fibrocollagenous tissue, bundles of striated muscle and mixed acute and chronic inflammation without malignant cells. Considering the pathological report, a cyst drainage was performed (figure 3) and crizotinib treatment continued in a lower dose of 250 mg X 1 with no evidence of disease until this report.

      Result

      Crizotinib has been shown to act clinically as a targeted selective inhibitor of ALK activity in NSCLC. It is a multi-kinase inhibitor of c-MET and ROS1 oncogenic tyrosine kinase. C-MET receptors are normally present in renal tubular epithelium. Previous publications have described complex renal cyst development as a side effect of crizotinib treatment[iv] [v]. It is not clear yet whether its target of c-MET may explain the crizotinib relation to pseudotumors and renal cysts development. Therefor cases of renal cysts should be registered and reported as rare side effects of crizotinib treatment.

      Conclusion

      "Section not applicable"

      figure 1.jpg

      figure 2.jpg

      Only Active Members that have purchased this event or have registered via an access code will be able to view this content. To view this presentation, please login or select "Add to Cart" and proceed to checkout.