Appointment sheet
MET exon 14 and MET-amplified non-small-cell lung cancer
Prepared with OnCo (onco.cc/prep/met-altered-nsclc/). Orientation, not medical advice; your team knows your case.
My details
Name
Date of appointment
Hospital and clinician
Who is coming with me
What I know, what is unclear, changes to discuss
Saved in this browserWhat I know so far
What is unclear to me
Changes since last time
My questions
18 on the sheetNewly diagnosed
- 1.What is my exact diagnosis, stage, and grade, and which tests established them?
- 2.Which biomarkers have been tested on my tumour (for example MET exon 14 skipping by RNA or DNA sequencing, MET gene copy number by fluorescence in situ hybridisation or sequencing, c-Met immunohistochemistry, MET amplification in plasma or tissue at progression on osimertinib, Peripheral oedema and creatinine on MET inhibitors), and what were the results?
- 3.Which subtype is my cancer, and does that change the recommended treatment?
- 4.Is germline (inherited) genetic testing recommended for me or my family?
Advanced MET exon 14, first line or later
- 5.For my situation (advanced met exon 14, first line or later), which of the standard options do you recommend and why?
- 6.Am I a candidate for Capmatinib, Tepotinib, Capmatinib & tepotinib or related drugs, and what side effects should I expect?
- 7.How do the results of GEOMETRY mono-1 and Tepotinib Phase II in NSCLC Harboring MET Alterations (VISION) apply to someone like me?
MET amplification after osimertinib in EGFR-mutated disease
- 8.For my situation (met amplification after osimertinib in egfr-mutated disease), which of the standard options do you recommend and why?
- 9.Am I a candidate for Osimertinib, Savolitinib, Amivantamab, and what side effects should I expect?
- 10.How do the results of Osimertinib Plus Savolitinib in EGFRm+/MET+ NSCLC Following Prior Osimertinib and A Study of Amivantamab and Lazertinib in Combination With Platinum-Based Chemotherapy Compared With Platinum-Based Chemotherapy in Patients With Epidermal Growth Factor Receptor (EGFR)-Mutated Locally Advanced or Metastatic Non- Small Cell Lung Cancer After Osimertinib Failure apply to someone like me?
c-Met overexpression, previously treated non-squamous
- 11.For my situation (c-met overexpression, previously treated non-squamous), which of the standard options do you recommend and why?
- 12.Am I a candidate for Telisotuzumab vedotin, Docetaxel, and what side effects should I expect?
- 13.How do the results of LUMINOSITY and TeliMET NSCLC-01 apply to someone like me?
Any stage
- 14.Are there clinical trials I could join, for example of TeliMET NSCLC-01, Telisotuzumab adizutecan, Savolitinib, Osimertinib Plus Savolitinib in EGFRm+/MET+ NSCLC Following Prior Osimertinib?
- 15.Would a second opinion at a high-volume centre change anything, and can you help arrange it?
- 16.What supportive care (symptom control, nutrition, exercise, mental health, financial help) is available from the start?
- 17.I read that “MET amplification has no agreed threshold and results differ between assays”. How does that affect my plan?
- 18.I read that “Peripheral oedema limits the dose of every MET inhibitor and has no good treatment”. How does that affect my plan?
The words I may hear
- MET amplification (bypass resistance): When lung cancer switches on the MET receptor to bypass a blocked EGFR pill.
- Driver mutation: One of the few mutations in a tumour that actually causes it to grow.
- Tyrosine kinase inhibitor (TKI): Pills that block the on-switch enzyme (a kinase) that a particular cancer depends on: imatinib for CML, osimertinib for EGFR lung cancer, ibrutinib for CLL.
- Drug resistance (primary and acquired): Why cancer drugs stop working: the tumour either never depended on the target or evolves around the block.
Tests and results to bring
Biomarker results to ask for: MET exon 14 skipping by RNA or DNA sequencing (DNA panels miss some intronic variants), MET gene copy number by fluorescence in situ hybridisation or sequencing, c-Met immunohistochemistry (3+ in 50 percent or more of cells for telisotuzumab vedotin), MET amplification in plasma or tissue at progression on osimertinib, Peripheral oedema and creatinine on MET inhibitors.
Scans and tests linked to this cancer: Comprehensive genomic profiling.
Bring copies of scan reports, pathology and blood results, and a list of every medicine and supplement.
The treatments I may be offered
- MET amplification after osimertinib in EGFR-mutated disease: Osimertinib plus savolitinib (SAVANNAH, SACHI) where available; amivantamab plus chemotherapy; platinum-pemetrexed. (Osimertinib, Savolitinib, Osimertinib Plus Savolitinib in EGFRm+/MET+ NSCLC Following Prior Osimertinib, Amivantamab, A Study of Amivantamab and Lazertinib in Combination With Platinum-Based Chemotherapy Compared With Platinum-Based Chemotherapy in Patients With Epidermal Growth Factor Receptor (EGFR)-Mutated Locally Advanced or Metastatic Non- Small Cell Lung Cancer After Osimertinib Failure, MET amplification (bypass resistance))
- Advanced MET exon 14, first line or later: Capmatinib (GEOMETRY mono-1) or tepotinib (VISION); platinum-pemetrexed with or without pembrolizumab if the inhibitor is not tolerated or after it. (Capmatinib, GEOMETRY mono-1, Tepotinib, Tepotinib Phase II in NSCLC Harboring MET Alterations (VISION), Capmatinib & tepotinib, Pemetrexed, Carboplatin)
- c-Met overexpression, previously treated non-squamous: Telisotuzumab vedotin (LUMINOSITY) after platinum chemotherapy; TeliMET NSCLC-01 versus docetaxel is confirmatory. (Telisotuzumab vedotin, LUMINOSITY, TeliMET NSCLC-01, Docetaxel)
From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.
Answers and next steps
Saved in this browserWhat I was told
Agreed next steps, dates and who to call