NTRK fusion-positive non-small-cell lung cancer
Prepared with OnCo (onco.cc/prep/ntrk-fusion-nsclc/). Orientation, not medical advice; your team knows your case.
My details
What I know, what is unclear, changes to discuss
Saved in this browserMy questions
12 on the sheet- 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 NTRK1, NTRK2 and NTRK3 fusions by RNA sequencingor DNA panel, Pan-TRK immunohistochemistry as a screen, NTRK resistance mutationsat progression, Brain MRI), 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?
- 5.For my situation (advanced, first line or after chemotherapy), which of the standard options do you recommend and why?
- 6.Am I a candidate for Larotrectinib, Entrectinib, Repotrectinib or related drugs, and what side effects should I expect?
- 7.How do the results of NAVIGATE and Basket Study of Entrectinib (RXDX-101) for the Treatment of Patients With Solid Tumors Harboring NTRK 1/2/3 (Trk A/B/C), ROS1, or ALK Gene Rearrangeme apply to someone like me?
- 8.Are there clinical trials I could join, for example of Repotrectinib, A Study of Repotrectinib (TPX-0005) in Patients With Advanced Solid Tumors Harboring ALK, ROS1, or NTRK1-3 Rearrangements?
- 9.Would a second opinion at a high-volume centre change anything, and can you help arrange it?
- 10.What supportive care (symptom control, nutrition, exercise, mental health, financial help) is available from the start?
- 11.I read that “Fusions are missed when only DNA panels are run”. How does that affect my plan?
- 12.I read that “Neurological side effects from TRK inhibition are class-wide”. How does that affect my plan?
The words I may hear
- On-target resistance mutations (gatekeeper, solvent-front, compound): When a cancer becomes resistant to a targeted pill, it often does so by changing the exact spot where the drug binds: a 'gatekeeper' or 'solvent-front' mutation.
- Oncogene addiction: When a cancer depends so completely on one mutated gene that blocking it collapses the tumour.
- Gene fusion: A gene fusion is two genes broken and joined together, creating a hybrid protein that can drive cancer.
- Tumour-agnostic (tissue-agnostic) approval: A tumour-agnostic approval lets a drug be used for any cancer carrying a specific molecular feature, regardless of where it started.
- Brain metastases (intracranial disease): Tumour deposits that have travelled to the brain from a cancer elsewhere, ten times more common than cancers that start in the brain, mostly from lung, breast, melanoma and kidney cancer.
Tests and results to bring
Biomarker results to ask for: NTRK1, NTRK2 and NTRK3 fusions by RNA sequencing (preferred) or DNA panel, Pan-TRK immunohistochemistry as a screen, NTRK resistance mutations (solvent front, gatekeeper) at progression, Brain MRI.
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
- Advanced, first line or after chemotherapy: Larotrectinib or entrectinib under their tumour-agnostic approvals; repotrectinib after resistance to either; chemoimmunotherapy as for driver-negative disease before or after. (Larotrectinib, NAVIGATE, Entrectinib, Basket Study of Entrectinib (RXDX-101) for the Treatment of Patients With Solid Tumors Harboring NTRK 1/2/3 (Trk A/B/C), ROS1, or ALK Gene Rearrangeme, Repotrectinib, Tumour-agnostic (tissue-agnostic) approval, Pembrolizumab, Carboplatin, Pemetrexed)
From the standard of care recorded for this cancer; which apply depends on your stage and biomarkers. Ask which the team recommends and why.